PINK MONTH- BREAST CANCER AWARENESS WEEK

[drmithila]

As the entire world takes steps forward in helping women all over fight against breast cancer, as doctors its our duty to be a part of this….let us all try and do our bit in raising as much awareness we can….CELEBRATE THE PINK MONTH….SPREAD AWARENESS

Put up awareness charts in your clinics to help and reach anyone you can…

        

[drmithila]

Striking new evidence suggesting that diet and related factors early in life can boost the risk for breast cancer — totally independent of the body’s production of the hormone estrogen — has been uncovered by a team of researchers at the University of California, Davis.
The findings provide new insights into the processes that regulate normal breast development, which can impact the risk of developing breast cancer later in life. The study will be published Sept. 17 in the early edition of the Proceedings of the National Academy of Sciences.
"It’s long been assumed that circulating estrogens from the ovaries, which underlie normal female reproductive development, were crucial for the onset of breast growth and development," said Russ Hovey, a UC Davis associate professor of animal science and senior author on the study.
"Our findings, however, suggest that diet and shifts in body metabolism that parallel changes seen during obesity and Type 2 diabetes can also stimulate breast growth entirely independent of estrogen’s effects," he said.
The studies with mice used a diet supplemented with a form of the fatty acid known as 10, 12 conjugated linoleic acid or 10, 12 CLA, which mimics specific aspects of a broader metabolic syndrome.
In humans, this syndrome is linked to a broad array of changes associated with obesity that can increase the risk of Type 2 diabetes and cardiovascular disease.
The 10, 12 CLA was added to the diet of the test group of mice because it is known to disrupt normal metabolic processes. In this study, the supplement stimulated the mammary ducts to grow, despite the fact that the mice lacked estrogen.
The researchers demonstrated that the diet-induced breast development also increased the formation of mammary tumors in some of the mice.
They ruled out a role for estrogen as the possible cause for how diet increased growth of the breast tissues by giving the supplement to male mice and to female mice in which the function of estrogen was blocked.
The research team also discovered that various mouse strains responded differently to the dietary supplement despite similar metabolic changes, suggesting that there may be a genetic component for how diet and related metabolic changes affect breast cancer risk in different populations, Hovey said.
He noted that results from the study would likely have significant implications for better understanding human breast development before puberty and after menopause, when estrogens are less present.
"The findings of this study are particularly important when we superimpose them on data showing that girls are experiencing breast development at earlier ages, coincident with a growing epidemic of childhood obesity," Hovey said.
Adam Lock, an assistant professor of dairy cattle nutrition at Michigan State University, was co-principal investigator with Hovey on the original Dairy Management Inc. grant that supported studies leading to the PNAS publication.
"The biology of conjugated linoleic acid fatty acids has stimulated much scientific and public interest over the last two decades," said Lock. "These recent findings will further our understanding of the biology of this specific CLA isomer and also further advance our understanding of the role of bioactive fatty acids in health maintenance and disease prevention."
Other members of the research team are graduate students Grace Berryhill and Julia Gloviczki, Project Scientist Josephine Trott, postdoctoral researchers Lucila Aimo and Whitney Petrie, undergraduate student Carly Paul, and Professor Robert Cardiff, all of UC Davis; and Research Assistant Professor Jana Kraft of the University of Vermont.
The study was supported in part by Dairy Management Inc., the UC Davis Cancer Center and the Department of Defense

 

        

[drmithila]

A University of Cincinnati (UC) cancer biology team reports breakthrough findings about specific cellular mechanisms that may help overcome endocrine (hormone) therapy-resistance in patients with estrogen-positive breast cancers, combating a widespread problem in effective medical management of the disease.
Xiaoting Zhang, PhD, and his colleagues have identified a specific estrogen receptor co-activator — known as MED1 — as playing a central role in mediating tamoxifen resistance in human breast cancer. The team reports its findings in the Nov. 1, 2012, issue of Cancer Research, a scientific journal of the American Association for Cancer Research.
According to the National Cancer Institute, nearly 227,000 women are diagnosed with breast cancer annually in the United States. About 75 percent have estrogen-positive tumors and require adjuvant hormone therapy such as tamoxifen, a drug that works by interfering with estrogen’s ability to stimulate breast cancer cell growth.
Despite advances in hormone therapy drugs, cancer surveillance research has shown that 50 percent of patients will develop resistance to the drug and experience a cancer relapse.
The hormones estrogen and progesterone can stimulate the growth of some breast cancers. Hormone therapy is used to stop or slow the growth of these tumors. Hormone-sensitive (i.e., positive) breast cancer cells contain specific proteins known as hormone receptors that become activated once hormones bind to them, leading to cancer growth.
Based on new findings, UC Cancer Institute scientists believe that tamoxifen resistance may be driven by a novel molecular “crosstalk” point between the estrogen and HER2 (human epidermal growth factor receptor 2) signaling pathways.
Testing in both pre-clinical models and human breast cancer tissue samples showed that MED1 co-amplifies and co-expresses with HER2, a gene that has an increased presence in 20-30 percent of invasive human breast cancer and plays a major role in tamoxifen resistance.
HER2 over-expression led to MED1 activation while reduction of MED1 caused breast cancer cells that were otherwise tamoxifen-resistant to respond and stop dividing. Further mechanistic studies showed that HER2 activation of MED1 resulted in the recruitment of co-activators instead of co-repressors by tamoxifen-bound estrogen receptor. This, explains Zhang, drives expression of not only traditional estrogen receptor-positive cancer target genes, but also HER2 and those estrogen receptor target genes abnormally activated by HER2.
“Together, these findings suggest this ‘crosstalk’ could play a central role in mediating tamoxifen resistance in human breast cancer, especially because recent published data also indicated that high MED1 expression levels correlate with poor treatment outcome and disease-free survival of patients who underwent endocrine therapy,” explains Zhang, an assistant professor of cancer biology at the UC College of Medicine and breast cancer researcher with the UC Cancer Institute.
“We are currently utilizing RNA-based nanotechnology to target MED1 in an effort to simultaneously block both estrogen and HER2 pathways to overcome endocrine-resistant breast cancer.”
UC study collaborators include cancer biologists Jiajun Cui, PhD, Katherine Germer, MD, Shao-chun Wang, PhD; environmental health researcher Tianying Wu, PhD; and pathologist Jiang Wang, MD. Qianben Wang, PhD of the Ohio State University College of Medicine, and Jia Luo, PhD, of the University of Kentucky, also contributed to this study.
The study was supported with start-up funding from the UC Cancer Institute, Ride Cincinnati/Marlene Harris Pilot Grant, Susan G. Komen for the Cure Foundation and the Center for Clinical and Translational Science and Training — home to UC’s institutional Clinical and Translational Science Award program grant from the National Institutes of Health.

        

[Author]

Posts