Physicians who treat women with the breast cancer susceptibility gene BRCA1 often remove their patients’ ovaries to eliminate the source of estrogen they believe fuels cancer growth. Yet they also know that anti-estrogen therapies don’t work to treat breast or ovarian cancer that might develop. That paradox has led scientists to question exactly how, or if, estrogen is involved in cancer development and whether removal of ovaries makes sense.
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1. Sorting Out Membrane-Initiated Estrogen EffectsMarissa I. Boulware, Holly Kordasiewicz, and Paul G. MermelsteinThe caveolins (CAV1-3) are, not surprisingly, integral components of caveolae, pockets within the plasma membrane capable of signal transduction. In this week’s Journal, Boulware et al. describe two distinct estrogen receptor signaling pathways that require caveolins, thus providing a potential mechanism for the membrane effects of estrogens.
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More than 10 percent of women with breast cancer stopped taking a commonly prescribed drug because of joint and muscle pain, according to a new study from researchers at the University of Michigan Comprehensive Cancer Center.The women in the study were taking aromatase inhibitors, a type of drug designed to block the production of estrogen, which fuels some breast cancers.
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Scientists have discovered new information about an immune pathway in mice that explains how oxidative stress that results from acute estrogen deficiency leads to the loss of bone. The finding, published in the Proceedings of the National Academy of Sciences, could help in identifying a new drug target for preventing postmenopausal bone loss.
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The deterioration in immune function that occurs as an individual ages is thought to occur because the thymus involutes with age, causing a dramatic decrease in T cell output. New data generated by Dennis Taub and colleagues from the National Institutes of Health, Baltimore, suggest that in mice, thymic involution is caused by a decrease upon aging in thymic expression of both a hormone that is better known as a stimulator of food intake (ghrelin) and its receptor.
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A specific gene mutation may be useful in predicting the level of aggression of thyroid cancer and help guide treatment options and follow-up care, according to new study findings.The mutation, called BRAF V600E, is a genetic alteration in the BRAF oncogene, a modified gene believed to cause cancer. The new research is reported in the September issue of the Annals of Surgery.
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New insights into the role of estrogen receptor in mammary gland development may help scientists better understand the molecular origin of breast cancer, according to new research from the University of Cincinnati (UC).About a decade ago, U.S. scientists at the National Institutes of Health (NIH) developed a standard estrogen receptor (ER) gene knock-out mouse model to study the estrogen receptor’s role in human diseases.
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