High Vitamin D Levels associated with an 82% reduction in Breast Cancer Incidence

High Vitamin D Levels associated with an 82% reduction in Breast Cancer Incidence

High Vitamin D Levels associated with an 82% reduction in Breast Cancer Incidence

“We found that participants with blood levels of 25(OH)D that were above 60 ng/ml had one-fifth the risk of breast cancer compared to those with less than 20 ng/ml,” said principal investigator and co-author Cedric F. Garland, DrPH, adjunct professor in the UC San Diego Department of Family Medicine and Public Health. Risk of cancer appeared to decline with greater levels of serum vitamin D.

Breast cancer risk markedly lower with serum 25-hydroxyvitamin D concentrations 60 vs 20 ng/ml (150 vs 50 nmol/L): Pooled analysis of two randomized trials and a prospective cohort McDonnell SL, Baggerly CA, French CB, Baggerly LL, Garland CF, et al. (2018) Breast cancer risk markedly lower with serum 25-hydroxyvitamin D concentrations 60 vs 20 ng/ml (150 vs 50 nmol/L): Pooled analysis of two randomized trials and a prospective cohort. PLOS ONE 13(6): e0199265. https://doi.org/10.1371/journal.pone.0199265

Scientists halt breast cancer spread

Scientists halt breast cancer spread

 

Scientists have discovered that an amino acid called asparagine is essential for breast cancer spread, and by restricting it, cancer cells stopped invading other parts of the body in mice, according to new research.

Citation: Asparagine bioavailability governs metastasis in a model of breast cancer. Nature, 2018; DOI: 10.1038/nature25465

Asparagine, breast cancer, head cancer, neck cancer, spread, metastasis, halt, diet

Annual screening does not cut breast cancer deaths, suggests Canadian study

Highlights:
– Annual screening in women aged 40-59 does not reduce mortality from breast cancer beyond that of physical examination
– .Canada decided to compare breast cancer incidence and mortality up to 25 years in over 89,000 women aged 40-59 who did or did not undergo mammography screening
– During the 25 year study period, 3,250 women in the mammography arm and 3,133 in the control arm were diagnosed with breast cancer and 500 and 505, respectively, died of breast cancer
– Furthermore, the study shows that 22% of screen detected breast cancers were over-diagnosed
* 25-year study from Canada published on bmj.com today. FEB 2014 Continue reading “Annual screening does not cut breast cancer deaths, suggests Canadian study”

LSUHSC research finds combo of plant nutrients killed 100% of sample breast cancer cells

Contact: Leslie Capo lcapo@lsuhsc.edu 504-568-4806 Louisiana State University Health Sciences Center

New Orleans, LA – A study led by Madhwa Raj, PhD, Research Professor in Obstetrics and Gynecology at LSU Health Sciences Center New Orleans and its Stanley S. Scott Cancer Center, has found that a super cocktail of six natural compounds in vegetables, fruits, spices and plant roots killed 100% of sample breast cancer cells without toxic side effects on normal cells. The results, which also revealed potential treatment target genes, are published in the November 2013 issue of The Journal of Cancer.

Continue reading “LSUHSC research finds combo of plant nutrients killed 100% of sample breast cancer cells”

Young breast cancer patients often overestimate benefit of having healthy breast removed (unlikely to improve their chance of survival )

Contact: Robbin Ray robbin_ray@dfci.harvard.edu 617-632-4090 Dana-Farber Cancer Institute

BOSTON — Young women with breast cancer often overestimate the odds that cancer will occur in their other, healthy breast, and decide to have the healthy breast surgically removed, a survey conducted by Dana-Farber Cancer Institute investigators indicates. The survey also shows that many patients opt for the procedure  —  known as a contralateral prophylactic mastectomy, or CPM  —  despite knowing it will be unlikely to improve their chance of survival.

The study, published in the Sept. 17 issue of the Annals of Internal Medicine, shows a certain disconnect between what many patients know on an abstract, intellectual level  —  that CPM has little impact on survival rates for most women  —  and the choices they make after receiving the anxiety-inducing diagnosis of breast cancer, the authors say.

“An increasing percentage of women treated for early-stage breast cancer are choosing to have CPM,” says the study’s lead author, Shoshana Rosenberg, ScD, MPH, of the Susan F. Smith Center for Women’s Cancers at Dana-Farber. “The trend is particularly notable among younger women.”

The survey results, explains Rosenberg, suggest that many patients are going into this decision with an unrealistic sense of the benefits of CPM, and of the risks. “Improving the communication of those risks and benefits  —  together with better management of anxiety surrounding diagnosis  —  and providing patients with the support they need to make decisions based on solid evidence  —  are worthwhile steps,” says Rosenberg.

In the survey, researchers canvassed 123 women age 40 or younger who had undergone a bilateral mastectomy  —  the removal of both breasts  —  despite having cancer in only one breast. Respondents answered questions about their reasons for having the procedure, their knowledge of its risks and benefits, and their satisfaction with the outcome.

Almost all the women said they opted for CPM out of a desire to improve their chances of survival and prevent the cancer from spreading to other parts of the body. At the same time, however, most understood that removing both breasts does not extend survival for women who are free of an inherited genetic predisposition to breast cancer.

To explain this apparent contradiction, the authors write, “Most women acknowledge that CPM does not improve survival, but anxiety and fear of recurrence probably influence them during the decision-making process.”

The survey also indicated that women who don’t inherit an increased genetic risk of breast cancer tend to overestimate the chance that cancer will develop in both breasts. They estimated that 10 out of 100 women with cancer in one breast would develop cancer in the other breast within five years. The actual risk of that happening is approximately 2 to 4 percent.

By contrast, respondents who did have an inherited predisposition to breast cancer  —  as a result of a mutation in the genes BRCA1 or BRCA2, for example  —  more accurately perceived their risk for cancer in both breasts.

Even as they overestimated the benefits of CPM, many of the participants underestimated the severity of some of its side effects. Many respondents said the effect of CPM on their appearance was worse than they had expected. A substantial proportion of the respondents  —  42 percent  —  reported that their sense of sexuality after CPM was worse than expected, although other studies have not found sexual problems to be prevalent.

“Our findings underscore how important it is that doctors effectively communicate the risks and benefits of CPM to women,” Rosenberg says. “We need to be sure that women are making informed decisions, supported decisions, based on an accurate understanding of the pros and cons of the procedure, and in a setting where anxiety and concerns can be addressed.”

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The senior author of the study is Ann Partridge, MD, MPH, of the Susan F. Smith Center for Women’s Cancers and director of the Program for Young Women with Breast Cancer at Dana-Farber.

Co-authors are Michaela Tracy, Meghan Meyer, Shari Gelber, MS, MSW, Judi Hirshfield-Bartek, MS, and Eric Winer, MD, of the Susan F. Smith Center for Women’s Cancers at Dana-Farber; Karen Sepucha, PhD, and Lidia Schapira, MD, of Massachusetts General Hospital; Susan Troyan, MD, of Brigham and Women’s Hospital; Monica Morrow, MD, of Memorial Sloan-Kettering Cancer Center; and Steven Come, MD, of Beth Israel Deaconess Medical Center.

Funding for the study was provided by the National Cancer Institute (NIH 5 R25 CA057711) and Susan G. Komen for the Cure.

Written by Rob Levy

About Dana-Farber Cancer Institute

Dana-Farber Cancer Institute is a principal teaching affiliate of the Harvard Medical School and is among the leading cancer research and care centers in the United States. It is a founding member of the Dana-Farber/Harvard Cancer Center, designated a comprehensive cancer center by the National Cancer Institute. It provides adult cancer care with Brigham and Women’s Hospital as Dana-Farber/Brigham and Women’s Cancer Center and it provides pediatric care with Boston Children’s Hospital as Dana-Farber/Boston Children’s Cancer and Blood Disorders Center. Dana-Farber is the top ranked cancer center in New England, according to U.S. News & World Report, and one of the largest recipients among independent hospitals of National Cancer Institute and National Institutes of Health grant funding. Follow Dana-Farber on Facebook and on Twitter.

Antihypertensives linked with increased breast cancer risk in postmenopausal women

Contact: Kristen Woodward media@fhcrc.org 206-667-2210 Fred Hutchinson Cancer Research Center

Calcium-channel blockers in particular are associated with significantly increased risk

SEATTLE – Older women who take certain types of medication to combat high blood pressure may be putting themselves at greater risk for developing breast cancer, according to a new study by a team of Fred Hutchinson Cancer Research Center scientists led by Christopher Li, M.D., Ph.D. The study is the first to observe that long-term use of a class of antihypertensive drugs known as calcium-channel blockers in particular are associated with breast cancer risk. The team’s findings will be published online Aug. 5 in JAMA Internal Medicine.

Antihypertensive drugs are the most frequently prescribed type of medications in the United States, with more than 678 million prescriptions filled in 2010, nearly 98 million of which were for calcium-channel blockers.

Despite widespread and often long-term use of these drugs, studies and evidence linking antihypertensives to breast cancer have been sparse and inconsistent.

“Because hypertension is a chronic condition, most people with high blood pressure use antihypertensive drugs chronically and will often stay on the same regimen for long periods of time,” said Li, head of the Translational Research Program and member of the Public Health Sciences Division at Fred Hutch. “Characterizing their potential associations with the most common cancer in women is an important clinical and public health issue, particularly with the increasing availability of alternative options to manage hypertension.”

In addition to calcium-channel blockers, other classes of antihypertensive drugs include angiotensin-converting-enzyme (ACE) inhibitors, angiotensin-receptor blockers, beta blockers and diuretics. Combinations of such drugs are also prescribed. “Each drug has different potential benefits as well as side effects,” Li said. “Choice of which regimen a patient is given depends on their tolerance of medication, other conditions, and whether their hypertension can be managed by a single drug or requires a combination of drugs.”

The purpose of the Hutch study was to assess the relationship between the major classes of antihypertensive drugs and risk of the two most common histological types of breast cancers in the United States: invasive ductal carcinomas, which represent approximately 70 percent of all breast cancers; and invasive lobular carcinomas, which represent an estimated 20 percent.

The study’s key finding was that women currently taking calcium-channel blockers who have used them for 10 years or longer had an approximately two and a half times higher risk of both invasive ductal and invasive lobular cancers compared to those who never used such calcium-channel blockers and compared to users of other forms of antihypertensives.  In contrast, the study found that use of other classes of antihypertensive drugs, including diuretics, beta blockers and angiotensin-receptor blockers, were not associated with an increased risk of breast cancer, even when used long term.

Li’s team interviewed 1,763 study participants, all between the ages of 55-74 from the Puget Sound region, including 880 with invasive ductal cancer, 1,027 with invasive lobular cancer, and 856 cancer-free controls. Participants were interviewed in person to establish detailed histories of hypertension and heart disease, as well as risk factors for cancer, including family history, obesity, smoking and alcohol use.  Through a series of structured questions, researchers also gathered detailed data regarding use of antihypertensive drugs, including beginning and end dates of use, drug names, dose, route of administration, pattern of use and indication.

While calcium-channel blockers in particular appear to have an implication for increased cancer risk in cases of long-term use, the drugs have a broad spectrum of physiological effects, and more research will be required to understand the underlying biological mechanisms potentially responsible for the added risk. Calcium-channel blockers function by regulating the influx of calcium into muscle cells, decreasing arterial resistance and heart muscle oxygen demand. Some hypothesize that these drugs may increase cancer risk because they inhibit programmed cell death, or apoptosis, but supporting evidence is lacking.

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The National Cancer Institute funded the study.

Editor’s note: Please contact Kristen Woodward, Fred Hutch media relations, to schedule an interview. To obtain a copy of the JAMA Internal Medicine paper, “Use of Antihypertensive Medications and Breast Cancer Risk Among Women 55-74 Years of Age,” please contact the journal at 312-464-5262 or mediarelations@jamanetwork.org.

About Fred Hutchinson Cancer Research Center

At Fred Hutchinson Cancer Research Center, home to three Nobel laureates, interdisciplinary teams of world-renowned scientists seek new and innovative ways to prevent, diagnose and treat cancer, HIV/AIDS and other life-threatening diseases. Fred Hutch’s pioneering work in bone marrow transplantation led to the development of immunotherapy, which harnesses the power of the immune system to treat cancer with minimal side effects. An independent, nonprofit research institute based in Seattle, Fred Hutch houses the nation’s first and largest cancer prevention research program, as well as the clinical coordinating center of the Women’s Health Initiative and the international headquarters of the HIV Vaccine Trials Network. Private contributions are essential for enabling Fred Hutch scientists to explore novel research opportunities that lead to important medical breakthroughs. For more information visit http://www.fredhutch.org or follow Fred Hutch on Facebook, Twitter or YouTube.

Statins risk for women: Taking cholesterol-lowering drug for more than ten years ‘doubles chances of the most common breast cancer’

  • Previous studies had shown  cholesterol-lowering drugs can reduce the risk of certain cancers
  • Research had only looked at women on drugs  for less than five years
  • Experts say drugs could affect hormone  regulation which could lead to breast cancer

By  Pat Hagan

PUBLISHED: 16:17 EST, 19  July 2013 |  UPDATED: 18:05 EST, 19 July 2013

Statins are a major weapon against heart disease. The new findings raise concerns over the long-term safety of the drugs 

Statins are a major weapon against heart disease. The  new findings raise concerns over the long-term safety of the drugs

Women who take statins for more than a decade  face double the risk of contracting the most common type of breast  cancer.

Alarming findings raise new concerns over the  long-term safety of a widely prescribed medicine in the UK.

Previous studies have suggested the  cholesterol-lowering drugs, used by an estimated eight million men and women,  can reduce the risk of certain cancers – including the breast form of the  disease.

However, most research looked at patients who  had only been on them for five years or less.

The latest findings identified invasive  ductal carcinoma (IDC) which starts in the ducts of the breast before spreading  inwards. It accounts for around seven out of ten breast cancer cases.

The experts at the Fred Hutchinson Cancer  Research Centre in Seattle, US, also found the chances of getting invasive  lobular carcinoma, which accounts for ten to 15 per cent of breast cancers, went  up almost 2.5 times in some women on statins long-term.

Around 48,000 women in Britain are diagnosed  with breast cancer each year, equal to around 130 a day. A woman has a one in  nine chance of developing the disease at some point in her life.

The reasons why the anti-cholesterol pills  might stimulate cancer growth are unclear.

The researchers said one explanation may be  that statins affect hormone regulation in the body, especially as the study  found women on the drugs were significantly more likely to suffer cancers driven  by the hormone oestrogen.

 

They said it’s possible that while short-term  use does appear to have a protective effect against breast cancer, in the  long-run statins may damage certain chemical pathways that lead to growth of  tumours.

The report found: ‘As more women are taking  them and for longer durations it is possible we will observe effects that prior  studies could not detect.’

Last night, leading UK cancer bodies called  for urgent research to clarify the risks to women.

But they urged patients on statins not to  stop taking them without consulting their GP.

The researchers said statins could affect hormone regulation in the body, especially as the study found women on the drugs were significantly more likely to suffer cancers driven by the hormone oestrogen 

The researchers said statins could affect hormone  regulation in the body, especially as the study found women on the drugs were  significantly more likely to suffer cancers driven by the hormone  oestrogen

Sally Greenbrook, from the charity  Breakthrough Breast Cancer, said: ‘Any study suggesting a potential link between  statins and breast cancer risk should not be taken lightly. But these drugs are  extremely effective at reducing the risk of cardiovascular  disease.’

Jessica Harris, of Cancer Research UK, said:  ‘There’s been a huge amount of research into the link between statins and  cancer.

‘But so far there’s no conclusive answer,  with some studies showing a reduced risk, some no link, and others showing a  raised risk.’

Statins have also emerged as a major weapon  against heart disease in the last 20 years.

The latest research, published in the journal  Cancer Epidemiology Biomarkers and Prevention, examined how long-term statin use  affected breast cancer risk in women aged between 55 and 74.

The researchers studied just under 2,000  women diagnosed with either IDC or ILC between 2000 and 2008 and a separate  group of 902 women of a similar age profile but who were free of  cancer.

Around 370 men a year in the UK are diagnosed  with breast cancer – but the latest research did not investigate the cancer risk  of men taking statins.

Read more: http://www.dailymail.co.uk/health/article-2370825/Statins-risk-women-Taking-cholesterol-lowering-drug-years-doubles-chances-common-breast-cancer.html#ixzz2ZY2BmQQY Follow us: @MailOnline on Twitter | DailyMail on Facebook

Omega-3 fatty acids more effective at inhibiting growth of triple-negative breast cancer

Contact: Diana Quattrone diana.quattrone@fccc.edu 215-728-7784 Fox Chase Cancer Center

 

 

WASHINGTON, DC (April 9, 2013)—Researchers from Fox Chase Cancer Center have found that omega-3 fatty acids and their metabolite products slow or stop the proliferation, or growth in the number of cells, of triple-negative breast cancer cells more effectively than cells from luminal types of the disease. The omega-3s worked against all types of cancerous cells, but the effect was observed to be stronger in triple-negative cell lines, reducing proliferation by as much as 90 percent. The findings will be presented at the AACR Annual Meeting 2013 on Tuesday, April 9.

Omega-3 fatty acids are found in oily fish like sardines and salmon, and also in oils derived from plants like hemp and flax. Previous studies suggest these compounds can negatively affect critical mechanisms in cancer cells, namely those responsible for proliferation and for apoptosis, or programmed cell death. Lead author on the study Thomas J. Pogash, a scientific technician in the Fox Chase Cancer Center lab of Jose Russo, MD, says the new work underscores the important role common compounds found in food may play in keeping cancer at bay.

“Diet can play a critical role in breast cancer prevention,” says Pogash. “When you compare a western diet to a mediterranean diet, which has more omega-3s, you see less cancer in the mediterranean diet. They eat much more fish.”

Breast cancer is a heterogeneous group of cancers comprising diseases that differ on the molecular level. Patients with different types of breast cancer respond differently to treatments. Four distinct categories of the disease are generally recognized. Two of those, luminal A and luminal B, grow in the luminal cells that line milk ducts in the breast and have receptors for estrogen and progesterone (prognosis is generally better for patients with luminal A than with luminal B). A third category includes tumors that test positive for the HER2 receptor.

Tumors in the fourth category, triple-negative, lack receptors for progesterone, estrogen, and a protein called HER2/neu. As a result, this type of disease is insensitive to treatments like trastuzumab, which disrupts the HER2 receptor, and tamoxifen, which targets the estrogen receptor.

Russo notes that no targeted therapies are currently available for patients diagnosed with triple-negative breast cancer. Combination chemotherapies are the standard of care for early-stage disease.

“This type of cancer, which is found more frequently in Latina and African-American women, is highly aggressive and has a low survival rate,” says Russo. “There is not any specific treatment for it.”

When a cancer cell digests omega-3s, the fatty acid is broken down into smaller molecules called metabolites. Russo, Pogash, and their colleagues tested the effect of large omega-3 parent molecules, as well as their smaller metabolic derivatives, on three luminal cell lines and seven lines that included basal-type triple-negative cells.

Omega-3 and its metabolites were observed to inhibit proliferation in all cell lines, but the effect was dramatically more pronounced in the triple-negative cell lines. In addition, the metabolites of omega-3 reduced the motility, or ability to move, by 20-60 percent in the triple-negative basal cell lines.

This study is part of a consortium between Fox Chase Cancer Center and Pennsylvania State University under a five-year grant awarded by the Komen Foundation. Russo is the principal investigator of the project at Fox Chase. Andrea Manni, MD, leader of the Pennsylvania State University team, has extended this work to animal models, studying the anticancer effects of omega-3s and its metabolites on mouse models of triple-negative breast cancer.

Russo and his colleagues are working on two related projects, one on the role of epigenetic events in the mechanism of cell transformation and another on the potential action of peptides of the hormone human chorionic gonadotropin (hCG) on breast cancer prevention.

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In addition to Russo, Manni, and Pogash, investigators on this project included Ricardo López de Cicco, Benjamin Pressly, and Irma H. Russo at Fox Chase Cancer Center; and Julie A. Himmelberger at DeSales University; and Shantu Amin, Krishne Gowda, and Karam El-Bayoumy at Pennsylvania State University.

Fox Chase Cancer Center, part of Temple University Health System, is one of the leading cancer research and treatment centers in the United States. Founded in 1904 in Philadelphia as one of the nation’s first cancer hospitals, Fox Chase also was among the first institutions to receive the National Cancer Institute’s prestigious comprehensive cancer center designation in 1974. Fox Chase researchers have won the highest awards in their fields, including two Nobel Prizes. Fox Chase physicians are routinely recognized in national rankings, and the Center’s nursing program has achieved Magnet status for excellence three consecutive times. Fox Chase conducts a broad array of nationally competitive basic, translational, and clinical research and oversees programs in cancer prevention, detection, survivorship, and community outreach. For more information, call 1-888-FOX-CHASE (1-888-369-2427) or visit http://www.foxchase.org.

OMEGA-3s Inhibit Breast Cancer Tumour Growth, U of G Study Finds

February 21, 2013 – News Release

A lifelong diet rich in omega-3 fatty acids can inhibit growth of breast cancer tumours by 30 per cent, according to new research from the University of Guelph.

The study, published recently in the Journal of Nutritional Biochemistry, is believed to be the first to provide unequivocal evidence that omega-3s reduce cancer risk.

“It’s a significant finding,” said David Ma, a professor in Guelph’s Department of Human Health and Nutritional Sciences, and one of the study’s authors.

“We show that lifelong exposure to omega-3s has a beneficial role in disease prevention – in this case, breast cancer prevention. What’s important is that we have proven that omega-3s are the driving force and not something else.”

Breast cancer remains the most common form of cancer in women worldwide and is the second leading cause of female cancer deaths.

Advocates have long believed diet may significantly help in preventing cancer. But epidemiological and experimental studies to back up such claims have been lacking, and human studies have been inconsistent, Ma said.

“There are inherent challenges in conducting and measuring diet in such studies, and it has hindered our ability to firmly establish linkages between dietary nutrients and cancer risk,” he said.

“So we’ve used modern genetic tools to address a classic nutritional question.”

For their study, the researchers created a novel transgenic mouse that both produces omega-3 fatty acids and develops aggressive mammary tumours. The team compared those animals to mice genetically engineered only to develop the same tumours.

“This model provides a purely genetic approach to investigate the effects of lifelong omega-3s exposure on breast cancer development,” Ma said.

“To our knowledge, no such approach has been used previously to investigate the role of omega-3s and breast cancer.”

Mice producing omega-3s developed only two-thirds as many tumours – and tumours were also 30-per-cent smaller – as compared to the control mice.

“The difference can be solely attributed to the presence of omega-3s in the transgenic mice – that’s significant,” Ma said.

“The fact that a food nutrient can have a significant effect on tumour development and growth is remarkable and has considerable implications in breast cancer prevention.”

Known as an expert in how fats influence health and disease, Ma hopes the study leads to more research on using diet to reduce cancer risk and on the benefits of healthy living.

“Prevention is an area of growing importance. We are working to build a better planet, and that includes better lifestyle and diet,” he said.

“The long-term consequences of reducing disease incidence can have a tremendous effect on the health-care system.”

The study also involved lead author Mira MacLennan, a former U of G graduate student who is now studying medicine at Dalhousie University; U of G pathobiology professor Geoffrey Wood; former Guelph graduate students Shannon Clarke and Kate Perez; William Muller from McGill University; and Jing Kang from Harvard Medical School.

Funding for this research came from the Canadian Breast Cancer Research Alliance/Canadian Institutes of Health Research, the Canada Foundation for Innovation and the Ontario Research Fund.

Contact: Prof. David Ma Department of Human Health and Nutritional Sciences davidma@uoguelph.ca 519 824-4120, Ext: 52272/53906

For media questions, contact Communications and Public Affairs: Lori Bona Hunt, 519-824-4120, Ext. 53338, or lhunt@uoguelph.ca; or Kevin Gonsalves, Ext. 56982, or kgonsalves@uoguelph.ca.

Liver cancer survival time tripled by virus: JX-594

The virus used in the vaccine that helped eradicate smallpox is now working its magic on liver cancer. A genetically engineered version of the vaccinia virus has trebled the average survival time of people with a severe form of liver cancer, with only mild, flu-like side effects.Thirty people with hepatocellular carcinoma received three doses of the modified virus – code-named JX-594 – directly into their liver tumour over one month. Half the volunteers received a low dose of the virus, the other half a high dose. Members of the low and high-dose groups subsequently survived for, on average, 6.7 and 14.1 months respectively. By contrast, trials several years ago showed that sorafenib, the best existing medication for this cancer, prolonged life by only three months.

Two of the patients on the highest viral dose were still alive more than two years after the treatment. “It’s a very substantial survival benefit,” says Laurent Fischer, president of Jennerex, the company in San Francisco developing the treatment under the trade name Pexa-Vec.

Besides shrinking the primary tumour, the virus was able to spread to and shrink any secondary tumours outside the liver. “Some tumours disappeared completely, and most showed partial destruction on MRI scans,” says David Kirn, head of the study at Jennerex. Moreover, the destruction was equally dramatic in the primary and secondary tumours.

“This clinical trial is an exciting step forward to help find a new way of treating cancers,” says Alan Melcher of the University of Leeds, UK, who was not involved in the study. “It helps demonstrate the cancer-fighting potential of viruses, which have relatively few side effects compared with traditional chemo or radiotherapy,” he says. “If it proves effective in larger trials, it could be available to patients within five years.”

The fact that the virus appears able to spread to secondary tumours suggests that simply injecting the virus into the bloodstream may be effective. A trial to compare this treatment with injecting the virus directly into a tumour is under way.

Targeted at cancer

The virus has had a gene coding for an enzyme called thymidine kinase snipped out. The enzyme enables the virus to recognise and infect dividing cells. By removing the gene, the virus’s developers have reduced the likelihood of healthy dividing cells being infected.

Instead, the virus exclusively attacks cancerous tissue, by targeting two genes that have increased activity in tumour cells. One genes is associated with an epidermal growth factor receptor, which stimulates the cancer to grow. The other is associated with a vascular endothelial growth factor, which enables the cancer to recruit its own blood supply. The virus reduces the activity of both genes, causing the infected cancer cell to wither and die.

What’s more, the virus carries extra genes to prod the body’s own immune system into action against the cancer. One produces granulocyte colony stimulating factor, a protein that encourages production of extra white blood cells at sites of infection. The other produces a protein not naturally found in humans, called Lac-Z, that earmarks infected cells for destruction.

Fischer says that to date, more than 200 people have received the virus, which has also shown promise against other types of cancer, including those of the kidney and skin. But he warns that not everyone sees a benefit. “We know why patients respond, but not why they don’t,” he says.

Journal reference: Nature Medicine, DOI: 10.1038/nm.3089

http://www.newscientist.com/article/dn23154-liver-cancer-survival-time-tripled-by-virus.html

 

Vitamin D Holds Promise in Battling a Deadly Breast Cancer, SLU Researchers Say

January 22, 2013

Carrie Bebermeyer
314.977.8015
Fight Against Triple-Negative Breast Cancer Takes Three Steps Forward
ST. LOUIS — In research published in the Jan. 21 issue of The Journal of Cell Biology, a team led by Susana Gonzalo, Ph.D., assistant professor of biochemistry and molecular biology at Saint Louis University, has discovered a molecular pathway that contributes to triple-negative breast cancer, an often deadly and treatment resistant form of cancer that tends to strike younger women. In addition, Gonzalo and her team identified vitamin D and some protease inhibitors as possible new therapies and discovered a set of three biomarkers that can help to identify patients who could benefit from the treatment.

Susana Gonzalo, Ph.D. with members of her lab team. From left to right, Stanley Kanai, Ignacio Gonzalez-Suarez, David Grotsky, Sree Yaddanapudi, Susana Gonzalo, Abena Redwood and Martin Neumann. This photo appeared in The Journal of Cell Biology.

In the recent breakthrough, which was funded in part by a $500,000 Department of Defense grant, Gonzalo’s lab identified one pathway that is activated in breast cancers with the poorest prognosis, such as those classified as triple-negative. These cancers often strike younger women and are harder to treat than any other type of breast cancer. Women who are born with BRCA1 gene mutations are at increased risk for developing breast and ovarian cancers within their lifetime, and the tumors that arise are frequently the triple-negative type. Although chemotherapy is the most effective treatment for triple-negative breast cancer, it has profound secondary effects. Understanding the biology of triple-negative breast cancers will help to develop less toxic therapeutic strategies.

Experiments performed in Gonzalo’s laboratory, in collaboration with the laboratories of Xavier Matias-Guiu and Adriana Duso (IRBLleida, Spain), showed that activation of this novel pathway not only allows tumor cells to grow unchecked, but also explains the reduced sensitivity of these types of tumors to current therapeutic strategies. Importantly, vitamin D plays a role in turning off this pathway, providing a safe and cost-effective strategy to fight these types of tumors.

THE SCIENCE

For molecular biologists like Gonzalo who look for answers below the cellular level to discover why some people develop cancer, the search often involves tracing a chain of events to try to understand cause and effect of the behavior between several genes and the proteins which they express. In order to understand these complex pathways, researchers often turn levels of proteins on or off by expressing one gene or suppressing another. Part of a researcher’s challenge is determining what the function of each component of a pathway is.

The cell employs a complex mechanism to protect genetic information and ensure that damaged DNA is not passed on to daughter cells. Cells have built in checkpoints and fail safes to ensure the accuracy of their DNA code and are able to slow or stop their own proliferation if the information is compromised. Loss of these checkpoints and the accumulation of damaged DNA often leads to cancer.

The Pathway BRCA1 is a well-established tumor suppressor gene. Women who carry mutations in this gene have a high risk of developing breast and ovarian cancer. Tumors that arise often lack expression of three receptors: estrogen, progesterone and HER2 (thus, “triple-negative”), and do not respond to hormone therapy.

BRCA1 is important because it is involved in repairing DNA double-strand breaks, a kind of DNA damage that is especially dangerous for the integrity of our genome. BRCA1 also is involved in cell-cycle checkpoints after damage, which are control mechanisms during cell proliferation that make sure the DNA information has been accurately replicated and transferred to the daughter cells. Thus, BRCA1 is considered a safeguard of the genome.

Loss of BRCA1 is bad news for the information contained in a cell’s genetic blueprint. It results in genomic instability characterized by unrepaired DNA breaks and chromosomal aberrations that compromise cell viability. How BRCA1-mutated cells are able to form tumors has been a long-standing question. Investigators recently showed that loss of another DNA repair factor, 53BP1, allows proliferation and survival of BRCA1-deficient cells. In addition, decreased levels of 53BP1 were observed in triple-negative breast cancers, and correlated with resistance to drugs at the forefront of cancer treatment, such as PARP inhibitors.

Gonzalo’s team has found a pathway responsible for the loss of 53BP1 in breast cancers with poor prognosis, specifically BRCA1 mutated and triple-negative. It turns out that loss of BRCA1 increases the expression of a protease, known as cathepsin L (CTSL), which causes the degradation of 53BP1. Cells that have lost both BRCA1 and 53BP1 have the ability to repair DNA, maintain the integrity of the genome, and proliferate. Thus, the protease helps cells with faulty BRCA1 to survive.

The Fix If lowering the levels of 53BP1 allows BRCA1 deficient cells to thrive and do their worst, increasing the levels of the protein offers a promising strategy for treatment of breast tumors.

So, how to do this? In previous research, Gonzalo’s team showed that vitamin D inhibits CTSL-mediated degradation of 53BP1 in non-tumor cells, as efficiently as specific CTSL inhibitors. This time, they found that treatment of BRCA1-deficient tumor cells with vitamin D restores high levels of 53BP1, which results in increased genomic instability and reduced proliferation. Importantly, their evidence suggests that vitamin D treatment might restore the sensitivity to PARP inhibitors in patients who become resistant. Thus, a combination of vitamin D and PARP inhibitors could represent a novel therapeutic strategy for breast cancers with poor prognosis.

So, with this chain of events, Gonzalo and colleagues demonstrated a pathway by which triple-negative breast cancers proliferate: BRCA1-deficient cells activate CTSL which minimizes levels of 53BP1 to overcome genomic instability and growth arrest.

The Patients In a final exceptionally useful discovery, Gonzalo and collaborators found that high levels of nuclear CTSL and low levels of 53BP1 and nuclear vitamin D receptor (VDR) are a clear marker that identifies certain triple-negative breast cancer patients, biomarkers that offer the potential to customize future breast cancer therapies. In particular, this triple-biomarker signature will allow the identification of patients in whom the pathway is on and who might benefit the most from vitamin D treatment.

BOTTOM LINE:

  • Researchers have discovered a way in which one of the deadliest and most difficult to treat breast cancers allows tumor cells to grow unchecked and how these tumors resist treatment. Specifically, they found that BRCA1-deficient cells activate CTSL which leads to lower levels of the protein 53BP1 which, in turn, allows cancer cells to grow unchecked.
  • In addition, they discovered the potential for a new therapy involving vitamin D, and identified biomarkers that can help identify which patients could benefit from this therapy.
  • In the future, women with triple-negative breast cancer may benefit from a treatment that includes vitamin D.  As with all laboratory research, vitamin D therapy will have to be studied in a clinical trial before doctors know how safe or effective it will be.
  • Researchers’ next steps will be to study molecular mechanisms behind the activation of the degradation of 53BP1 by CTSL. In addition, preclinical studies with vitamin D and cathepsin inhibitors as single agents or in combination with different drugs are underway in mouse models of breast cancers.

Established in 1836, Saint Louis University School of Medicine has the distinction of awarding the first medical degree west of the Mississippi River. The school educates physicians and biomedical scientists, conducts medical research, and provides health care on a local, national and international level. Research at the school seeks new cures and treatments in five key areas: cancer, liver disease, heart/lung disease, aging and brain disease, and infectious disease.

Harms from breast cancer screening outweigh benefits if death caused by treatment is included

Contact: Emma Dickinson edickinson@bmjgroup.com 44-020-738-36529 BMJ-British Medical Journal

Cancer expert remains to be convinced by breast screening review

Harms from breast cancer screening outweigh benefits if death caused by treatment is included

Michael Baum, Professor emeritus of surgery at University College London says that, while deaths from breast cancer may be avoided, any benefit will be more than outweighed by deaths due to the long term adverse effects of treatment.

He estimates that, for every 10, 000 women invited for screening, three to four breast cancer deaths are avoided at the cost of 2.72 to 9.25 deaths from the long term toxicity of radiotherapy.

These figures contrast with an independent report on breast cancer screening, led by Sir Michael Marmot and published in November last year. Marmot and his committee were charged with asking whether the screening programme should continue, and if so, what women should be told about the risks of overdiagnosis.

They concluded that screening should continue because it prevented 43 deaths from breast cancer for every 10,000 women invited for screening.

The downside was an estimated 19% rate of overdiagnosis: 129 of the 681 cancers detected in those 10,000 women would have done them no harm during their lifetime. However, those women would have undergone unnecessary treatment, including surgery, radiotherapy and chemotherapy.

But despite this higher than previous estimate of overdiagnosis, they concluded that the breast screening programme should continue.

The report also judged that screening reduces the risk of dying from breast cancer by 20%. But Professor Baum disputes these figures, saying the analysis takes no account of improvements in treatment since these trials were done, which will reduce the benefits of screening. Nor does it make use of more recent observational data.

With these data included, estimated rates of overdiagnosis as a result of screening increase to up to 50%, he argues.

This is important because it can change the decisions women make when invited for screening. In a study also published today, researchers at the University of Sydney explored attitudes to screening in a sample of 50 women. Many of the women were surprised when they were told about overdiagnosis and most said they would attend screening if overdiagnosis rates were 30% or lower, but a rate of 50% made most of them reconsider.

An accompanying editorial points out that the harms of screening will reduce as more effective diagnostic  processes develop to inform less harmful and more personalised treatments. In the meantime, it says women need up to date and transparent information about the benefits and harms of screening to help them make informed choices.

Herbal treatments for postmenopausal symptoms can be recommended as an alternative to HRT

Contact: Rebecca Jones rjones@rcog.org.uk 020-777-26444 Wiley

Herbal and complementary medicines could be recommended as an alternative to hormone replacement therapy (HRT) for treating postmenopausal symptoms says a new review published today in The Obstetrician and Gynaecologist (TOG).

The review outlines the advantages and limitations of both pharmacological and herbal and complementary treatments for women with postmenopausal symptoms.

The menopause is defined as the time after a woman’s menstrual periods have ceased (12 months after a woman’s final menstrual period). It is associated with an estrogen deficiency and can cause an increase in vasomotor symptoms (hot flushes), genitourinary symptoms (vaginal dryness, sexual dysfunction, frequent urinary tract infections, urinary incontinence), and musculoskeletal symptoms (joint pain) as well as sleep and mood disturbance.

One of the most common menopausal symptoms is hot flushes; approximately two-thirds of postmenopausal women will experience them, and 20% of women can experience them for up to 15 years, states the review.

Estrogen deficiency can also lead to longer-term health issues such as cardiovascular disease and osteoporosis. While pharmacological agents are available to treat postmenopausal symptoms, many non-pharmacological treatment options are also available.

HRT is the most effective treatment of hot flushes, improving symptoms in 80 – 90% of women, says the review. However, the author notes that there are possible health risks associated with HRT, such as links to breast cancer, blood clots, stroke, and cardiovascular problems.

Due to these possible risks, other treatment options may be equally effective, such as behaviour modification and herbal and complimentary medicines, says the author.

The review states that as many as 50 – 75% of postmenopausal women use herbal options to treat hot flushes, and of the complimentary therapies, soy, red clover and black cohosh have been the most investigated.

Soy is the most common plant containing estrogen, found naturally in food and supplements. Previous research has shown a reduction in hot flush symptoms with soy ranging from 20 – 55%. Red clover, a legume also containing estrogen, and black cohosh, a plant originating from the eastern United States and Canada, have also been reported to ease postmenopausal symptoms.

The author of the review recommends these herbal treatments as there are no significant adverse side effects associated with them, as long as they are used in women who do not have a personal history of breast cancer, are not at high risk for breast cancer, and are not taking tamoxifen. However, the review notes that herbal medicines are not regulated in many countries, and therefore the contents of a given product may vary from sample to sample.

Iris Tong, Director of Women’s Primary Care at the Women’s Medicine Collaborative, The Warren Alpert Medical School of Brown University, Rhode Island, and author of the review said:

“Up to 75% of women use herbal and complimentary medicines to treat their postmenopausal symptoms. Therefore, it is vitally important for healthcare providers to be aware of and informed about the non-pharmacological therapies available for women who are experiencing postmenopausal symptoms and who are looking for an alternative to HRT.”

TOG‘s Editor –in-Chief, Jason Waugh said:

“Postmenopausal symptoms can be very distressing and it is important to review the advantages and limitations of the non-pharmacological treatments available as well as the pharmacological ones. Even simple behaviour modification can make a difference to postmenopausal symptoms, including keeping the room temperature cool, wearing layered clothing, relaxation techniques and smoking cessation.”

Watercress may ‘turn off’ breast cancer signal

2010 study posted for filing

Contact: Sophie Docker S.Docker@soton.ac.uk 0044-023-805-98933 University of Southampton

The research, unveiled at a press conference today (14 September 2010), shows that the watercress compound is able to interfere with the function of a protein which plays a critical role in cancer development.

As tumours develop they rapidly outgrow their existing blood supply so they send out signals which make surrounding normal tissues grow new blood vessels into the tumour which feed them oxygen and nutrients.

The research, led by Professor Graham Packham of the University of Southampton, shows that the plant compound (called phenylethyl isothiocyanate) found in watercress can block this process, by interfering with and ‘turning off’ in the function of a protein called Hypoxia Inducible Factor (HIF).

Professor Packham, a molecular oncologist at the University of Southampton, comments: “The research takes an important step towards understanding the potential health benefits of this crop since it shows that eating watercress may interfere with a pathway that has already been tightly linked to cancer development.

“Knowing the risk factors for cancer is a key goal and studies on diet are an important part of this. However, relatively little work is being performed in the UK on the links between the foods we eat and cancer development.”

Working with Barbara Parry, Senior Research Dietician at the Winchester and Andover Breast Unit, Professor Packham performed a pilot study in which a small group of breast cancer survivors, underwent a period of fasting before eating 80g of watercress  (a cereal bowl full) and then providing a series of blood samples over the next 24 hours.

The research team was able to detect significant levels of the plant compound PEITC in the blood of the participants following the watercress meal, and most importantly, could show that the function of the protein HIF was also measurably affected in the blood cells of the women.

The two studies, which have been published in the British Journal of Nutrition and Biochemical Pharmacology, provide new insight into the potential anti-cancer effects of watercress, although more work still needs to be done to determine the direct impact watercress has on decreasing cancer risk.

Watercress Alliance member Dr Steve Rothwell says: “We are very excited by the outcome of Professor Packham’s work, which builds on the body of research which supports the idea that watercress may have an important role to play in limiting cancer development.”

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A summary of the research has been accepted for inclusion in the Breast Cancer Research Conference which is taking place in Nottingham from 15 to 17 September.

Breast cancer is the most common cancer in women in the western world and currently affects approximately 1 in 9 women during their lifetime.

Study shows how dietary supplement may block cancer cells

2010 study posted for filing

 

Contact: Darrell E. Ward Darrell.Ward@osumc.edu 614-293-3737 Ohio State University Medical Center

COLUMBUS, Ohio – Researchers at the Ohio State University Comprehensive Cancer Center-Arthur G. James Cancer Hospital and Richard J. Solove Research Institute (OSUCCC-James) have discovered how a substance that is produced when eating broccoli and Brussels sprouts can block the proliferation of cancer cells.

Compelling evidence indicates that the substance, indole-3-carbinol (I3C), may have anticancer effects and other health benefits, the researchers say. These findings show how I3C affects cancer cells and normal cells.

The laboratory and animal study discovered a connection between I3C and a molecule called Cdc25A, which is essential for cell division and proliferation. The research showed that I3C causes the destruction of that molecule and thereby blocks the growth of breast cancer cells.

The study was published online June 29 in the journal Cancer Prevention Research.

“Cdc25A is present at abnormally high levels in about half of breast cancer cases, and it is associated with a poor prognosis,” says study leader Xianghong Zou, assistant professor of pathology at the Ohio State University Medical Center.

The molecule also occurs at abnormally high levels in cancers of the breast, prostate, liver, esophagus, endometrium and colon, and in non-Hodgkin lymphoma, and in other diseases such as Alzheimer’s disease, he noted.

“For this reason, a number of anti-Cdc25 agents have been identified, but they have not been successful for cancer prevention or treatment due to concerns about their safety or efficacy,” says Zou, who is also a member of the OSUCCC-James Molecular Carcinogenesis and Chemoprevention program.

“I3C can have striking effects on cancer cells,” he explains, “and a better understanding of this mechanism may lead to the use of this dietary supplement as an effective and safe strategy for treating a variety of cancers and other human diseases associated with the overexpression of Cdc25A,” Zou says.

For this study, Zou and his colleagues exposed three breast cancer cell lines to I3C. These experiments revealed that the substance caused the destruction of Cdc25A. They also pinpointed a specific location on that molecule that made it susceptible to I3C, showing that if that location is altered (because of a gene mutation), I3C no longer causes the molecule’s destruction.

Last, the investigators tested the effectiveness of I3C in breast tumors in a mouse model. When the substance was given orally to the mice, it reduced tumor size by up to 65 percent. They also showed that I3C had no affect on breast-cell tumors in which the Cdc25A molecule had a mutation in that key location.

Peaches, plums induce deliciously promising death of breast cancer cells

2010 study posted for filing

 

Contact: Kathleen Phillips ka-phillips@tamu.edu 979-845-2872 Texas A&M AgriLife Communications

      AUDIO:   Breast cancer cells — even the most aggressive type — died after treatments with peach and plum extracts in lab tests at Texas AgriLife Research recently, and scientists say the…Click here for more information.

 

COLLEGE STATION — Breast cancer cells – even the most aggressive type – died after treatments with peach and plum extracts in lab tests at Texas AgriLife Research recently, and scientists say the results are deliciously promising. Not only did the cancerous cells keel over, but the normal cells were not harmed in the process.

AgriLife Research scientists say two phenolic compounds are responsible for the cancer cell deaths in the study, which was published in the Journal of Agriculture and Food Chemistry. The phenols are organic compounds that occur in fruits. They are slightly acidic and may be associated with traits such as aroma, taste or color.

“It was a differential effect which is what you’re looking for because in current cancer treatment with chemotherapy, the substance kills all cells, so it is really tough on the body,” said Dr. David Byrne, AgriLife Research plant breeder who studies stone fruit. “Here, there is a five-fold difference in the toxic intensity. You can put it at a level where it will kill the cancer cells – the very aggressive ones – and not the normal ones.”

Byrne and Dr. Luis Cisneros-Zevallos originally studied the antioxidants and phytonutrients in plums and found them to match or exceed the blueberry which had been considered superior to other fruits in those categories.

“The following step was to choose some of these high antioxidant commercial varieties and study their anticancer properties,” Cisneros-Zevallos said. “And we chose breast cancer as the target because it’s one of the cancers with highest incidence among women. So it is of big concern.”

According to the National Cancer Institute, there were 192,370 new cases of breast cancer in females and 1,910 cases in males in 2009. That year, 40,170 women and 440 men died from breast cancer. The World Health Organization reports that breast cancer accounts for 16 percent of the cancer deaths of women globally.

      IMAGE:   Breast cancer cells — even the most aggressive type — died after treatments with peach and plum extracts in lab tests at Texas AgriLife Research.Click here for more information.

 

Cisneros-Zevallos, an AgriLife Research food scientist, said the team compared normal cells to two types of breast cancer, including the most aggressive type. The cells were treated with an extract from two commercial varieties, the “Rich Lady” peach and the “Black Splendor” plum.

“These extracts killed the cancer cells but not the normal cells,” Cisneros-Zevallos said.

A closer look at the extracts determined that two specific phenolic acid components – chlorogenic and neochlorogenic – were responsible for killing the cancer cells while not affecting the normal cells, Cisneros-Zevallos said.

The two compounds are very common in fruits, the researchers said, but the stone fruits such as plums and peaches have especially high levels.

“So this is very, very attractive from the point of view of being an alternative to typical chemotherapy which kills normal cells along with cancerous ones,” Byrne added.

The team said laboratory tests also confirmed that the compounds prevented cancer from growing in animals given the compounds.

Byrne plans to examine more fully the lines of the varieties that were tested to see how these compounds might be incorporated into his research of breeding plums and peaches. Cisneros-Zevallos will continue testing these extracts and compounds in different types of cancer and conduct further studies of the molecular mechanisms involved.

###

The work documenting the health benefits of stone fruit has been supported by the Vegetable and Fruit Improvement Center at Texas A&M University, the U.S. Department of Agriculture and the California Tree Fruit Agreement.

79th Health Research Report 08 APR 2010 – Reconstruction

 

In this Issue:

 

1. Chemical exposure before mid-30s may be critical in breast cancer development Postmenopausal breast cancer and occupational exposures

2. American industry’s thirst for water: First study of its kind in 30 years

3. Medicine residues may threaten fish reproduction

4. Researchers show some cells in pancreas can spontaneously change into insulin-producing cells

5. Exposure to 3 classes of common chemicals may affect female development

6. Did seasonal flu vaccination increase the risk of infection with pandemic H1N1 flu?

7. Eating eggs for breakfast helps reduce calorie consumption throughout the day by 18 percent

8. Mouth Breathing Can Cause Major Health Problems

9. Supplement your stem cells

10. BUSPH study links rheumatoid arthritis to vitamin D deficiency

Public release date: 31-Mar-2010

Chemical exposure before mid-30s may be critical in breast cancer development Postmenopausal breast cancer and occupational exposures

Occupational exposure to certain chemicals and pollutants before a woman reaches her mid-30s could treble her risk of developing cancer after the menopause, suggests research published in Occupational and Environmental Medicine .

Women exposed to synthetic fibres and petroleum products during the course of their work seem to be most at risk, the research suggests.

The researchers base their findings on more than 1100 women, 556 of whom were diagnosed with breast cancer in 1996/7 in Montreal, Canada, when aged between 50 and 75 and who had gone through the menopause.

The other 613 women, who were matched for age and date of diagnosis, had a range of other cancers, and were intended to act as a comparison group.

An expert team of chemists and industrial hygienists then set about investigating the women’s levels of exposure to around 300 different substances throughout the course of their employment history.

After taking account of the usual factors associated with an increased risk of breast cancer, the analysis indicated a link between occupational exposure to several of these substances.

Compared with the comparison group, this risk peaked for exposures before the age of 36, and was magnified with each additional decade of exposure before this age.

This resulted in women occupationally exposed to acrylic fibres running a seven-fold risk of breast cancer, while those exposed to nylon fibres almost doubled their risk.

When tumours were divided into their hormonal responsiveness, women whose cancers responded to oestrogen, but not progesterone, were at least twice as likely to have breast cancer for every 10 year period they were exposed to monaromatic hydrocarbons (a byproduct of crude oil) and acrylic and rayon fibres.

Exposure to polycyclic aromatic hydrocarbons, found in petroleum products, before the age of 36, tripled the risk for women whose tumours were responsive to both oestrogen and progesterone.

The authors concede that their findings could be due to chance alone, but say they are consistent with the theory that breast tissue is more sensitive to harmful chemicals if the exposure occurs when breast cells are still active – in other words, before a woman reaches her 40s. And they point to the rising incidence of breast cancer in developed countries, which is likely to be due to a range of factors, including diagnosis of small slow growing tumours and changes in alcohol consumption.

But environmental and workplace factors are also thought to have a role, they suggest, with previously published evidence implicating exposure to certain chemicals, low frequency electromagnetic fields, and disruption of the body clock.

Public release date: 31-Mar-2010

American industry’s thirst for water: First study of its kind in 30 years

How many gallons of water does it take to produce $1 worth of sugar, dog and cat food, or milk? The answers appear in the first comprehensive study in 30 years documenting American industry’s thirst for this precious resource. The study, which could lead to better ways to conserve water, is in ACS’ Environmental Science & Technology, a semi-monthly journal.

Chris Hendrickson and colleagues note in the new study that industry (including agriculture) long has been recognized as the biggest consumer of water in the United States. However, estimates of water consumption on an industry-by-industry basis are incomplete and outdated, with the last figures from the U.S. Census Bureau dating to 1982.

They estimated water use among more than 400 industry sectors — from finished products to services — using a special computer model. The new data shows that most water use by industry occurs indirectly as a result of processing, such as packaging and shipping food crops to the supermarket, rather than direct use, such as watering crops. Among the findings for consumer products: It takes almost 270 gallons of water to produce $1 worth of sugar; 200 gallons of water to make $1 worth of dog and cat food; and 140 gallons of water to make $1 worth of milk. “The study gives a way to look at how we might use water more efficiently and allows us to hone in on the sectors that use the most water so we can start generating ideas and technologies for better management,” the scientists note.

Public release date: 31-Mar-2010

Medicine residues may threaten fish reproduction

Researchers at Umeå University and the Sahlgrenska Academy at the University of Gothenburg have discovered that traces of many medicines can be found in fish that have been swimming in treated waste water. One such medicine, the hormone levonorgestrel, was found in higher concentrations in the blood of fish than in women who take the contraceptive pill. Elevated levels of this hormone can lead to infertility in fish.

The study is published in the journal Environmental Science and Technology. The fish in the study were exposed to treated waste water from three sewage treatment works in Stockholm, Umeå and Gothenburg. The study shows that levonorgestrel – which is found in many contraceptive pills, including the morning-after pill – can impact on the environment and constitutes a risk factor for the ability of fish to reproduce. Levonogestrel is designed to mimic the female sex hormone progesterone and is produced synthetically.

A study from Germany showed very recently that less than a billionth of a gram of levonorgestrel per litre inhibited the reproduction of fish in aquarium-based trials.

”We are finding these levels in treated waste water in Sweden,” explains Jerker Fick at the Department of Chemistry at Umeå University.

For around ten years it has been known that synthetic oestrogen from contraceptive pills can affect fish that live downstream from sewage treatment works. The new study shows that synthetic progesterone-like hormones in contraceptive pills also carry risks.

The fish in the study were exposed to undiluted waste water, whilst in the natural environment there tends to be a degree of dilution in watercourses. But the study pointed out that there are also watercourses with very little dilution, and probably treatment plants that filter out the hormone less effectively than those included in the study. These findings will help to improve our understanding of which substances need to be removed from waste water.

”If we know how our medicines affect the environment, we will be in a better position to choose environmentally friendly alternatives, though we must always put the health of patients first,” says Joakim Larsson at the Sahlgrenska Academy, one of the researchers behind the study.

Public release date: 5-Apr-2010

Researchers show some cells in pancreas can spontaneously change into insulin-producing cells

NEW YORK, April 5, 2010 – Alpha cells in the pancreas, which do not produce insulin, can convert into insulin-producing beta cells, advancing the prospect of regenerating beta cells as a cure for type 1 diabetes. The findings come from a study at the University of Geneva, co-funded by the Juvenile Diabetes Research Foundation, that is published today in the online edition of the scientific journal Nature.

The researchers, led by Dr. Pedro L. Herrera, demonstrated that beta cells will spontaneously regenerate after near-total beta cell destruction in mice and the majority of the regenerated beta cells are derived from alpha cells that had been reprogrammed, or converted, into beta cells. Using a unique model of diabetes in mice, in which nearly all of the beta cells are rapidly destroyed, the researchers found that if the mice were maintained on insulin therapy, beta cells were slowly and spontaneously restored, eventually eliminating the need for insulin replacement. Alpha cells normally reside alongside beta cells in the pancreas and secrete a hormone called glucagon, which works opposite to insulin to regulate the levels of sugar in the blood. Alpha cells are not attacked by the autoimmune processes that destroy beta cells and causes type 1 diabetes.

Type 1 diabetes is a chronic, autoimmune disease that affects children, adolescents and adults, in which the immune system attacks the beta cells in the pancreas that produce insulin, a hormone that enables people to convert food into energy. People with type 1 diabetes are dependent on insulin treatment for the rest of their life.

Dr. Herrera’s results are the first to show that beta cell reprogramming can occur spontaneously, without genetic alterations. Previous efforts to reprogram non-beta cells into beta cells relied on genetic manipulations – processes that can not be easily translated into therapies.

According to Dr. Andrew Rakeman, JDRF Program Manager in Beta Cell Therapies, the breakthrough in Dr. Herrera’s work is the demonstration that alpha- to-beta-cell reprogramming can be a natural, spontaneous process., “If we can understand the signals that are triggering this conversion, it will open a whole new potential strategy for regenerating beta cells in people with type 1 diabetes,” he said. “It appears that the body can restore beta cell function either through reprogramming alpha cells to become beta cells or, as previously shown by others, by increasing growth of existing beta cells. This path may be particularly useful in individuals who have had the disease for a long time and have no, or very few, remaining beta cells.”

Role of Removing Beta Cells

Dr. Herrera’s team genetically engineered the animals to be susceptible to a toxin that would destroy only their beta cells. When the mice were exposed to the toxin, the beta cells were rapidly and efficiently destroyed – greater than 99% just 15 days after treatment. Then, to track the source of newly regenerated beta cells, Dr. Herrera’s team used another genetic manipulation to permanently label mature alpha cells and all their descendents with a fluorescent protein. This “genetic lineage tracing” approach allowed the scientists to track the fate of the alpha cells and their progeny; the presence of fluorescently labeled beta cells in the recovered animals gave conclusive evidence that alpha cells had reprogrammed into beta cells.

The Geneva researchers pointed out that the critical factor in sparking the alpha-to- beta-cell reprogramming was removing (or ablating) nearly all the original insulin-producing cells in the mice. In mice where the loss of beta cells was more modest, the researchers either found no evidence of beta cell regeneration (when only half the cells were destroyed) or less alpha cell reprogramming (when less than 95% of cells were destroyed).

“The amount of beta-cell destruction thus appears to determine whether regeneration occurs. Moreover, it influences the degree of cell plasticity and regenerative resources of the pancreas in adult organisms,” said Dr. Herrera.

Regeneration Research

In type 1 diabetes, the immune system attacks beta cells, stopping a person’s pancreas from producing insulin, the hormone that enables people to get energy from sugar. JDRF has been at the forefront of diabetes research looking to develop therapeutics to drive the regeneration of insulin-producing cells within a person’s body (as an alternative to transplanting insulin-producing cells from other sources). Beta cell regeneration involves triggering the body to grow its own new insulin producing cells, either by copying existing ones – some are usually still active, even in people who have had diabetes for decades – or causing the pancreas to create new ones.

This study is another step forward for JDRF’s research focus on Regeneration as a potential pathway to restore insulin production – and normal blood sugar in people with type 1 diabetes. JDRF has become a leader in this new and exciting research field, funding a wide range of research projects, including studies like Dr. Herrera’s, and an innovative diabetes drug discovery and development partnership with the Genomics Institute of the Novartis Foundation (GNF), focused on regeneration approaches.

In addition to regenerating or replacing insulin producing cells, a cure for type 1 diabetes will also require stopping the autoimmune attack that causes diabetes, and reestablishing excellent glucose control.

Public release date: 5-Apr-2010

Exposure to 3 classes of common chemicals may affect female development

Researchers at Mount Sinai School of Medicine have found that exposure to three common chemical classes—phenols, phthalates and phytoestrogens—in young girls may disrupt the timing of pubertal development, and put girls at risk for health complications later in life. The study, the first to examine the effects of these chemicals on pubertal development, is currently published online in the journal Environmental Health Perspectives.

“Research has shown that early pubertal development in girls can have adverse social and medical effects, including cancer and diabetes later in life,” said Dr. Mary Wolff, Professor of Preventive Medicine and Oncological Sciences at Mount Sinai School of Medicine. “Our research shows a connection between chemicals that girls are exposed to on a daily basis and either delayed or early development. While more research is needed, these data are an important first step in continuing to evaluate the impact of these common environmental agents in putting girls at risk.”

Phenols, phthalates and phytoestrogens are among chemicals known as endocrine disruptors, which interfere with the body’s endocrine, or hormone, system. They are found in a wide range of consumer products, such as nail polishes, where they increase durability, and in cosmetics, perfumes, lotions, and shampoos, where they carry fragrance. Some are used to increase the flexibility and durability of plastics such as PVC, or are included as coatings on medications or nutritional supplements to make them timed-release.

Dr. Wolff, co-principal investigator Susan Teitelbaum, PhD, Associate Professor, Preventive Medicine, and their team from Mount Sinai’s departments of Pediatrics and Microbiology recruited girls from the neighborhood of East Harlem, a unique minority population considered high risk. Working with Cincinnati Children’s Hospital and Kaiser Permanente Northern California, they analyzed the impact of exposure to environmental agents in a study that included 1,151 girls from New York, greater Cincinnati and northern California.

The girls were between 6- and 8-years-old at enrollment and between 7 and 9 at analysis. Researchers collected urine samples from the study participants and analyzed them for phenols, phthalates, and phytoestrogens, including 19 separate urine biomarkers.

The data showed that the three classes of chemical compounds were widely detectable in the study population, and that high exposure to certain chemicals was associated with early breast development. The strongest links were seen with phthalates and phytoestrogens, which were also among the highest exposures. One phenol, two phytoestrogens, and a subset of phthalates (those found in building products and plastic tubing) were associated with later puberty. However, the phthalates found in personal products such as lotion and shampoo, especially those with fragrance, were related to earlier breast and pubic hair development.

“We believe that there are certain periods of vulnerability in the development of the mammary gland, and exposure to these chemicals may influence breast cancer risk in adulthood,” Dr. Wolff continued. “Dietary habits may also have an impact. Further study is needed to determine how strong the link is.”

Consistent with previous studies, researchers also found that body-mass index (BMI) played a role in the onset of puberty. About a third of the girls were considered overweight, which is also an indicator of early breast development. As a result, some of the chemical associations differed in more or less obese girls. Researchers continue to study the impact of diet on pubertal development and eventual breast cancer risk.

“Exposure to these chemicals is extremely common,” Dr. Wolff continued. “As such, while the association between chemicals and pubertal development seems small, the impact on the overall population is significant.”

 

Public release date: 6-Apr-2010

 

Did seasonal flu vaccination increase the risk of infection with pandemic H1N1 flu?

In September 2009, news stories reported that researchers in Canada had found an increased risk of pandemic H1N1 (pH1N1) influenza in people who had previously been vaccinated against seasonal influenza. Their research, consisting of four different studies, has now undergone further scientific peer review and is published in the open access journal PLoS Medicine.

Did previous vaccination against seasonal flu increase the risk of getting pH1N1 flu? Based on these studies – conducted by a large network of investigators across Canada led by Principal Investigator Danuta Skowronski of the British Columbia Centre for Disease Control in Vancouver, in collaboration with provincial leads Gaston De Serres in Quebec, Natasha Crowcroft in Ontario and Jim Dickinson in Alberta – the answer remains: “possibly.”

In a school outbreak of pH1N1 in spring 2009, people with cough and fever were found to have received prior seasonal flu vaccination more often than those without. Several public health agencies in Canada therefore undertook four additional studies during the summer of 2009 to investigate further. Taken together, the four studies included approximately 2,700 people with and without pH1N1.

The first of the studies used an ongoing sentinel monitoring system to assess the frequency of prior vaccination with the 2008󈝵 seasonal vaccine in people with pH1N1 influenza (cases) compared to people without evidence of infection with an influenza virus (controls). This study confirmed that the seasonal vaccine provided protection against seasonal influenza, but found it to be associated with an increased risk of approximately 68% for pH1N1 disease.

 

The further 3 studies (which included additional case-control investigations in Ontario and Quebec, as well as a transmission study in 47 Quebec households where pH1N1 influenza had occurred) similarly found between 1.4𔃀.5 times increased likelihood of pH1N1 illness in people who had received the seasonal vaccine compared to those who had not. Prior seasonal vaccination was not associated with an increase in hospitalization among those who developed pH1N1 illness.

These studies do not show whether there was a true cause-and-effect relationship between seasonal flu vaccination and subsequent pH1N1 illness (as might occur if, for example, the seasonal vaccine modified the immune response to pH1N1), or whether the observed association was not a result of vaccination, but was instead due to differences in some unidentified factor(s) among the groups being studied.

If the findings from these studies are real they raise important questions about the biological interactions between pre-existing and novel pandemic influenza strains. The researchers note, however, that the World Health Organization has recommended that pH1N1 be included in subsequent seasonal vaccine formulations. This will provide direct protection against pH1N1 and thereby obviate any risk that might have been due to the seasonal vaccine in 2009, which did not include pH1N1.

In an accompanying commentary in PLoS Medicine, Lone Simonsen and Cécile Viboud, who were not involved in the studies, write: “Given the uncertainty associated with observational studies, we believe it would be premature to conclude that increased the risk of 2009 pandemic illness, especially in light of six other contemporaneous observational studies in civilian populations that have produced highly conflicting results.” They conclude that “this perplexing experience should teach us how to best react to disparate and conflicting studies and prepare us for the next public health crisis, so that we can better manage future alerts for unexpected risk factors.”

Public release date: 6-Apr-2010

Eating eggs for breakfast helps reduce calorie consumption throughout the day by 18 percent

New research reports that eating protein in the morning helps manage hunger

Park Ridge, Ill. (April 6, 2010) – A new study demonstrates that eating protein-rich eggs for breakfast reduces hunger and decreases calorie consumption at lunch and throughout the day. The study, published in the February issue of Nutrition Research, found that men who consumed an egg-based breakfast ate significantly fewer calories when offered an unlimited lunch buffet compared to when they ate a carbohydrate-rich bagel breakfast of equal calories.(1) This study supports previous research which revealed that eating eggs for breakfast as part of a reduced-calorie diet helped overweight dieters lose 65 percent more weight and feel more energetic than dieters who ate a bagel breakfast of equal calories and volume.(2)

“There is a growing body of evidence that supports the importance of high-quality protein in the diet for overall health and in particular the importance of protein at the breakfast meal,” said Maria Luz Fernandez, Ph.D., study author and professor in the department of nutritional sciences at the University of Connecticut. “We examined two typical American breakfasts, and the participants’ self-reported appetite ratings reveal that a protein-rich breakfast helps keep hunger at bay.”

Public release date: 6-Apr-2010

Mouth Breathing Can Cause Major Health Problems

Dentists May Be First to Diagnose Patients Who Mouth Breathe

CHICAGO (April 6, 2010) – For some, the phrase “spring is in the air” is quite literal. When the winter snow melts and flowers bloom, pollen and other materials can wreak havoc on those suffering from seasonal allergies, usually causing a habit called “mouth breathing.” The physical, medical and social problems associated with mouth breathing are not recognized by most health care professionals, according to a study published in the January/February 2010 issue of General Dentistry, the peer-reviewed clinical journal of the Academy of General Dentistry (AGD). Dentists typically request that their patients return every six months, which means that some people see their dentist more frequently than they see their physician. As a result, dentists may be the first to identify the symptoms of mouth breathing. And, because dentists understand the problems associated with mouth breathing, they can help prevent the adverse effects.

“Allergies can cause upper airway obstruction, or mouth breathing, in patients,” said Yosh Jefferson, DMD, author of the study. “Almost every family has someone with mouth breathing problems.”

Over time, children whose mouth breathing goes untreated may suffer from abnormal faci al and dental development, such as long, narrow faces and mouths, gummy smiles, gingivitis and crooked teeth. The poor sleeping habits that result from mouth breathing can adversely affect growth and academic performance. As

Dr. Jefferson notes in his article, “Many of these children are misdiagnosed with attention deficit disorder (ADD) and hyperactivity.” In addition, mouth breathing can cause poor oxygen concentration in the bloodstream, which can cause high blood pressure, heart problems, sleep apnea and other medical issues.

“Children who mouth breathe typically do not sleep well, causing them to be tired during the day and possibly unable to concentrate on academics,” Dr. Jefferson said. “If the child becomes frustrated in school, he or she may exhibit behavioral problems.”

Treatment for mouth breathing is available and can be beneficial for children if the condition is caught early. A dentist can check for mouth breathing symptoms and swollen tonsils. If tonsils and/or adenoids are swollen, they can be surgically removed by an ear-nose-throat (ENT) specialist. If the face and mouth are narrow, dentists can use expansion appliances to help widen the sinuses and open nasal airway passages.

“After surgery and/or orthodontic intervention, many patients show improvement in behavior, energy level, academic performance, peer acceptance and growth,” says Leslie Grant, DDS, spokesperson for the AGD. “Seeking treatment for mouth breathing can significantly improve quality of life.”

At this time, many health care professionals are not aware of the health problems associated with mouth breathing. If you or your child suffers from this condition, speak with a health care professional who is knowledgeable about mouth breathing.

Public release date: 7-Apr-2010

Supplement your stem cells

A nutritional supplement could stimulate the production of stem cells integral for repairing the body. Research published in BioMed Central’s open access Journal of Translational Medicine suggests that a commercially-available supplement can increase the blood circulation of hematopoietic stem cells, which can give rise to all blood cells, and endothelial progenitor cells, which repair damage to blood vessels.

Thomas E. Ichim from Medistem Incorporated, USA worked with a team of 13 researchers from industry and academia to further investigate whether this supplement, containing a cocktail of green tea, astralagus, goji berry extracts, ‘good’ bacteria Lactobacillus fermentum, antioxidant ellagic acid, immune enhancer beta 1,3 glucan and vitamin D3, was able to increase the number of stem cells circulating in the blood. They recruited 18 healthy adults aged between 20 and 72 who stopped any other dietary supplements 4-5 days before starting a two-week course of this supplement, taking it twice daily. The researchers took blood from the participants before they started the course and on days 1, 2, 7 and 14 to test for signs of stem cell activity by looking for cells expressing the genetic stem cell markers CD133, CD34 and KDR. They then confirmed whether taking the supplement changed the overall levels of hematopoietic stem cells and endothelial progenitor cells in the blood by using HALO (Hematopoietic Assay via Luminescent Output) and colony forming assays respectively.

Hematopoietic stem cells and endothelial progenitor cells increased after taking the nutritional supplement, suggesting that the supplement may be a useful stimulator for both types of stem cells. In this study, the levels of these stem cells peaked at 2-7 days and started to drop at 14 days, suggesting that this supplement could be used for continuous treatment for conditions associated with decreases in these stem cells such as Alzheimer’s Disease. Other therapeutic treatments used to recruit hematopoietic stem cells are not viable as long-term solutions due to costs and increased health risks caused by the extremely high levels of stem cells that these treatments maintain in the blood.

“To our knowledge, this is the first study demonstrating profound mobilization effect with possible clinical significance by a food supplement-based approach”, say the authors, adding, “Indeed it may be possible that our supplement could be beneficial in conditions associated with reduced progenitor cells such as diabetes or in smokers which possess lower baseline values as compared to controls”. Although they are quick to add, “However, given commercial pressures associated with this largely unregulated field, we propose detailed scientific investigations must be made before disease-associated claims are made by the scientific community”.

Public release date: 7-Apr-2010

BUSPH study links rheumatoid arthritis to vitamin D deficiency

Women living in the northeastern United States are more likely to develop rheumatoid arthritis (RA), suggesting a link between the autoimmune disease and vitamin D deficiency, says a new study led by a Boston University School of Public Health researcher.

In the paper, which appears online in the journal Environmental Health Perspectives, a spatial analysis led by Dr. Verónica Vieira, MS, DSc, associate professor of environmental health, found that women in states like Vermont, New Hampshire and southern Maine were more likely to report being diagnosed with RA.

“There’s higher risk in the northern latitudes,” Dr. Vieira said. “This might be related to the fact that there’s less sunlight in these areas, which results in a vitamin D deficiency.”

The study looked at data from the Nurses’ Health Study, a long-term cohort study of U.S. female nurses. Looking at the residential addresses, health outcomes and behavioral risk factors for participants between 1988 and 2002, researchers based their findings on 461 women who had RA, compared to a large control group of 9,220.

RA is a chronic inflammatory disease that affects the lining of the joints, mostly in the hands and knees. This chronic arthritis is characterized by swelling and redness and can wear down the cartilage between bones. RA is two to three times more common in women than in men.

Although the cause of RA is unknown, the researchers wrote, earlier studies have shown that vitamin D deficiency, which can be caused by a lack of sunlight, has already been associated with a variety of other autoimmune diseases.

“A geographic association with northern latitudes has also been observed for multiple sclerosis and Crohn’s disease, other autoimmune diseases that may be mediated by reduced vitamin D from decreased solar exposure and the immune effects of vitamin D deficiency,” the authors wrote.

The authors said further research is needed to look into the relationship between vitamin D exposure and RA.

Dr. Vieira said she and her co-authors were somewhat surprised by the findings. A previous geographic study of RA had suggested an ecologic association with air pollution, she said.

“The results were unexpected,” Dr. Vieira said. “Prior to the analysis, we were more interested in the relationship with air pollution. I hadn’t given latitudes much thought.”

In addition to the geographic variation, the study suggested that the timing of residency may influence RA risk. “Slightly higher odds ratios were observed for the 1988 analysis suggesting that long term exposure may be more important than recent exposure,” the study said.

Dr. Vieira and other BUSPH researchers previously have used innovative spatial-temporal analyses to study the incidence of breast cancer, specifically focused on Cape Cod.

________________________________

 

These reports are done with the appreciation of all the Doctors, Scientist, and other

Medical Researchers who sacrificed their time and effort. In order to give people the

ability to empower themselves. Without the base aspirations for fame, or fortune.

Just honorable people, doing honorable things.

Health Research Report

79th Issue 08 APR 2010

Compiled By Ralph Turchiano

www.healthresearchreport.me www.vit.bz

www.youtube.com/vhfilm www.facebook.com/engineeringevil

www.engineeringevil.com

Chemical exposure before mid-30s may be critical in breast cancer development

2010 study posted for filing

Contact: Emma Dickinson edickinson@bmjgroup.com 44-020-738-36529 BMJ-British Medical Journal

Postmenopausal breast cancer and occupational exposures

Occupational exposure to certain chemicals and pollutants before a woman reaches her mid-30s could treble her risk of developing cancer after the menopause, suggests research published in Occupational and Environmental Medicine .

Women exposed to synthetic fibres and petroleum products during the course of their work seem to be most at risk, the research suggests.

The researchers base their findings on more than 1100 women, 556 of whom were diagnosed with breast cancer in 1996/7 in Montreal, Canada, when aged between 50 and 75 and who had gone through the menopause.

The other 613 women, who were matched for age and date of diagnosis, had a range of other cancers, and were intended to act as a comparison group.

An expert team of chemists and industrial hygienists then set about investigating the women’s levels of exposure to around 300 different substances throughout the course of their employment history.

After taking account of the usual factors associated with an increased risk of breast cancer, the analysis indicated a link between occupational exposure to several of these substances.

Compared with the comparison group, this risk peaked for exposures before the age of 36, and was magnified with each additional decade of exposure before this age.

This resulted in women occupationally exposed to acrylic fibres running a seven-fold risk of breast cancer, while those exposed to nylon fibres almost doubled their risk.

When tumours were divided into their hormonal responsiveness, women whose cancers responded to oestrogen, but not progesterone, were at least twice as likely to have breast cancer for every 10 year period they were exposed to monaromatic hydrocarbons (a byproduct of crude oil) and acrylic and rayon fibres.

Exposure to polycyclic aromatic hydrocarbons, found in petroleum products, before the age of 36, tripled the risk for women whose tumours were responsive to both oestrogen and progesterone.

The authors concede that their findings could be due to chance alone, but say they are consistent with the theory that breast tissue is more sensitive to harmful chemicals if the exposure occurs when breast cells are still active – in other words, before a woman reaches her 40s. And they point to the rising incidence of breast cancer in developed countries, which is likely to be due to a range of factors, including diagnosis of small slow growing tumours and changes in alcohol consumption.

But environmental and workplace factors are also thought to have a role, they suggest, with previously published evidence implicating exposure to certain chemicals, low frequency electromagnetic fields, and disruption of the body clock.

###

Mango effective in preventing, stopping certain colon, breast cancer cells

2010 study posted for filing

 

Contact: Kathleen Phillips ka-phillips@tamu.edu 979-845-2872 Texas A&M AgriLife Communications

COLLEGE STATION – Mango. If you know little about this fruit, understand this: It’s been found to prevent or stop certain colon and breast cancer cells in the lab.

That’s according to a new study by Texas AgriLife Research food scientists, who examined the five varieties most common in the U.S.: Kent, Francine, Ataulfo, Tommy/Atkins and Haden.

Though the mango is an ancient fruit heavily consumed in many parts of the world, little has been known about its health aspects. The National Mango Board commissioned a variety of studies with several U.S. researchers to help determine its nutritional value.

“If you look at what people currently perceive as a superfood, people think of high antioxidant capacity, and mango is not quite there,” said Dr. Susanne Talcott, who with her husband, Dr. Steve Talcott, conducted the study on cancer cells. “In comparison with antioxidants in blueberry, acai and pomegranate, it’s not even close.”

But the team checked mango against cancer cells anyway, and found it prevented or stopped cancer growth in certain breast and colon cell lines, Susanne Talcott noted.

“It has about four to five times less antioxidant capacity than an average wine grape, and it still holds up fairly well in anticancer activity. If you look at it from the physiological and nutritional standpoint, taking everything together, it would be a high-ranking super food,” she said. “It would be good to include mangoes as part of the regular diet.”

The Talcotts tested mango polyphenol extracts in vitro on colon, breast, lung, leukemia and prostate cancers. Polyphenols are natural substances in plants and are associated with a variety of compounds known to promote good health.

Mango showed some impact on lung, leukemia and prostate cancers but was most effective on the most common breast and colon cancers.

“What we found is that not all cell lines are sensitive to the same extent to an anticancer agent,” she said. “But the breast and colon cancer lines underwent apotosis, or programmed cell death. Additionally, we found that when we tested normal colon cells side by side with the colon cancer cells, that the mango polyphenolics did not harm the normal cells.”

The duo did further tests on the colon cancer lines because a mango contains both small molecules that are readily absorbed and larger molecules that would not be absorbed and thus remain present in a colon.

“We found the normal cells weren’t killed, so mango is not expected to be damaging in the body,” she said. “That is a general observation for any natural agent, that they target cancer cells and leave the healthy cells alone, in reasonable concentrations at least.”

The Talcotts evaluated polyphenolics, and more specifically gallotannins as being the class of bioactive compounds (responsible for preventing or stopping cancer cells). Tannins are polyphenols that are often bitter or drying and found in such common foods as grape seed, wine and tea.

The study found that the cell cycle, which is the division cells go through, was interrupted. This is crucial information, Suzanne Talcott said, because it indicates a possible mechanism for how the cancer cells are prevented or stopped.

“For cells that may be on the verge of mutating or being damaged, mango polyphenolics prevent this kind of damage,” she said.

The Talcotts hope to do a small clinical trial with individuals who have increased inflamation in their intestines with a higher risk for cancer.

“From there, if there is any proven efficacy, then we would do a larger trial to see if there is any clinical relevance,” she said.

###

According to the National Mango Board, based in Winter Park, Fla., most mangoes consumed in the U.S. are produced in Mexico, Ecuador, Peru, Brazil, Guatemala and Haiti. Mangoes are native to southeast Asia and India and are produced in tropical climates. They were introduced to the U.S. in the late 1800s, and a few commercial acres still exist in California and Florida.

Spices halt growth of breast stem cells, U-M study finds ( Curcumin, piperine )

2009 study posted for filing

Contact: Nicole Fawcett nfawcett@umich.edu 734-764-2220 University of Michigan Health System

ANN ARBOR, Mich. — A new study finds that compounds derived from the spices turmeric and pepper could help prevent breast cancer by limiting the growth of stem cells, the small number of cells that fuel a tumor’s growth.

Researchers at the University of Michigan Comprehensive Cancer Center have found that when the dietary compounds curcumin, which is derived from the Indian spice turmeric, and piperine, derived from black peppers, were applied to breast cells in culture, they decreased the number of stem cells while having no effect on normal differentiated cells.

“If we can limit the number of stem cells, we can limit the number of cells with potential to form tumors,” says lead author Madhuri Kakarala, M.D., Ph.D., R.D., clinical lecturer in internal medicine at the U-M Medical School and a research investigator at the VA Ann Arbor Healthcare System.

Cancer stem cells are the small number of cells within a tumor that fuel the tumor’s growth. Current chemotherapies do not work against these cells, which is why cancer recurs and spreads. Researchers believe that eliminating the cancer stem cells is key to controlling cancer. In addition, decreasing the number of normal stem cells – unspecialized cells that can give rise to any type of cell in that organ – can decrease the risk of cancer.

In this study, a solution of curcumin and piperine was applied to the cell cultures at the equivalent of about 20 times the potency of what could be consumed through diet. The compounds are available at this potency in a capsule form that could be taken by mouth. (Note: This work has not been tested in patients, and patients are not encouraged to add curcumin or piperine supplements to their diet at this time.)

The researchers applied a series of tests to the cells, looking at markers for breast stem cells and the effects of curcumin and piperine, both alone and combined, on the stem cell levels. They found that piperine enhanced the effects of curcumin, and that the compounds interrupted the self-renewal process that is the hallmark of cancer-initiating stem cells. At the same time, the compounds had no affect on cell differentiation, which is the normal process of cell development.

“This shows that these compounds are not toxic to normal breast tissue,” Kakarala says. “Women at high risk of breast cancer right now can choose to take the drugs tamoxifen or raloxifene for prevention, but most women won’t take these drugs because there is too much toxicity. The concept that dietary compounds can help is attractive, and curcumin and piperine appear to have very low toxicity.”

Curcumin and piperine have been explored by other researchers as a potential cancer treatment. But this paper, published online in the journal Breast Cancer Research and Treatment, is the first to suggest these dietary compounds could prevent cancer by targeting stem cells.

In addition, tamoxifen or raloxifene are designed to affect estrogen, which is a factor in most, but not all breast cancers. In fact, the aggressive tumors that tend to occur more often in women with a family history or genetic susceptibility are typically not affected by estrogen. Because curcumin and piperine limit the self renewal of stem cells, they would impact cancers that are not estrogen sensitive as well as those that are.

Researchers are planning an initial Phase I clinical trial to determine what dose of curcumin or piperine can be tolerated in people. The trial is not expected to begin accruing participants until spring.

###

Breast cancer statistics: 194,280 Americans will be diagnosed with breast cancer this year and 40,610 will die from the disease, according to the American Cancer Society

Additional authors: Dean Brenner, Hasan Korkaya, Connie Cheng, Karim Tazi, Christophe Ginestier, Suling Liu, Gabriel Dontu and Max Wicha, all from U-M

Funding: National Institutes of Health; curcumin and piperine were donated by Sabinsa Co.

Reference: Breast Cancer Research and Treatment, DOI: 10.1007/s10549-009-0612-x

Resources: U-M Cancer AnswerLine, 800-865-1125 U-M Comprehensive Cancer Center, www.mcancer.org Cancer’s Stem Cell Revolution, www.mcancer.org/stemcells

Breast cancer screening saves lives, says study??? that screening only narrowly decreased risks that a 50-year-old woman would die from breast cancer within 10 years — from 0.53 percent to 0.46 percent.

Engineering Evil Note: There seems to be conflicting studies being utilized to favor screening. I found this report stating that they used no current data for the meta analysis. The data they claimed to have used here was over 20 years old. I am withholding my humble opinion to see if there were current studies, and if they used the superior MRI  overt he  antiquated mammograms. There seems to be a few different press releases quoting different studies, in addition now to a few broken links to those reports.

i.e. http://todayhealth.today.com/_news/2012/10/29/14787480-breast-cancer-checks-save-lives-despite-over-diagnosis-reportsays?lite

Breast cancer screening saves lives, says study

PARIS (AFP)  Benefits of preemptive breast cancer screening outweigh the risks, a study said Tuesday, insisting the practice saves thousands of lives.The new research adds to the debate about the dangers of overdiagnosis, which sees some women undergo invasive treatment for cancers that would never have made them ill or even been diagnosed were it not for the scans.”Breast screening extends lives,” concluded a panel of researchers in The Lancet medical journal.

The team had analysed data from other trials conducted over many years in Britain, where women aged 50 to 70 are invited for a screening mammogram every three years.

The data, it said, pointed to a 20 percent reduction in mortality — or one death prevented for every 180 women screened.

This meant that the UK screening programmes “probably prevent about 1,300 breast cancer deaths every year,” said the report.

But there is a cost.

Nearly 20 percent of breast cancer diagnosed by screening would never have caused any problems, said the study.

The panel, set up to advise British policymakers, estimated that among every 10,000 women invited to screening from the age of 50 in the Britain, 681 cancers would be discovered, of which 129 would be overdiagnoses, and 43 deaths prevented.

The report showed that “the UK breast-screening programme extends lives and that, overall, the benefits outweigh the harms,” The Lancet wrote in an editorial.

“Women need to have full and complete access to this latest evidence in order to make an informed choice about breast cancer screening.”

The team conceded there were limitations to its work, including that all the data scrutinised was more than 20 years old.

Cancer experts have been at loggerheads for years about whether the benefits of screening outweigh the harm of overdiagnosis.

All cancer, once picked up in the screening process, is treated, often with surgery as well as radio- and chemotherapy, as it is impossible to tell which growths would have remained undetected for the remainder of a woman’s life.

In August, medical experts Steven Woloshin and Lisa Schwartz wrote in the British Medical Journal (BMJ) that screening only narrowly decreased risks that a 50-year-old woman would die from breast cancer within 10 years — from 0.53 percent to 0.46 percent.

Up to half of women screened annually over 10 years experienced at least one false alarm that required a biopsy, they said.

And in 2010, a report in the New England Journal of Medicine said mammograms have only a “modest” impact on reducing breast cancer deaths.

The latest panel had been created by the national cancer director for England, Mike Richards and Cancer Research UK chief executive officer Harpal Kumar.

Its work, said The Lancet, “should begin to lay the benefits versus harm controversy to rest”.

http://www.afp.com/en/news/topstories/breast-cancer-screening-saves-lives-says-study

Long-term tamoxifen use increases risk of an aggressive, hard to treat type of second breast cancer: 4 fold increase

2009 study posted for filing

Contact: Kristen Woodward kwoodwar@fhcrc.org 206-667-5095 Fred Hutchinson Cancer Research Center

Study finds a more than four-fold increased risk of ER negative second cancers

SEATTLE – While long-term tamoxifen use among breast cancer survivors decreases their risk of developing the most common, less aggressive type of second breast cancer, such use is associated with a more than four-fold increased risk of a more aggressive, difficult-to-treat type of cancer in the breast opposite, or contralateral, to the initial tumor. These findings by Christopher Li, M.D., Ph.D., and colleagues at Fred Hutchinson Cancer Research Center were published online Aug. 25 in the journal Cancer Research.

Hormonal therapy with drugs like tamoxifen is one of the most common treatments for breast cancer because it has been shown to reduce the risk of dying from the disease but, as this study suggests, it does have risks.

Comparing breast-cancer patients who received the estrogen-blocking drug tamoxifen to those who did not, the researchers found that while the drug was associated with a 60 percent reduction in estrogen receptor-positive, or ER positive, second breast cancer – the more common type, which is responsive to estrogen-blocking therapy – it also appeared to increase the risk of ER negative second cancer by 440 percent. “This is of concern, given the poorer prognosis of ER-negative tumors, which are also more difficult to treat,” said Li, an associate member of the Hutchinson Center’s Public Health Sciences Division.

These findings confirm preliminary research by Li and colleagues, published in 2001, which was the first to suggest a link between long-term tamoxifen use and an increased risk of ER-negative second cancers. “The earlier study had a number of limitations. For example, we did not have information on the duration of tamoxifen therapy the women received,” Li said. “The current study is larger, is based on much more detailed data, and is the first study specifically designed to determine whether tamoxifen use among breast cancer survivors influences their risk of different types of second breast cancers,” Li said.

This new study assessed history of tamoxifen use among 1,103 breast cancer survivors from the Seattle-Puget Sound region who were initially diagnosed with ER positive breast cancer between the ages of 40 and 79. Of these, 369 of the women went on to develop a second breast cancer. Nearly all of the women in the study who took adjuvant hormonal therapy used tamoxifen specifically. Detailed information about tamoxifen use was ascertained from telephone interviews and medical record reviews.

While the study confirmed a strong association between long-term tamoxifen therapy and an increased risk of ER-negative second cancer, it does not suggest that breast cancer survivors should stop taking hormone therapy to prevent a second cancer, Li said.

“It is clear that estrogen-blocking drugs like tamoxifen have important clinical benefits and have led to major improvements in breast cancer survival rates. However, these therapies have risks, and an increased risk of ER negative second cancer may be one of them. Still, the benefits of this therapy are well established and doctors should continue to recommend hormonal therapy for breast cancer patients who can benefit from it,” Li said.

###

 

The National Cancer Institute funded the research.

At Fred Hutchinson Cancer Research Center, our interdisciplinary teams of world-renowned scientists and humanitarians work together to prevent, diagnose and treat cancer, HIV/AIDS and other diseases. Our researchers, including three Nobel laureates, bring a relentless pursuit and passion for health, knowledge and hope to their work and to the world. For more information, please visit fhcrc.org.

Asian Spice Could Reduce Breast Cancer Risk in Postmenopausal Women Exposed to Hormone Replacement Therapy, MU Study Finds

2009 study posted for filing

 

July 13, 2009

 

COLUMBIA, Mo. – Previous studies have found that postmenopausal women who have taken a combined estrogen and progestin hormone replacement therapy have increased their risk of developing progestin-accelerated breast tumors. Now, University of Missouri researchers have found that curcumin, a popular Indian spice derived from the turmeric root, could reduce the cancer risk for women after exposure to hormone replacement therapy.

 

“Approximately 6 million women in the United States use hormone replacement therapy to treat the symptoms of menopause,” said Salman Hyder, the Zalk Endowed Professorship in Tumor Angiogenesis and professor of biomedical sciences in the College of Veterinary Medicine and the Dalton Cardiovascular Research Center. “This exposure to progestin will predispose a large number of post-menopausal women to future development of breast cancer. The results of our study show that women could potentially take curcumin to protect themselves from developing progestin-accelerated tumors.”

 

In the study, researchers found that curcumin delayed the first appearance, decreased incidence and reduced multiplicity of progestin-accelerated tumors in an animal model. Curcumin also prevented the appearance of gross morphological abnormalities in the mammary glands. In previous studies, MU researchers showed that progestin accelerated the development of certain tumors by increasing production of a molecule called VEGF that helps supply blood to the tumor. By blocking the production of VEGF, researchers could potentially reduce the proliferation of breast cancer cells. Curcumin inhibits progestin-induced VEGF secretion from breast cancer cells, Hyder said.

 

“Curcumin and other potential anti-angiogenic compounds should be tested further as dietary chemopreventive agents in women already exposed to hormone replacement therapy containing estrogen and progestin in an effort to decrease or delay the risk of breast cancer associated with combined hormone replacement therapy,” Hyder said.

 

The study, “Curcumin delays development of MPA-accelerated DMBA-induced mammary tumors,” has been accepted for publication in Menopause, a journal of the North American Menopause Society. It was coauthored by Hyder; Candace Carroll, graduate student of biomedical sciences; Cynthia Besch-Williford, associate professor of veterinary pathobiology in the MU College of Veterinary Medicine; and Mark Ellersieck, professor and researcher in the MU Experiment Station Statistics

58th Health Research Report 09 JUN 2009 – Reconstruction

 

Editors Top Five:

 

1. Recycled radioactive metal contaminates consumer products

2. Illness, medical bills linked to nearly two-thirds of bankruptcies: Harvard study

3. Bird flu virus remains infectious up to 600 days in municipal landfills

4. How many scientists fabricate and falsify research?

5. Wet ear wax and unpleasant body odors signal breast cancer risk

In this Issue:

1. Use of acid-suppressive medications associated with increased risk of hospital-acquired pneumonia

2. Cancer drug causes patient to lose fingerprints and be detained by US immigration

3. Green tea extract shows promise in leukemia trials

4. History of hyperactivity off-base, says researcher

5. How many scientists fabricate and falsify research?

6. Omega fatty acid balance can alter immunity and gene expression

7. Bird flu virus remains infectious up to 600 days in municipal landfills

8. Silver nanoparticles show “immense potential” in prevention of blood clots

9. Wet ear wax and unpleasant body odors signal breast cancer risk

10. Commonly used medications may produce cognitive impairment in older adults

11. Why dishing does you good: U-M study

12. Sedatives may increase suicide risk in older patients

13. Illness, medical bills linked to nearly two-thirds of bankruptcies: Harvard study

14. Association Found Between Parkinson’s Disease and Pesticide Exposure in French Farm Workers

15. Multivitamins in pregnancy reduce risk of low birth weights

16. Stopping diabetes damage with vitamin C

17. Recycled radioactive metal contaminates consumer products

Health Research Report

58th Issue Date 09 JUN 2009

Compiled By Ralph Turchiano

www.healthresearchreport.me  www.vit.bz

www.youtube.com/vhfilm  http://www.facebook.com/engineeringevil

www.engineeringevil.com

How big business cashes in on breast cancer: Junk food, Barbie dolls and even power tools are jumping on this month’s pink ribbon bandwagon

By Linda Kelsey

PUBLISHED:16:40 EST, 14  October 2012| UPDATED:18:00 EST, 14 October 2012

Most people must be aware that we’re in the  middle of Breast Cancer Awareness Month.

Since the beginning of October, I’ve been  accosted by women (and men) wearing pink nylon wigs and brandishing collection  boxes, almost mown down by people in pink sportswear doing fundraising runs  round my local park and been exhorted to ‘shop without guilt’ for everything  from a pink Avon Breast Cancer Crusade emery board (£1.95) to a pink Coast dress  (£135), available online at Breakthrough Breast Cancer.

On Saturday, walking near my home, I came  across a trio of eight-year-olds selling home-made pink cupcakes at £1.50 each  just outside their front gate.

Increasing concerns are being raised about the methods used to encourage us to part with our money (posed by model)
Increasing concerns are being raised about the methods  used to encourage us to part with our money (posed by model)

I felt obliged to buy six of them even  though I promptly threw the lumps of pink goo in the bin.

Every year, the whole world seems to turn  pink in October.

Earlier this week, Elizabeth Hurley turned up  at the British Museum wearing a lacy pink confection and showing maximum  cleavage, accompanied by Shane Warne, who had a pink ribbon pinned to his lapel.

The great and good (well, journalists and  celebrities) had gathered to celebrate the 20th anniversary of Estee Lauder’s  Breast Cancer Awareness campaign and to illuminate the museum with a pink glow,  guaranteeing headlines for the campaign and the billion-dollar business that has  grown up behind it.

Debenhams has commissioned its top designers — including Matthew Williamson, Jasper Conran and Julien Macdonald — to design  T-shirts in support of their Think Pink campaign, with 25 per cent of sales  going to three breast cancer charities including The Pink Ribbon Foundation.

Launched by a number of celebrities (Tess  Daly, Donna Air and Sadie Frost for starters) these T-shirts are certain to  raise lots of money for a great cause as well as generate loads of  publicity — and extra profit — for Debenhams.

Every day, 130 women in the UK are diagnosed  with breast cancer.

DID  YOU KNOW?

ONE  IN EIGHT WOMEN WILL BE DIAGNOSED WITH BREAST CANCER

And, as Breakthrough Breast Cancer  points out, that’s 4,000 mums, daughters, sisters and friends hearing the  dreadful news during Breast Cancer Awareness month alone.

While no one would deny the importance of  raising the millions of pounds needed to fund research and improve early  detection and survival rates, increasing concerns are being raised about the  methods used to encourage us to part with our money.

‘Buys that save lives’ says the slogan next  to a pair of pink stretch M&S jeggings or a pink Breast Cancer   Awareness USB flash drive on the Breakthrough website.

But will my purchase of a pair of pink  jeggings I don’t need — and will never wear — really help save lives?

Launched by a number of celebrities these T-shirts are certain to raise lots of money for a great cause as well as generate loads of publicity ¿ and extra profit ¿ for DebenhamsLaunched by a number of celebrities these T-shirts are certain to raise lots of money for a great cause as well as generate loads of publicity ¿ and extra profit ¿ for Debenhams

Launched by a number of celebrities  these T-shirts  are certain to raise lots of money for a great cause as well as generate loads  of publicity — and extra profit — for Debenhams

Wouldn’t my contribution to saving a life be  greater if I simply wrote out a cheque to a charity and popped it in the post?

Perhaps I shouldn’t carp on about Asda’s  Tickled Pink campaign, given that over the past 16 years, they’ve donated £29 million to cancer charities.

But when you consider that our unhealthy  Western diet and the rise in obesity is a prime cause of breast cancer, how can  it be a good thing to encourage us to buy pink-boxed Jaffa Cakes, which may be  low in fat, but are high in sugar?

And how about Stokes Real Mayonnaise with its  pink lid? Or Lucozade’s pink lemonade? Of course, there would be no real health  risk for most people in consuming such products occasionally, but this  association with fat and sugar-laden foods is an uncomfortable one.

As Woman’s Hour presenter Jenni Murray — who  has suffered breast cancer — says: ‘I have no problem with big companies  contributing to cancer research, but disapprove of them selling us products,  including unhealthy junk foods, in the belief we’re making our contribution.

‘I also wonder how much of what we spend  actually goes to breast cancer research. It’s cynical marketing. Better to  contribute to your favourite cancer charity and buy anything but  pink!’

One in eight women will be diagnosed with breast cancer
One in eight women will be diagnosed with breast  cancer

The commercialisation of the fight against  breast cancer surely reached a nadir two years ago when KFC — whose jumbo  containers of fried chicken and chips might be regarded more as part of certain  health problems than as a solution — controversially started peddling garish  pink Buckets For The Cure in the U.S.

A Pink Ribbon Barbie, clad in a frothy pink  gown with pink ribbon, doesn’t fill me with glee either. As one cancer sufferer,  Jeanne Sather, posted on her blog (assertivecancerpatient.com): ‘As a woman  living with breast cancer (and minus one breast) who is forced to run a gauntlet  of pink products every October, my question is this: What does this beauty  queen, fairy princess, doll in a pink formal gown say about me and my experience  with breast cancer?

‘The answer is: Nothing. This doll does not  offer hope. This doll does not offer a positive image of a strong woman living  with cancer. And the doll is not a fundraising effort I can support.’

Breast Cancer Action, a campaigning and  fundraising group in the U.S., has been one of the main organisations to  highlight the sometimes dubious links between companies that raise funds for  breast cancer while producing products that may contribute to the disease.

In 2008, they took on the dairy industry,  focusing on Yoplait’s pink-lidded yoghurt, which was sold to raise money for  breast cancer, but was made with milk from cows stimulated with the hormone rBGH  that has been linked to breast cancer. As a result of their protest campaign  Yoplait is rBGH free.

But nothing sinks so low as a pink Smith & Wesson gun, a weapon that kills, being flogged to save lives. Unless you  think a porn site offering to make donations based on how many ‘boob searches’ are made on its website is even more despicable. I wish I’d made up both  examples, but I haven’t.

By turning the unarguably good cause of breast cancer awareness and research into a crass consumer spending spree, and linking shopping for everything from cake tins to porn to saving lives, we are in danger of turning the disease into little more than a commodity, one that fails to take account of real women’s experiences of breast cancer and leaves them feeling conflicted and guilty about their unwillingness to embrace all this pinkification of cancer.

OBESITY  IS A PRIME CAUSE OF CANCER- SO HOW CAN IT BE HELPFUL TO BUY JAFFA  CAKES?

A friend who underwent a mastectomy,  radiotherapy and chemotherapy seven years ago and now counsels other breast  cancer victims says: ‘Please don’t reveal my name for this article.

‘I volunteer for a cancer charity and they  are all dedicated, hard-working people. But the products sold through their  website are beginning to make me cringe.

‘All this pink nonsense turns breast cancer  awareness into something resembling a giant hen party. It’s gone too  far.’

The official name given to this type of  corporate philanthropy is ‘cause marketing’. A study of its effects by two  professors at the University of Michigan found that companies can raise prices  and make higher profits on the sale of products that benefit a cause.

These companies’ brand portfolios can  experience a ‘spillover’ increase in sales and profits, which more than  compensate for the money given to charity.

Other research has shown that 79  per cent of  consumers would seriously consider switching to a brand that supports a good  cause, providing the product meets their needs.

Elizabeth Hurley went pink when she turned up at the British Museum wearing a lacy dress revealing a lot of cleavage
Elizabeth Hurley went pink when she turned up at the  British Museum wearing a lacy dress revealing a lot of cleavage

Moreover, cause marketing actually reduces  direct charitable giving by consumers.

It’s interesting that some cancer campaigns  associated with men — such as testicular cancer — raise funds and awareness  through sponsored growing of moustaches, for example, rather than linking with  commercial partners to flog products aimed at men.

It’s probably for three reasons: first, all  these charities are in their infancy; men aren’t as sappy as women when it comes  to shopping; and the taboo around these topics is still there, so commercial  interests haven’t yet cottoned on.

Breasts are seen as sexy and eminently  saleable, while men’s bits aren’t.

It’s all a far cry from 20 years ago when  pink ribbons were a demonstration of solidarity with cancer sufferers with no  taint of commercialism.

Then, in 1992, the late Evelyn Lauder (who  died from ovarian cancer last year), an executive at her husband’s family firm  of Estee Lauder, created the pink ribbon campaign for breast  cancer awareness with her friend Alexandra Penney, then editor-in-chief of  Self magazine.

The campaign began on a small scale with  Lauder and her husband Leonard financing the little pink bows that  were given to women at department store make-up counters alongside a card  describing how to conduct breast self-examination.

Kylie Minogue and Sheryl Crow are both breast cancer survivors Kylie Minogue and Sheryl Crow are both breast cancer survivors

Kylie Minogue and Sheryl Crow are both breast cancer  survivors

Soon after they collected more than 200,000  pink ribbon petitions urging the White House to increase funding for research.

The campaign grew to raise millions of  dollars, launching the Breast Cancer Research Foundation and helping to  establish the Evelyn H. Lauder Breast Centre at Memorial Sloan-Kettering Cancer  Centre in New York.

‘There had been no publicity about breast  cancer,’ Lauder said, shortly before she died. ‘But a confluence of events — the  pink ribbon, the colour, the Press, partnering with Elizabeth Hurley, having  Estee Lauder as an advertiser in magazines and persuading so many of my health  and beauty editor friends to do stories about breast health — got people  talking.’

Certainly, breast cancer was a largely taboo  subject until awareness campaigns took off. It was under-funded in terms of  research and treatment, and women who had undergone mastectomies went to great  lengths to hide their suffering.

‘Every  year more than £5 million is  received from Breakthrough’s corporate partners  and this money plays an  instrumental role in helping fund groundbreaking  research and improve  service and treatments for women affected by breast  cancer’

Now, thanks to increased awareness and  celebrities — from Kylie to Jennifer Saunders — speaking openly about their  experiences of breast cancer, women can share their pain.

Of course, the charities involved argue that  all publicity and types of fundraising are worthwhile. A spokesman for  Breakthrough Breast Cancer says: ‘We very much value and depend on the support  that our corporate partners give to us.

The vital life-saving work that we do to stop  women dying from the disease is reliant to a large degree on the money raised  through companies such as Marks & Spencer, Avon, Ghd, Adidas and many others  who have supported us generously over the years.

‘Every year more than £5 million is received  from Breakthrough’s corporate partners and this money plays an instrumental role  in helping fund groundbreaking research and improve service and treatments for  women affected by breast cancer.’

Nevertheless, perhaps the time has come not  to ‘think pink’ but to ‘think before you pink’.

Instead of buying a ‘Cancer Can Kiss My  Tatas’ T-shirt, with little idea of how much of your money will be used to  profit cancer research, why not arrange an easy bank transfer that will do the  job your donation is intended for — and make so much more of a  difference.

DOES BUYING PINK ADD UP?

Jaffa Cake Bars Tickled Pink Limited Edition, £1, donation 5pStokes Sauces Mayonnaise, £3.15, donation 10p

Jaffa Cake Bars Tickled Pink Limited Edition, £1,  donation 5p

Stokes Sauces Mayonnaise, £3.15, donation 10p

Makita drill, £84.99, donation £5Lucozade Pink Lemonade Tickled Pink Limited Edition, 31.99, donation 10p
Makita drill, £84.99, donation £5

Lucozade Pink Lemonade Tickled Pink Limited Edition,  31.99, donation 10p

Read more: http://www.dailymail.co.uk/femail/article-2217678/How-big-business-cashes-breast-cancer-Junk-food-Barbie-dolls-power-tools-jumping-months-pink-ribbon-bandwagon.html#ixzz29LPtthaZ Follow us: @MailOnline on Twitter | DailyMail on Facebook

Curcumin curbs metastases

Munich, 10/12/2012

Powdered turmeric has been used for centuries to treat osteoarthritis and other illnesses. Its active ingredient, curcumin, inhibits inflammatory reactions. A new study now shows that it can also inhibit formation of metastases. Prostate cancer is one of the most prevalent malignancies in the Western world, and is often diagnosed only after metastatic tumors have formed in other organs. In three percent of cases, these metastases are lethal. A research team led by PD Dr. Beatrice Bachmeier at LMU Munich has been studying the mode of action of a natural product that inhibits the formation of metastases. The compound is found in turmeric, a plant that has been used for medicinal purposes for thousands of years, and is a major ingredient of curry.

Bachmeier’s research centers on curcumin, the polyphenol responsible for the characteristic color of curry. Curcumin is well tolerated and is therefore, in principle, suitable both for prophylactic use (primary prevention) and also for the suppression of metastases in cases where an established tumor is already present (secondary prevention). In a previous study Bachmeier and her colleagues had demonstrated that the substance reduces statistically significantly the formation of lung metastases in an animal model of advanced breast cancer.

Mitigating metastasis

The new study was designed to investigate the efficacy of curcumin in the prevention of prostate cancer metastases, and to determine the agent’s mechanism of action. The researchers first examined the molecular processes that are abnormally regulated in prostate carcinoma cells. Breast and prostate cancers are often associated with latent or chronic inflammatory reactions, and in both cases, the tumor cells were found to produce pro-inflammatory immunomodulators including the cytokines CXCL1 und CXCL2.

The researchers went on to show that curcumin specifically decreases the expression of these two proteins, and in a mouse model, this effect correlated with a decline in the incidence of metastases. “Due to the action of curcumin, the tumor cells synthesize smaller amounts of cytokines that promote metastasis,” says Bachmeier. “As a consequence, the frequency of metastasis formation in the lungs is significantly reduced, in animals with breast cancer, as we showed previously, or carcinoma of the prostate, as demonstrated in our new study.”

Curcumin and chemoprevention

Bachmeier therefore believes that curcumin may be useful in the prevention of breast and prostate cancers – which are both linked to inflammation – and in reducing their metastatic potential. “This does not mean that the compound should be seen as a replacement for conventional therapies. However, it could play a positive role in primary prevention – before a full-blown tumor arises – or help to avert formation of metastases. In this context the fact that the substance is well tolerated is very important, because one can safely recommend it to individuals who have an increased tumor risk.”

A daily intake of up to 8g of curcumin is regarded as safe, and its anti-inflammatory properties have long been exploited in traditional oriental medicine. Men with benign hyperplasia of the prostate (BHP) are one possible target group for prophylaxis, as are women who have a family history of breast cancer. The agent might also be valuable as a supplement to certain cancer therapies. At all events, curcumin’s beneficial effects must first be confirmed in controlled clinical tests. Bachmeier is now planning such a trial in patients who suffer from therapy-resistant carcinoma of the prostate.

(Carcinogenesis online, 5 October 2012) bedo / suwe

Second lumpectomy for breast cancer REDUCES survival rates

2008 study posted for filing

Contact: Karen Finney
karen.finney@ucdmc.ucdavis.edu
916-734-9064
University of California – Davis Health System

UC Davis researchers find disturbing trend in treating recurrent breast cancer

(SACRAMENTO, Calif.) — A majority of women with breast cancer today are candidates for lumpectomy, allowing for conservation of most of their breast tissue. Results of a UC Davis study, however, show that a number of women whose cancer recurs in the same breast are treated with a second lumpectomy rather than a mastectomy, defying current treatment recommendations and cutting the number of years those women survive in half.

“We were surprised to find that so many women in our study — almost a quarter of them — had received another lumpectomy rather than a mastectomy,” said Steven Chen, a UC Davis Cancer Center surgical oncologist and lead author of the study, which appears in the October issue of the American Journal of Surgery. “It’s likely that patients are asking for lumpectomies when their cancer is diagnosed a second time, and their doctors are simply complying with that request. Whatever the reason, that decision can shorten life spans.”

Chen and study co-author, Steve Martinez, also a UC Davis Cancer Center surgical oncologist, gathered data from the National Cancer Institute’s Surveillance, Epidemiology and End Results database, which includes information on all cancers diagnosed in selected regions throughout the nation. Their study included 747 patients who previously received breast-conservation therapy and were diagnosed with cancer a second time in the same breast between 1988 and 2004.

The authors found that women who had mastectomies had a 78 percent survival rate after five years, while those who had second lumpectomies had a 67 percent survival rate. The 10-year survival rates were 62 percent for those who had mastectomies and 57 percent for those who had second lumpectomies. In all, 24 percent of women with recurrent breast cancer in the same breast had second lumpectomies.

The researchers went on to calculate the risk of dying for mastectomy patients compared to lumpectomy patients. They found that, after adjusting for factors that affect survival, there will be half as many survivors at any given time in the lumpectomy group versus the mastectomy group.

Chen explained that a mastectomy is the generally accepted surgical treatment for a second cancer because whole breast radiation, which typically accompanies a lumpectomy, is not usually recommended twice in a lifetime. This new study shows as well that there is a survival advantage to those who choose a mastectomy.

According to Martinez, knowledge of breast cancer and its treatments are continuously advancing, and second lumpectomies could at some point become a viable option.

“As therapy for breast cancer becomes more targeted and researchers come closer to identifying those factors that make some breast cancers more aggressive than others, we may have the option of recommending second and even third lumpectomies in select cases in the future. Until then, mastectomy remains the best option for women experiencing a same-breast recurrence of their breast cancer,” he said.

 

###

 

Breast cancer is currently the most common newly diagnosed malignancy among American women. The chance of developing invasive breast cancer at some time in a woman’s life is about 1 in 8. In the United States in 2008, an estimated 182,460 new cases of invasive breast cancer will be diagnosed, an additional 67,770 new cases of carcinoma in situ — or “pre-cancer” — will be discovered and 40,480 women will die from breast cancer.

Designated by the National Cancer Institute, UC Davis Cancer Center cares for 9,000 adults and children each year from throughout the Central Valley and inland Northern California. The center’s Breast Cancer Program provides comprehensive, multidisciplinary services for patients with all stages of the disease. Patients receive their care in one location, from a team of top academic physicians with expertise in hematology and oncology, surgical oncology, radiation oncology, pathology, plastic and reconstructive surgery, and diagnostic radiology/mammography. These experts work together to develop individualized treatment plans for each patient. For more information, visit www.ucdmc.ucdavis.edu/cancer/.

137th Health Research Report 07 SEP 2008

 Full Report at www.healthresearchreport.me

Editors Top Five:

 

1. Study Finds How BPA Affects Gene Expression, Anxiety; Soy Mitigates Effects

2. Vitamin B3 may offer new tool in fight against ‘superbugs’

3. Johns Hopkins team finds ICU misdiagnoses may account for as many annual deaths as breast cancer

4. Prenatal exposure to pesticide additive linked with childhood cough

5. Childhood virus RSV shows promise against adult cancer

 

 

In this Issue:

1. Vitamin B3 may offer new tool in fight against ‘superbugs’

2. How a virus might make you diabetic later in life

3. Adolescent pot use leaves lasting mental deficits

4. Nutrition tied to improved sperm DNA quality in older men

5. Energy drinks improve heart function

6. Breast milk promotes a different gut flora growth than infant formulas

7. Johns Hopkins team finds ICU misdiagnoses may account for as many annual deaths as breast cancer

8. WSU researcher documents links between nutrients, genes and cancer spread

9. Antibiotic residues in sausage meat may promote pathogen survival

10. Smoking after stroke increases death risk by 3-fold

11. The raccoon spreads dangerous diseases as it invades Europe

12. Chocolate: A sweet method for stroke prevention in men?

13. Bacterial cause found for skin condition rosacea

14. WSU researchers discover mechanism leading from trichomoniasis to prostate cancer

15. Lyme retreatment guidance may be flawed

16. Chemical exposure in the womb from household items may contribute to obesity

17. Affluent people less likely to reach out to others in times of chaos, study suggests

18. Coconut oil could combat tooth decay

19. Heavy drinking rewires brain, increasing susceptibility to anxiety problems

20. Even in normal range, high blood sugar linked to brain shrinkage

21. High doses of Vitamin D help tuberculosis patients recover more quickly

22. High levels of DDT in breast milk

23. Large Review Finds Some Evidence for “Chemo Brain” in Breast Cancer Survivors, Moffitt Cancer Center Says

24. Are restrictions to scientific research costing lives?

25. Toddlers increasingly swallowing liquid detergent capsules

26. Brainy beverage: Study reveals how green tea boosts brain cell production to aid memory

27. Children exposed to 2 phthalates have elevated risk of asthma-related airway inflammation

28. Prenatal exposure to pesticide additive linked with childhood cough

29. Nutritional supplement offers promise in treatment of unique form of autism

30. Diagnostic chest radiation before 30 may increase breast cancer risk

31. Report: Strategies to prevent noise-induced hearing loss, tinnitus in soldiers

32. Childhood virus RSV shows promise against adult cancer

33. Stress prompts some to retain as much salt as eating fries

34. Study Finds How BPA Affects Gene Expression, Anxiety; Soy Mitigates Effect

 

 

Health Technology Research Synopsis

137th Issue Date 07 SEP 2012

Compiled By Ralph Turchiano

www.healthresearchreport.me www.vit.bz

www.youtube.com/vhfilm http://www.facebook.com/vitaminandherbstore

www.engineeringevil.com


Ingredient found in green tea significantly inhibits breast cancer growth in female mice: EGCG decreases in TCSA (66%), tumor weight (68%) 5 weeks

Repost from 2008

Contact: Donna Krupa dkrupa@the-aps.org 703-967-2751 American Physiological Society

SAN DIEGO, CA — Green tea is high in the antioxidant EGCG (epigallocatechin-3- gallate) which helps prevent the body’s cells from becoming damaged and prematurely aged. Studies have suggested that the combination of green tea and EGCG may also be beneficial by providing protection against certain types of cancers, including breast cancer. A new study conducted by researchers at the University of Mississippi researchers now finds that consuming EGCG significantly inhibits breast tumor growth in female mice. These results bring us one step closer to better understanding the disease and potentially new and naturally occurring therapies.

The study was conducted by Jian-Wei Gu, Emily Young, Jordan Covington, James Wes Johnson, and Wei Tan, all of the Department of Physiology & Biophysics, University of Mississippi Medical Center, Jackson, MS. Dr. Gu will present his team’s findings, entitled, Oral Administration of EGCG, an Antioxidant Found in Green Tea, Inhibits Tumor Angiogenesis and Growth of Breast Cancer in Female Mice, at the  121st Annual Meeting of the American Physiological Society (APS; www.the-APS.org/press), part of the Experimental Biology 2008 scientific conference.

The Study

Epidemiological studies suggest that green tea and its major constituent, EGCG, can provide some protection against cancer. Because these studies were very limited, the anti-cancer mechanism of green tea and EGCG was not clear. As a result, the researchers examined whether drinking EGCG (just the antioxidant infused in water) inhibited the following: expression of VEGF (vascular endothelial growth factor, which is found in variety of breast cancer types); tumor angiogenesis (thought to help tumors to expand by supplying them with nutrients); and the growth of breast cancer in female mice.

Seven week old female mice were given EGCG (25 mg/50 ml) in drinking water for five weeks (approximately 50-100 mg/kg/day.) The control mice received regular drinking water. In the second week of the study mouse breast cancer cells were injected in the left fourth mammary glands of the mice. Tumor size was monitored by measuring the tumor cross section area (TCSA). Tumors were eventually isolated and measured for tumor weight, intratumoral microvessel (IM) density (using staining), and VEGF protein levels (using ELISA).

At the end of the five week period the researchers found that oral consumption of EGCG  caused significant decreases in TCSA (66%), tumor weight (68%), IM density 155±6 vs.111±20 IM#mm^2) and VEGF protein levels (59.0±3.7 vs. 45.7±1.4 pg/mg) in the  breast tumors vs. the control mice, respectively (N=8; P<0.01).  Further, VEGF plasma levels were lower in EGCG mice than in control mice (40.8±3.5 vs. 26.5±3.8 pg/ml P< 0.01).

Dr. Gu, the senior researcher for the study, hypothesized that the reason for the link between EGCG and the reductions in the cancer data was because EGCG directly targets both tumor blood vessels and tumor cells of breast cancer for suppressing the new blood vessels formation in breast tumor, the proliferation and migration of breast cancer cells.

Gu concluded by saying, “In this study we have demonstrated that the frequent ingestion of EGCG significantly inhibits breast tumor growth, VEGF expression and tumor angiogenesis in mice. We believe our findings will help lead to new therapies for the prevention and treatment of breast cancer in women.”

###

 

Physiology is the study of how molecules, cells, tissues and organs  function to create health or disease. The American Physiological Society (APS; www.The-APS.org/press) has been an integral part of this  discovery process since it was established in 1887.

NOTE TO EDITORS: The APS annual meeting is part of the Experimental Biology 2008 (EB ’08) gathering and will be held April 5-9, 2008 at the San Diego, CA Convention Center. To schedule an interview with Dr. Gu please contact Donna Krupa at 301.634.7209 (office), 703.967.2751 (cell) or DKrupa@the-APS.org.

Wormwood ( Artemesia ) may hold key to non-toxic Cancer and Leukemia treatment

Reposted at Request from 26-Nov-2001

Contact: Rob Harrill rharrill@u.washington.edu 206-543-2580 University of Washington

Two bioengineering researchers at the University of Washington have discovered a promising potential treatment for cancer among the ancient arts of Chinese folk medicine.

Research Professor Henry Lai and assistant research Professor Narendra Singh have exploited the chemical properties of a wormwood derivative to target breast cancer cells, with surprisingly effective results.  A study in the latest issue of the journal Life Sciences describes how the derivative killed virtually all human breast cancer cells exposed to it within 16 hours.

“Not only does it appear to be effective, but it’s very selective,” Lai said.  “It’s highly toxic to the cancer cells, but has a marginal impact on normal breast cells.”

The compound, artemisinin, isn’t new.  It apparently was extracted from the plant Artemesia  annua L., commonly known as wormwood, thousands of years ago by the Chinese, who used it to combat malaria.  However, the treatment was lost over time.  Artemisinin was rediscovered during an archaeological dig in the 1970s that unearthed recipes for ancient medical remedies, and has become widely used in modern Asia and Africa to fight the mosquito-borne disease.

The compound helps control malaria because it reacts with the high iron concentrations found in the malaria parasite.  When artemisinin comes into contact with iron, a chemical reaction ensues, spawning charged atoms that chemists call “free radicals.”  The free radicals attack cell membranes, breaking them apart and killing the single-cell parasite.

About seven years ago, Lai began to hypothesize that the process might work with cancer, too.

“Cancer cells need a lot of iron to replicate DNA when they divide,” Lai explained.  “As a result, cancer cells have much higher iron concentrations than normal cells.  When we began to understand how artemisinin worked, I started wondering if we could use that knowledge to target cancer cells.”

Lai devised a potential method and began to look for funding, obtaining a grant from the Breast Cancer Fund in San Francisco.  Meanwhile, the UW patented his idea.

The thrust of the idea, according to Lai and Singh, was to pump up the cancer cells with maximum iron concentrations, then introduce artemisinin to selectively kill the cancer.  To accommodate a rate of iron intake greater than normal cells, cancer cell surfaces feature greater concentrations of transferrin receptors – cellular pathways that allow iron into a cell.  Breast cancer cells are no exception.  They have five to 15 times more transferrin receptors on their surface than normal breast cells.

In the current study, the researchers subjected sets of breast cancer cells and normal breast cells to doses of holotransferrin (which binds with transferrin receptors to transport iron into cells), dihydroartemisinin (a more water-soluble form of artemisinin) and a combination of both compounds.  Cells exposed to just one of the compounds showed no appreciable effect.  Normal breast cells, exposed to both compounds, exhibited a minimal effect.  But the response by cancer cells when hit with first holotransferrin, then dihydroartemisinin, was dramatic.

After eight hours, just 25 percent of the cancer cells remained.  By the time 16 hours had passed, nearly all the cells were dead.

An earlier study involving leukemia cells yielded even more impressive results.  Those cells were eliminated within eight hours.  A possible explanation might be the level of iron in the leukemia cells.

“They have one of the highest iron concentrations among cancer cells,” Lai explained.  “Leukemia cells can have more than 1,000 times the concentration of iron that normal cells have.”

The next step, according to Lai, is animal testing.  Limited tests have been done in that area.  In an earlier study, a dog with bone cancer so severe it couldn’t walk made a complete recovery in five days after receiving the treatment.  But more rigorous testing is needed.

If the process lives up to its early promise, it could revolutionize the way some cancers are approached, Lai said.  The goal would be a treatment that could be taken orally, on an outpatient basis.

“That would be very easy, and this could make that possible,” Lai said.  “The cost is another plus – at $2 a dose, it’s very cheap.  And, with the millions of people who have already taken artemisinin for malaria, we have a track record showing that it’s safe.”

Whatever happens, Lai said, a portion of the credit will have to go to unknown medical practitioners, long gone now.

“The fascinating thing is that this was something the Chinese used thousands of years ago,” he said.  “We simply found a different application.”

###

For more information, contact Lai at (206) 543-1071 or hlai@u.washington.edu.  For more information on the journal Life Sciences, check the Web at:http://www.elsevier.com/locate/lifescie

The Cancer “Breakthroughs” that Cost Too Much and Do Too Little

Author

Laura Beil, Newsweek

Aug 27, 2012 1:00 AM EDT

‘Death panels’ are a bad idea. But asking hard questions about health care is not.

In his more than 35 years of practice, Dr. Lowell Schnipper has seen a lot of women die from breast cancer. A patient’s options start to dwindle by the time tumor cells set up outposts in the bones, lungs, and other organs, defying all attempts to keep them under control. But in June, when the government approved Perjeta, Schnipper had something new to offer. The drug is one of an innovative class of drugs known as “targeted therapies.”

As the chief of oncology at Beth Israel Deaconess Medical Center in Boston, Schnipper knew Perjeta was not a cure: added to a standard treatment with Herceptin—another targeted therapy that was hailed as a breakthrough in 1998—Perjeta gives the average woman only about six months more of calm before her disease starts to stir again. Given the limited benefit, the price was startling. For most women, a full course of the drug combination will cost $188,000—enough, he says, “to give anybody a cold sweat.”

Americans spent more than $23 billion last year for cancer drugs, more than we paid for prescriptions to treat anything else. But many oncologists are starting to question what we are getting in return for that bill, whether the war on cancer has become too much of a race to produce the next blockbuster. “In general, progress for cancer has been halting and slow,” says David Howard of the Department of Health Policy and Management at Emory University. So far, most new drugs offer only marginal extensions of life and few cures. Howard says new so-called breakthroughs “overpromise and underdeliver.” Consider the popularity of Avastin, a targeted drug approved for metastatic colon cancer in 2004. A recent study found that almost 70 percent of patients on chemotherapy were receiving Avastin within a year of its release. In clinical trials, the drug increased survival by about five months. The cost? About $10,000 a month.

Treating cancer has never been cheap, but today, the price of each new treatment seems to outpace the one before, with little bearing on its efficacy. According to figures from insurer United Healthcare, a standard cocktail of drugs for treating lung cancer used to run about $1,000 a month. Today’s regimens cost from more than $6,000 to almost $10,000—for about two more months of life. “There is no such thing as a cancer drug coming on the market that is some sort of regular drug price,” says Dr. Peter Bach of Memorial Sloan-Kettering Cancer Center in New York, who studies the impact of cancer costs on U.S. health care. “They’re all priced at spectacularly high levels.” Which leads to an unsettling question: how much is a little more time worth? Would you spend $50,000 for four more months? How about $15,000 for two weeks?

Of three frontiers in cancer treatment, targeted therapies like Perjeta are widely seen as the best hope for a cure. Traditional chemotherapy is notorious for side effects because it wields destruction indiscriminately throughout the body. Targeted therapies are designed to hit cancer cells only. Perjeta, for example, targets a protein produced in excess amounts in some breast cancers; Avastin hinders the ability of a tumor to form new blood vessels to feed itself.

Dan Dunkley / Gallerystock.com

Doctors envision the day when every patient will have therapy precisely matched to the genetic bull’s-eyes of their own cancers. The holdup has been that cancer has proven to be more genetically crafty than researchers once imagined. Scientists may build a drug to hit one target, but a tumor may also employ lots of yet-undiscovered genetic tricks to keep itself alive. Instead of a magic bullet, scientists now know that any particular tumor may need lots of magic bullets. With so many targets unknown, a lot of patients end up getting drugs that barely touch their cancers, which is why the effectiveness of many new drugs remains underwhelming.

Not that this keeps a drug from becoming a blockbuster. Patients with advanced cancer, and their physicians, are hungry for progress. As a result, almost all of the 10 bestselling cancer drugs are targeted therapies, many less than a decade old. All came on the market at thousands of dollars a month, a trend that continues today with gusto. The drug Afinitor, a daily pill, was approved in July for patients with breast cancer. It costs more than $200 a tablet. But price rarely matters to patients or even doctors, says Dr. Oliver Sartor, medical director of the Tulane Cancer Center in New Orleans. “People have already been told there is no cure for their disease,” he says. “Every increment, every improvement, gives hope, and when options are extremely limited, we all focus on the positive possibilities.”

In addition to targeted therapies, drugs have come on the market that can spur the body’s own immune cells to lead the charge. Significant hurdles have hindered this kind of treatment for years. But they are finally being overcome. The prostate cancer drug Provenge, which came on the market in 2010, was the first immune-therapy drug to gain governmental approval. It was followed the next year by Yervoy, when approved the only drug ever shown to extend survival in advanced melanoma. Men with a common kind of advanced prostate cancer who used Provenge lived an average of four months longer than the comparison group; patients on Yervoy got an average of 3.6 months. The gains are modest, but not the cost. When Sartor learned Provenge would run $93,000 per patient, “I was stunned,” he says. And even that was cheaper than Yervoy, which appeared the following year at $120,000 for four injections. He predicts the pricing of immune therapies may be seen as “a watershed moment” in the debate over health-care costs.

The third area of touted breakthroughs has been in radiation, most recently by using protons instead of traditional X-rays to kill cancer cells. It’s a controversial undertaking: many doctors believe that protons offer better precision, able to get rid of tumors without collateral damage to nearby healthy tissues. But whether protons can treat with fewer side effects than traditional radiation is, to date, a matter of debate for almost all but pediatric and certain neurological tumors.

As with new drugs, proton-beam radiation is expensive—it can run roughly twice as much as the current state-of-the-art form of radiation that uses X-rays. In the case of proton beams, much of the cost has to do with building a cyclotron to harvest the protons—a construction project that can cost upwards of $150 million. In 2001 just three centers in the country offered proton treatment, but that number is now up to 10, with a half dozen more planned. About three quarters of the proton patient population covered by Medicare are men with prostate cancer, which, because of the length of their therapy, are the most lucrative to treat.

Why do new drugs cost so much? Pharmaceutical companies say it’s payment for scientific creativity, that high prices are necessary to recover the expense of developing and manufacturing their products and to encourage more research. A spokeswoman for Bristol-Myers Squibb, which makes Yervoy, says the cost of drugs is “based on a number of factors, including the value they deliver to patients, the scientific innovation they represent, and the cost to develop them.” Part of the price is also an investment in drug discovery. “We look at not only the past research and development, but development in the future,” says Krysta Pellegrino, a spokeswoman for Genentech, which developed Perjeta.

That said, many cancer experts remain skeptical of the notion that drug companies are simply passing along the cost of doing business and funding the incubation of new drugs. In 2004 researchers tried to test the relationship between a drug’s development and its final asking price. In the Journal of Clinical Oncology, the scientists concluded “that the drug companies are not pricing their drugs to recuperate losses associated with research and development, marketing, and operating prices, but rather [the average wholesale price] depends on what the market itself can bear.”

“It’s a marketplace where the seller has all of the control,” says Bach, from Memorial Sloan-Kettering, because private insurance companies and Medicare—the largest purchasers of drugs—are powerless to bargain for a less expensive deal. “Prices are high because they can be,” Bach says. As one doctor observed, “we are always paying for a Ferrari but often getting a Ford.” The occasional Ferrari does exist. The targeted drug Gleevec, which treats certain forms of leukemia and intestinal tumors, has allowed patients to live for years with their cancer in check.

But while the track record for some new treatments is expected to improve, Dr. Otis Brawley, chief medical and scientific officer of the American Cancer Society, says that in most cases, “new cancer treatments cost an awful lot of money, and there is usually a very small incremental benefit.” Brawley, author of How We Do Harm: A Doctor Breaks Ranks About Being Sick in America, likes to cite the case of Tarceva, a targeted therapy approved for pancreatic cancer in 2005 to piggyback on the traditional drug gemcitabine. “The median survival of Tarceva and gemcitabine compared to gemcita-bine alone was 14 to 16 days greater. Seven months versus seven and a half months.” A 2007 analysis in the Journal of Clinical Oncology determined that those extra days add around $15,000 to the cost of care. “Instead of talking about rationing care,” Brawley says, “we need to talk about rational use of care.”

If new cancer treatments continue to push the boundaries of affordability, Americans will eventually be forced into dilemmas we have largely postponed. Innovative cancer treatments, says Emory’s Howard, “really symbolize the tradeoff that we face between improving health and saving money. At some point, society—including employers, the government, patients, and clinicians—have to make a tradeoff. I think if these drugs cured the disease, which none of them do, then no one would be questioning these prices. But we are seeing very high cost for relatively little return in patient benefit and survival.”

Other countries already consider a treatment’s effectiveness in national discussions about whether to pay for it. For example, this summer in Israel, a panel of radiation oncologists advised the Israeli Ministry of Health that, because of the unproven benefits, spending public money on proton-beam treatment is not yet warranted. “We can’t say it is a justifiable expense,” says Dr. Abraham Kuten, director of oncology at Rambam Medical Center in Haifa. The United Kingdom affirmed in July, for the second time, that it will not cover Avastin for advanced breast cancer. Australia, which has one of the world’s highest incidences of melanoma, decided in March that the benefits of Yervoy are not worth the cost to the country’s national health-care system; it based its decision on an independent government advisory committee, which cited the questionable benefit to patients and the drug’s “uncertain clinical place in therapy.”

Then there is the United States, where wider access to drugs may be one of the reasons our cancer survival times rank among the highest worldwide. But the question is how long we can afford what we’re getting. “I think we are the only industrialized country that doesn’t look at the cost balanced somehow with effectiveness in making decisions about drugs,” says Dr. Thomas Smith of the Sidney Kimmel Comprehensive Cancer Center in Baltimore. “What we have now are a bunch of blockbuster-ette drugs that give a little bit of benefit. If you’re that person, it could be a really big benefit to have three extra months before your disease starts growing again, but as a society we simply can’t pay for that for everybody.”

Yet aside from academics and insurance-company executives, few Americans are willing to consider the price of time, says Dr. Lee Newcomer, senior vice president for oncology at United Healthcare. This means that the government sinks further into debt, and insurance companies keep raising premiums to keep up. “If we’re going to continue to have a sustainable health system, we have to talk about that as a society. In 15 years, you will have to earn the equivalent of a year’s salary today to pay your health-insurance premiums,” he says. “We’re going to have to have the discussion.”

Laura Beil is an independent journalist based in Dallas

Virus kills breast cancer cells in laboratory

A nondisease-causing virus kills human breast cancer cells in the laboratory, creating opportunities for potential new cancer therapies, according to Penn State College of Medicine researchers who tested the virus on three different breast cancer types that represent the multiple stages of breast cancer development.

Adeno-associated virus type 2 (AAV2) is a virus that regularly infects humans but causes no disease. Past studies by the same researchers show that it promotes tumor cell death in cervical cancer cells infected with human papillomavirus. Researchers used an unaltered, naturally occurring version of AAV2 on human breast cancer cells.

“Breast cancer is the most prevalent cancer in the world and is the leading cause of cancer-related death in women,” said Samina Alam, Ph.D., research associate in microbiology and immunology. “It is also complex to treat.”

Craig Meyers, Ph.D., professor of microbiology and immunology, said breast cancer is problematic to treat because of its multiple stages.

“Because it has multiple stages, you can’t treat all the women the same. Currently, treatment of breast cancer is dependent on multiple factors such as hormone-dependency, invasiveness and metastases, drug resistance and potential toxicities. Our study shows that AAV2, as a single entity, targets all different grades of breast cancer.”

Cells have multiple ways of dying. If damage occurs in a healthy cell, the cell turns on production and activation of specific proteins that allow the cell to commit suicide. However, in cancer cells these death pathways are often turned off, while the proteins that allow the cell to divide and multiply are stuck in the “on” position.

One way to fight cancer is to find ways to turn on these death pathways, which is what researchers believe is happening with the AAV2 virus. In tissue culture dishes in the laboratory, 100 percent of the cancer cells are destroyed by the virus within seven days, with the majority of the cell death proteins activated on the fifth day. In another study, a fourth breast cancer derived cell line, which is the most aggressive, required three weeks to undergo cell death

“We can see the virus is killing the cancer cells, but how is it doing it?” Alam said. “If we can determine which viral genes are being used, we may be able to introduce those genes into a therapeutic. If we can determine which pathways the virus is triggering, we can then screen new drugs that target those pathways. Or we may simply be able to use the virus itself.”

Research needs to be completed to learn how AAV2 is killing cancer cells and which of its proteins are activating the death pathways.

According to Meyers, the cellular myc gene seems to be involved. While usually associated with cell proliferation, myc is a protein also known to promote cell death. The scientists have observed increased expression of myc close to the time of death of the breast cancer cells in the study. They report their results in a recent issue of Molecular Cancer.

AAV2 does not affect healthy cells. However, if AAV2 were used in humans, the potential exists that the body’s immune system would fight to remove it from the body. Therefore, by learning how AAV2 targets the death pathways, researchers potentially can find ways to treat the cancer without using the actual virus.

In ongoing studies, the Penn State researchers have also shown AAV2 can kill cells derived from prostate cancer, methoselioma, squamous cell carcinoma, and melanoma. A fourth line of breast cancer cells – representing the most aggressive form of the disease – was also studied in a mouse breast tumor model, followed by treatment with AAV2. Preliminary results show the destruction of the tumors in the mice, and researchers will report the findings of those mouse studies soon.

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Other researchers on this project are Brian S. Bowser and Mohd Israr, Department of Microbiology and Immunology; Michael J. Conway, Section of Infection Diseases, Yale School of Medicine; and Apurva Tandon, Department of Microbiology, Immunology and Pathology, Colorado State University.

The Pennsylvania Department of Health, Breast and Cervical Cancer Initiative supported this research. The researchers have filed for a U.S. patent on this work

Cancer conflict with chemotherapy treatment – Chemotherapy gave no Survival advantage

Contact: Charlotte Webber press@biomedcentral.com 44-020-763-19980 BioMed Central

Young women suffering from breast cancer do not necessarily benefit from chemotherapy treatment

Women under the age of forty with breast cancer who are given drugs in addition to lumpectomies or radiotherapy, known as adjuvant chemotherapy, may not be benefiting from these drugs. This is especially true if their tumors respond to changing levels of hormones such as estrogen, according to research published in the online journal, Breast Cancer Research.

“Developing breast cancer at a young age is very worrying in terms of survival,” explained lead researcher Dr J van der Hage. “But some young women may be undergoing not only unpleasant but also unnecessary chemotherapy, which can be avoided.”

Almost 10% of women diagnosed with breast cancer in Europe are under the age of forty. Two thirds of breast cancers, known as estrogen receptor positive (ER+), contain high levels of cells which contain estrogen receptors. These tumors tend to grow less aggressively than estrogen receptor negative (ER-) tumors. Young patients with breast cancer are currently advised to undergo courses of chemotherapy as well as removal of the tumor and/or entire breast. A research team of the European Organisation for Research and Treatment of Cancer (EORTC) selected patients from four EORTC-trials which were coordinated by Professor C.J.H. van de Velde from the Leiden University Medical Center, to study the effect of chemotherapy in young women. The research team found that ER+ patients, while they benefited from their chemotherapy treatment, did not survive at higher rates than ER- patients.

The difference in survival rates between the two treatment groups was just 5% (in favour of the ER- group), indicating that the chemotherapy gave no advantage. Of all the patients examined, including those who had only undergone primary treatment such as mastectomy, over 25% had died seven years after initial diagnosis.

“Adjuvant chemotherapy is a well established, but ineffective treatment in ER+ breast cancer patients aged 40 years or less . Hormone responsiveness is the key to tailoring therapy in the future fight against this disease for young women,” concluded Dr van der Hage.

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Article Efficacy of adjuvant chemotherapy according to hormone receptor status in young breast cancer patients Jos A. van der Hage, Sven J.S.D. Mieog, Marc J. van de Vijver and Cornelis J.H. van de Velde Breast Cancer Research (in press)

Notes to Editors:

  • Material taken from 480 breast cancer patients all under 40 years old form the basis for this study.
  • Patients were selected from four European Organisaiton for Research and Treatment of Cancer (EORTC) trials conducted by the EORTC Breast Cancer and radiotherapy group.
  • 9938 patients participated in the EORTC trials, 934 of whom were under the age 40 when diagnosed. 

During embargo, article available at:http://www.biomedcentral.com/imedia/1903911851162796_manuscript.pdf

After the embargo, article available at:http://breast-cancer-research.com/

Article citation and URL available on request at press@biomedcentral.com on the day of publication

Please quote the journal in any story you write. If you are writing for the web, please link to the article. All articles are available free of charge, according to BioMed Central’s Open Access policy.

For author contact details please contact Charlotte Webber (Press Office, BioMed Central) Phone: +44 (0)20 7631 9980 Email: press@biomedecentral.com

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Genetically engineering ‘ethical’ babies is a moral obligation, says Editor-in-chief of the Journal of Medical Ethics

Genetically screening our offspring to make them better people is just ‘responsible parenting’, claims an eminent Oxford academic

By

3:33PM BST 16 Aug 2012

Professor Julian Savulescu said that creating so-called designer babies could be considered a “moral obligation” as it makes them grow up into “ethically better children”.

The expert in practical ethics said that we should actively give parents the choice to screen out personality flaws in their children as it meant they were then less likely to “harm themselves and others”.

The academic, who is also editor-in-chief of the Journal of Medical Ethics, made his comments in an article in the latest edition of Reader’s Digest.

He explained that we are now in the middle of a genetic revolution and that although screening, for all but a few conditions, remained illegal it should be welcomed.

He said that science is increasingly discovering that genes have a significant influence on personality – with certain genetic markers in embryo suggesting future characteristics.

By screening in and screening out certain genes in the embryos, it should be possible to influence how a child turns out.

In the end, he said that “rational design” would help lead to a better, more intelligent and less violent society in the future.

“Surely trying to ensure that your children have the best, or a good enough, opportunity for a great life is responsible parenting?” wrote Prof Savulescu, the Uehiro Professor in practical ethics.

“So where genetic selection aims to bring out a trait that clearly benefits an individual and society, we should allow parents the choice.

“To do otherwise is to consign those who come after us to the ball and chain of our squeamishness and irrationality.

“Indeed, when it comes to screening out personality flaws, such as potential alcoholism, psychopathy and disposition to violence, you could argue that people have a moral obligation to select ethically better children.

“They are, after all, less likely to harm themselves and others.”

“If we have the power to intervene in the nature of our offspring — rather than consigning them to the natural lottery — then we should.”

He said that we already routinely screen embryos and foetuses for conditions such as cystic fibrosis and Down’s syndrome and couples can test embryos for inherited bowel and breast cancer genes.

Rational design is just a natural extension of this, he said.

He said that unlike the eugenics movements, which fell out of favour when it was adopted by the Nazis, the system would be voluntary and allow parents to choose the characteristics of their children.

“We’re routinely screening embryos and foetuses for conditions such as cystic fibrosis and Down’s syndrome, and there’s little public outcry,” he said.

“What’s more, few people protested at the decisions in the mid- 2000s to allow couples to test embryos for inherited bowel and breast cancer genes, and this pushes us a lot close to creating designer humans.”

“Whether we like it or not, the future of humanity is in our hands now. Rather than fearing genetics, we should embrace it. We can do better than chance.”

Full article appears in September issue of Reader’s Digest, out 21st August

http://www.telegraph.co.uk/science/science-news/9480372/Genetically-engineering-ethical-babies-is-a-moral-obligation-says-Oxford-professor.html

Red wine ingredient resveratrol stops breast cancer growth – FASEB Journal

Red wine ingredient resveratrol stops breast cancer growth

New research in the FASEB Journal shows that resveratrol blocks the growth effects of estrogen by reducing the specific breast cancer receptors

Bethesda, MD—Cheers! A new research report appearing in the October 2011 issue of The FASEB Journal (https://www.fasebj.org) shows that resveratrol, the “healthy” ingredient in red wine, stops breast cancer cells from growing by blocking the growth effects of estrogen. This discovery, made by a team of American and Italian scientists, suggests for the first time that resveratrol is able to counteract the malignant progression since it inhibits the proliferation of hormone resistant breast cancer cells. This has important implications for the treatment of women with breast cancer whose tumors eventually develop resistance to hormonal therapy.

“Resveratrol is a potential pharmacological tool to be exploited when breast cancer become resistant to the hormonal therapy,” said Sebastiano Andò, a researcher involved in the work from the Faculty of Pharmacy at the University of Calabria in Italy.

To make this discovery, Andò and colleagues used several breast cancer cell lines expressing the estrogen receptor to test the effects of resveratrol. Researchers then treated the different cells with resveratrol and compared their growth with cells left untreated. They found an important reduction in cell growth in cells treated by resveratrol, while no changes were seen in untreated cells. Additional experiments revealed that this effect was related to a drastic reduction of estrogen receptor levels caused by resveratrol itself.

“These findings are exciting, but in no way does it mean that should people go out and start using red wine or resveratrol supplements as a treatment for breast cancer,” said Gerald Weissmann, M.D., Editor-in-Chief of The FASEB Journal. “What it does mean, however, is that scientists haven’t finished distilling the secrets of good health that have been hidden in natural products such as red wine.”

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Receive monthly highlights from The FASEB Journal by e-mail. Sign up at http://www.faseb.org/fjupdate.aspx. The FASEB Journal (http://www.fasebj.org) is published by the Federation of the American Societies for Experimental Biology (FASEB) and celebrates its 25th anniversary in 2011. Over the past quarter century, the journal has been recognized by the Special Libraries Association as one of the top 100 most influential biomedical journals of the past century and is the most cited biology journal worldwide according to the Institute for Scientific Information.

FASEB comprises 24 societies with more than 100,000 members, making it the largest coalition of biomedical research associations in the United States. FASEB enhances the ability of scientists and engineers to improve—through their research—the health, well-being and productivity of all people. FASEB’s mission is to advance health and welfare by promoting progress and education in biological and biomedical sciences through service to our member societies and collaborative advocacy.

Details:  Francesca De Amicis, Francesca Giordano, Adele Vivacqua, Michele Pellegrino, Maria Luisa Panno, Donatella Tramontano, Suzanne A. W. Fuqua, and Sebastiano Andò.  Resveratrol, through NF-Y/p53/Sin3/HDAC1 complex phosphorylation, inhibits estrogen receptor α gene expression via p38MAPK/CK2 signaling in human breast cancer cells. FASEB J. 2011 25:3695-3707; doi:10.1096/fj.10-178871 ;  http://www.fasebj.org/content/25/10/3695.abstract

BPA exposure in utero may increase predisposition to breast cancer

Contact: Aaron Lohr alohr@endo-society.org 240-482-1380 The Endocrine Society

Study finds perinatal exposure to BPA has effect on mammary hormone response

Chevy Chase, MD—A recent study accepted for publication in Molecular Endocrinology, a journal of The Endocrine Society, found that perinatal exposure to environmentally relevant doses of bisphenol A (BPA) alters long-term hormone response and breast development in mice that may increase the propensity to develop cancer.

BPA, a man-made chemical produced and marketed largely for specific industrial purposes, is detected in body fluids of more than 90 percent of the human population. It was originally synthesized as an estrogenic compound and there has been concern that exposure to BPA could have developmental effects on various hormone-responsive organs including the mammary gland.

“I want it to be clear that we do not provide evidence that BPA exposure causes breast cancer per se,” said Cathrin Brisken, MD, of the Swiss Institute for Experimental Cancer Research and co-author of the study. “We do provide evidence that BPA exposure alters mammary gland development and that this may increase the predisposition of the breast to breast cancer.”

In this study, researchers mimicked human exposure to BPA as it occurs with beverages and food from BPA containing vessels (such as plastics and the lining of tin cans) by adding the compound to the drinking water of breeding mice. Female pups born from BPA-consuming parents were transferred to a BPA-free environment at weaning and followed over time.

Researchers analyzed changes in the mammary gland of female offspring that were exposed to BPA through their mothers in utero and while being breast fed. The mammary glands of BPA exposed females showed an increased response to the hormone progesterone. Lifetime exposure to progesterone has been linked to increase breast cancer risk.

Furthermore, researchers  found that adult females who had been exposed to BPA in utero and while breast fed, showed a 1.5 fold increase in cell numbers in their milk ducts. This is comparable to what is seen upon similar exposure to another estrogenic compound, diethyllbestrol (DES). Uterine exposure to DES in the human population has been shown to increase the relative risk of getting breast cancer two-fold as women reach their fifties.

“While we cannot extrapolate these results directly from mice to humans, the possibility that some of the increase in breast cancer incidence observed over the past decades may be attributed to exposure to BPA cannot be dismissed,” said Brisken. “Our study suggests that pregnant and breastfeeding mothers should avoid exposure to BPA as it may affect their daughters’ breast tissue.”

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Other researchers working on the study include Ayyakkannu Ayyanan, Ouahiba Laribi, Sonia Schuepbach-Mallepell, Christina Schrick, Maria Gutierrez, Tamara Tanos and Ozden Yalcin-Ozuysal of the Swiss Institute for Experimental Cancer Research; and Gregory Lefebvre and Jacques Rougemont of École polytechnique fédérale de Lausanne in Switzerland.

The article, “Perinatal exposure to bisphenol A increases adult mammary gland progesterone response and cell number,” appears in the November 2011 issue of Molecular Endocrinology.

Founded in 1916, The Endocrine Society is the world’s oldest, largest and most active organization devoted to research on hormones and the clinical practice of endocrinology.  Today, The Endocrine Society’s membership consists of over 14,000 scientists, physicians, educators, nurses and students in more than 100 countries. Society members represent all basic, applied and clinical interests in endocrinology. The Endocrine Society is based in Chevy Chase, Maryland. To learn more about the Society and the field of endocrinology, visit our site at www.endo-society.org.

High rate of false-positives with annual mammogram

During a decade of receiving mammograms, more than half of cancer-free women will be among those summoned back for more testing because of false-positive results, and about one in 12 will be referred for a biopsy.

Simply shifting screening to every other year lowers a woman’s probability of having one of these false-positive episodes by about a third – from 61 percent to 42 percent – over the course of a decade.

A new study delving into false-positives in mammography looked at nearly 170,000 women between the ages of 40 and 59 from seven regions around the United States, and almost 4,500 women with invasive breast cancer. Because of the added decade of testing alone, it found, women who start mammograms at 40 instead of 50 are more likely to have false-positive results that lead to more testing.

“This study provides accurate estimates of the risk of a false-positive mammography and breast biopsy for women undergoing repeat mammography in community practice, and so provides important information about the potential harms of undergoing regular mammography,” said co-author Karla Kerlikowske, a professor of medicine at the UCSF School of Medicine.

The study will be published in Annals of Internal Medicine. The research was led by Group Health Research Institute of Seattle for the Breast Cancer Surveillance Consortium.

“Recalls” for a second mammogram for what turn out to be non-cancer results, known as false positives, may cause inconvenience and anxiety. Recommendations for fine-needle aspiration or surgical biopsy are less common, but can lead to unnecessary pain and scarring. The additional testing also contributes to rising medical costs.

Kerlikowske is the lead author of an additional report – to be published in the same issue of Annals – that for the first time in the United States examines the accuracy of film mammography against digital, which has increasingly replaced older film screening.

That study looked at nearly 330,000 women between the ages of 40 and 79. The data was pooled from the Breast Cancer Surveillance Consortium, a collaborative network of mammography registries in the United States.

The researchers found that overall cancer detection rates were similar for both methods. However, digital screening may be better for women between the ages of 40 and 49 who are more likely to have extremely dense breasts associated with lower cancer detection. The study also found new evidence that digital mammography is better at detecting estrogen receptor-negative tumors, particularly in women aged 40 to 49 years.

Breast cancer may not be detected, the researchers caution, if a radiologist fails to identify a visible breast lesion or if a tumor is obscured by normal breast tissue. Additionally, an imperceptible tumor may grow quickly and be discovered through a clinical exam prior to the next mammogram.

Digital mammography was developed in part to improve the detection of breast cancer in dense breasts by improving the ability to distinguish normal dense breast tissue from isodense invasive cancer.

The authors note that for every 10,000 women 40 to 49 who are given digital mammograms, two more cases of cancer will be identified for every 170 additional false-positive examinations.

Healthy women will undergo 12 screening mammograms in their lifetimes if they follow U.S. Preventive Services Task Force guidelines that recommend biennial screening starting at age 50 and continuing until age 74. This is controversial, with many practitioners recommending annual mammograms.

If women start biennial screening at 40, they will undergo 17 exams; those who start annual screenings at age 40 will undergo 34 exams.

For the false-positive study, the researchers found that after a decade of annual screening, a majority of women will receive at least one false-positive result, and 7 to 9 percent will receive a false-positive biopsy recommendation.

“We conducted this study to help women know what to expect when they get regular screening mammograms over the course of many years,” said study leader Rebecca Hubbard, PhD, an assistant investigator at Group Health Research Institute. “We hope that if women know what to expect with screening, they’ll feel less anxiety if – or when – they are called back for more testing. In the vast majority of cases, this does not mean they have cancer.”

The researchers say that screening every other year would likely lessen the probability of false-positive results “but could also delay cancer diagnosis.”  However, for those diagnosed with cancer, the authors found women screened every two years were not significantly more likely to be diagnosed with late-stage cancer compared to those screened at one-year intervals.

The study stresses the importance of radiologists being able to review a patient’s previous mammograms because it “may halve the odds of a false-positive recall.”

US cancer body oversells mammograms: experts

AFP 2 Aug 2012

Medical experts on Friday accused a major US breast cancer foundation known for its high-profile “pink ribbon” campaign of overselling pre-emptive mammography and understating the risks.

The Susan G. Komen for the Cure foundation uses misleading statistics in its pro-screening campaigns, two doctors from The Dartmouth Institute for Health Policy and Clinical Practice in New Hampshire wrote in the BMJ medical journal.

“Unfortunately, there is a big mismatch between the strength of evidence in support of screening and the strength of Komen’s advocacy for it,” professors Steven Woloshin and Lisa Schwartz wrote.

They take issue with a Komen poster comparing the 98-percent five-year survival rate for breast cancer when caught early, with a of 23-percent rate for later diagnosis.

Comparing the two figures did not tell you anything about the benefits of screening, they argued, and in reality a mammogram only narrowly decreases the chances that a 50-year-old woman will die from breast cancer within 10 years from 0.53 percent to 0.46 percent.

Breast cancer treatments are more effective today, and some question whether screening mammography has any benefit whatsoever, wrote the pair.

They accused Komen of overlooking the potential harms, with up to half of women screened annually over 10 years experiencing at least one false alarm that requires a biopsy.

Screening also results in overdiagnosis — detecting cancers that would never have killed or even caused symptoms in a person’s lifetime, and unnecessary treatment.

“The Komen advertisement campaign failed to provide the facts,” said the piece. “Worse, it undermined decision making by misusing statistics to generate false hope about the benefit of mammography screening.”

In 2010, a report in the New England Journal of Medicine said mammograms have only a “modest” impact on reducing breast cancer deaths.

Komen, in a response to the BMJ comment, insisted that early detection enables early treatment, which gives the best shot at survival.

“Everyone agrees that mammography isn’t perfect, but it’s the best widely available detection tool that we have today,” said Chandini Portteus, the foundation’s vice president of research, evaluation and scientific programmes.

“We’ve said for years that science has to do better, which is why Komen is putting millions of dollars into research to detect breast cancer before symptoms start, through biomarkers, for example.”

In February, Komen was embroiled in a controversy over its decision to stop funding for an abortion clinic group in the United States.

New study supports claim that breast screening may be causing more harm than good

Requested Repost from Dec 2011

Research: Possible net harms of breast cancer screening: Updated modelling of Forrest report

A new study published on bmj.com today supports the claim that the introduction of breast cancer screening in the UK may have caused more harm than good.

Harms included false positives (abnormal results that turn out to be normal) and overtreatment (treatment of harmless cancers that would never have caused symptoms or death during a patient’s lifetime). This may be because the cancer grows so slowly that the patient dies of other causes before it produces symptoms, or the cancer remains dormant or regresses.

It shows that the harms of screening largely offset the benefits up to 10 years, after which the benefits accumulate, but by much less than predicted when screening was first started.

The Forrest report in 1986, which led to the introduction of breast cancer screening in the UK, estimated the number of screened and unscreened women surviving each year over a 15-year period.  Costs and benefits were measured in quality adjusted life years or QALYs (a combined measure of quantity and quality of life) but it omitted harms.

It suggested that screening would reduce the death rate from breast cancer by almost one third with few harms and at low cost.

Since the Forrest report, the harms of breast cancer screening have been acknowledged. So, researchers at the University of Southampton set out to update the report’s survival estimates by combining the benefits and harms of screening in one single measure.

The results are based on 100,000 women aged 50 and over surviving by year up to 20 years after entry to the screening programme.

Inclusion of false positives and unnecessary surgery reduced the benefits of screening by about half. The best estimates generated negative net QALYs for up to eight years after screening and minimal gains after 10 years.

After 20 years, net QALYs accumulate, but by much less than predicted by the Forrest report.

The authors say more research is needed on the extent of unnecessary treatment and its impact on quality of life. They also call for improved ways of identifying those most likely to benefit from surgery and for measuring the levels and duration of the harms from surgery. From a public perspective, the meaning and implications of overdiagnosis and overtreatment need to be much better explained and communicated to any woman considering screening, they add.

However, the continuing uncertainty surrounding the extent of overtreatment is apparent in a study of French women published on bmj.com last month, which put overdiagnosis of invasive breast cancer due to screening at around 1%.

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Avastin, Sutent increase breast cancer stem cells, U-M study shows

 

ANN ARBOR, Mich. — Cancer treatments designed to block the growth of blood vessels were found to increase the number of cancer stem cells in breast tumors in mice, suggesting a possible explanation for why these drugs don’t lead to longer survival, according to a new study by researchers at the University of Michigan Comprehensive Cancer Center.

The drugs Avastin and Sutent have been looked at as potential breast cancer treatments. But while they do shrink tumors and slow the time till the cancer progresses, the effect does not last, and the cancer eventually regrows and spreads.

“This study provides an explanation for the clinical trial results demonstrating that in women with breast cancer antiangiogenic agents such as Avastin delay the time to tumor recurrence but do not affect patient survival. If our results apply to the clinic, it suggests that in order to be effective, these agents will need to be combined with cancer stem cell inhibitors, an approach now being explored in the laboratory,” says study author Max S. Wicha, M.D., director of the U-M Comprehensive Cancer Center.

The researchers treated mice with breast cancer using Avastin (bevacizumab) and Sutent (sunitinib), both of which work by stopping the growth and formation of blood vessels, a process called angiogenesis. The researchers found that tumors treated with these drugs developed more cancer stem cells, the small number of cells within a tumor that fuel a cancer’s growth and spread and that are often resistant to standard treatment. Both the number of cancer stem cells and the percentage of cancer stem cells that make up the tumor increased after being treated with each of these therapies.

The researchers found that the cancer stem cells increased because of a cellular response to low oxygen, a condition called hypoxia. And they were able to determine the specific pathways involved in hypoxia that activate the cancer stem cells.

Results of the study appear online in the Proceedings of the National Academy of Sciences Early Edition.

The U.S. Food and Drug Administration recently revoked approval of Avastin for treating breast cancer, although the drug is approved for use in other types of cancer. The reversal was in response to clinical trials showing that the drug’s benefit was short-lived, with breast cancer patients quickly relapsing and the cancer becoming more invasive and spreading further throughout the body. Overall, the drug did not help patients live any longer.

The current study suggests the possibility of combining anti-angiogenesis drugs with a cancer stem cell inhibitor to enhance the benefit of this treatment. The researchers are testing this approach in mice and preliminary data looks promising.

Breast cancer statistics: 209,060 Americans will be diagnosed with breast cancer this year and 40,230 will die from the disease, according to the American Cancer Society

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Additional authors: Sarah J. Conley, Elizabeth Gheordunescu, Pramod Kakarala, Bryan Newman, Hasan Korkaya, Amber N. Heath and Shawn G. Clouthier, all from U-M

Funding: Breast Cancer Research Foundation, National Institutes of Health and the U-M Taubman Institute

Disclosure: Wicha is a consultant for Pfizer and OncoMed Pharmaceuticals and holds equity in OncoMed Pharmaceuticals.

Reference: Proceedings of the National Academy of Sciences Early Edition, DOI: 10.1073/pnas.1018866109