MAYWOOD, Ill. -- A new study is providing insight into how estrogen fuels many breast cancers, and researchers say the findings could lead to new cancer-fighting drugs.

Researchers found that estrogen inhibits a protein called MLK3 that causes normal cell death. Blocking MLK3 leads to uncontrolled growth of cancer cells and resistance to chemotherapyterm.

Researchers from Loyola University Health System and three other centers reported the findings in the journal Cancer Research.

SAN ANTONIO – Anti-estrogens as therapy for breast cancer may also reduce the risk of death from lung cancer, according to study results presented at the CTRC-AACR San Antonio Breast Cancer Symposium, held here Dec. 9-13, 2009.

Washington, D.C. – Researchers at Georgetown University Medical Center have discovered a novel way in which breast cancer cells become resistant to tamoxifen, the world's largest-selling breast cancer prevention and treatment drug. They say the findings could provide a way to identify tamoxifen users who are no longer benefiting from the drug, allowing doctors to try another therapy option sooner.

In the November 1 issue of the journal Cancer Research, the researchers show that breast cancer cells that are resistant to tamoxifen display few of the "alpha" estrogen receptors that the drug is designed to bind on to and inhibit, but many more "gamma" estrogen-related receptors, which tamoxifen seems to activate. These two receptors are not closely related – they are more like distant cousins than siblings, researchers say, adding that understanding how these gamma estrogen-related receptors work may— eventually— help in designing new, more effective drugs targeting these receptors.

Women taking aromatase inhibitors to treat breast cancer or prevent its recurrence should think twice before also taking a soy-based dietary supplement, researchers report.

Genistein, a soy isoflavone that mimics the effects of estrogen in the body, can negate the effectiveness of aromatase inhibitors, which are designed to reduce the levels of estrogens that can promote tumor growth in some types of breast cancer.

The new study, which included researchers from the University of Illinois, Virginia Polytechnic and State University and the National Center for Toxicological Research, appears in the journal Carcinogenesis.

Aromatase inhibitors are a mainstay of breast cancer treatment in post-menopausal women. These drugs work by interfering with the enzyme aromatase, which catalyzes a crucial step in converting precursor molecules to estradiol, the main estrogen in the body.

About two-thirds of all cases of breast cancer diagnosed in the U.S. are estrogen dependent or estrogen sensitive, which means that the tumors grow more rapidly in the presence of estrogen.

Most women diagnosed with breast cancer are post-menopausal, so their ovaries are no longer producing normal levels of estrogen. Other tissues, however, produce a steroid hormone, androstenedione (AD), which – with the help of aromatases – is converted to testosterone and estrogens. The estrogens produced from AD can stimulate the growth of some types of breast cancer tumors.

Women whose breast cancer came back after treatment had almost twice as much estrogen in their blood than did women who remained cancer-free – despite treatment with anti-estrogen drugs in a majority of the women –according to researchers in a study published in the March issue of Cancer Epidemiology, Biomarkers and Prevention, a journal of the American Association for Cancer Research.

The findings suggest that high levels of estrogen contribute to an increased risk of cancer recurrence, just as they lead to the initial development of breast cancer, said the study’s lead author, Cheryl L. Rock, Ph.D., a professor in the Department of Family and Preventive Medicine at the University of California, San Diego.

SEATTLE – Postmenopausal women who take combined estrogen/progestin hormone-replacement therapy for three years or more face a fourfold increased risk of developing various forms of lobular breast cancer, according to new findings by researchers at Fred Hutchinson Cancer Research Center.

“Previous research indicated that five or more years of combined hormone-therapy use was necessary to increase overall breast-cancer risk,” said Christopher I. Li, M.D., Ph.D., the lead author of the report, published in the January issue of Cancer Epidemiology, Biomarkers and Prevention. “Our study, the first specifically designed to evaluate the relationship between combined HRT and lobular breast cancers, suggests that a significantly shorter length of exposure to such hormones may confer an increased risk.”

LOS ANGELES, April 17 – A new study from the University of Pittsburgh Cancer Institute's Center for Environmental Oncology suggests that fish caught in Pittsburgh rivers contain substances that mimic the actions of estrogen, the female hormone. Since fish are sentinels of the environment, and can concentrate chemicals from their habitat within their bodies, these results suggest that feminizing chemicals may be making their way into the region's waterways.

The study, abstract number 3458, being presented at the annual meeting of the American Association for Cancer Research, April 14-18, at the Los Angeles Convention Center, also demonstrated that the chemicals extracted from the local fish can cause growth of estrogen-sensitive breast cancer cells cultured in the laboratory. Extracts of fish caught in areas heavily polluted by industrial and municipal wastes resulted in the greatest amount of cell growth.