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Archive - Nov 3, 2012

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New Clues for Overcoming Tamoxifen-Resistant Breast Cancer

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, Ph.D., 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 reported its findings online 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.

Multicenter Team Identifies Promising Treatment for Polycystic Kidney Disease

A drug therapy shows promise for treating an inherited form of kidney disease called autosomal dominant polycystic kidney disease (ADPKD), Mayo Clinic researchers say. The medication, tolvaptan, slowed the pace of kidney cyst growth over the three years of the study. The phase three clinical trial results were being presented on November 3, 2012 at the American Society of Nephrology annual meeting and published online in the New England Journal of Medicine. The multicenter study found tolvaptan demonstrated a nearly 50 percent reduction in the rate of increase in total kidney volume (a measurement of kidney cyst growth) in ADPKD patients over the study period, compared to placebo. "ADPKD is the most common inherited and the fourth most common overall cause of kidney failure worldwide," says lead author Vicente Torres, M.D., Ph.D., Mayo Clinic nephrologist. "In most patients with this disease, relentless cyst growth within the kidneys destroys the tissue, causes hypertension and painful complications, and negatively impacts the quality of life," Dr. Torres says. "The results of this study reveal a potential treatment that blunts kidney growth, lessens associated symptoms, and slows kidney function decline when given over three years." While the trial findings are encouraging, tolvaptan has not yet been approved for this indication, Dr. Torres notes. [Press release] [New England Journal of Medicine]