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Neil Spector: Getting the Right Drug to the Right Patient

October 29, 2008

By Elizabeth Whittington

Herceptin (trastuzumab) was approved in 1998 as treatment for metastatic breast cancer, marking the beginning of the era of targeted therapies. While the drug, which targeted the HER2 receptor on the surface of breast cancer cells, became the next great hope in cancer therapy, Neil Spector, MD, was developing a small-molecule compound at GlaxoSmith-Kline called GW572016, now known as Tykerb (lapatinib).  With the success and publicity of Herceptin, Spector’s team convinced the company to test the compound in breast cancer.

Why cancer’s gaining on us

October 28, 2008

By Rita Arditti

Rita Arditti is one of the founders of the Cambridge-based Women’s Community Cancer Project, a grassroots organization committed to cancer prevention. She has been living with metastatic breast cancer since 1979. http://cache.boston.com/bonzai-fba/File-Based_Image_Resource/dingbat_story_end_icon.gifOctober 27, 2008  THE BOSTON GLOBE

FOR ALL the pink ribbons, breast-cancer awareness events, fund-raisers, and celebrations of “survivorship,” the facts remain grim. In this country, a woman’s lifetime risk of breast cancer is one in eight. In 1975, the risk was about one in 11.

Aromasin® Does Not Improve Survival of Metastatic Hormone-Positive Breast Cancer Compared to Nolvadex®

October 26, 2008

By CancerConsultants.com

Researchers affiliated with the European Organisation for the Research and Treatment of Cancer (EORTC) and the Breast Cancer Cooperative Group have reported that initial treatment of metastatic hormone receptor-positive breast cancer with Aromasin (exemestane) prolongs progression-free survival, but does not improve overall survival compared to Nolvadex (tamoxifen). The details of this study were published in the October 20, 2008 issue of the Journal of Clinical Oncology.1 

The use of the third-generation non-steroidal aromatase inhibitors Aromasin, Arimidex® (anastrozole) and Femara® (letrozole) is becoming increasingly widespread in the treatment of postmenopausal, hormone-positive breast cancer. All three of these agents are approved by the U.S. Food and Drug Administration for the treatment of hormone-positive breast cancer. Aromatase inhibitors have significant activity in patients who have failed Nolvadex. There are also ongoing clinical trials of aromatase inhibitors for prevention of breast cancer in high-risk women. Clinical trials have suggested that aromatase inhibitors may be superior to Nolvadex for adjuvant treatment of post-menopausal women with hormone receptor-positive breast cancer. Three other studies have compared aromatase inhibitiors to Nolvadex for the initial treatment of metastatic breast cancer and found aromatase inhibitors to be somewhat superior or the same as Nolvadex but with no impact on survival.

Circulating Tumor Cells: New Stratification for Women with Metastatic Breast Cancer?

October 21, 2008

By CancerConsultants.com

Researchers from the MD Anderson Cancer Center have reported that circulating tumor cells are a strong predictor of survival in women with metastatic breast cancer. The details of this study appeared in the October 20, 2008 issue of the Journal of Clinical Oncology.1

In women with localized breast cancer, the presence of tumor cells in the bone marrow has been predictive of a worse outcome, and bone marrow examinations have been suggested as routine staging procedures. A previous multi-center trial in the U.S. has determined that women with breast cancer who have five or more circulating tumor cells have shorter progression-free and overall survivals compared to women with fewer than five circulating tumor cells (see first item of related news). In a more recent trial, researchers from France have reported that circulating tumor cells were present in 59% of women with metastatic breast cancer. They concluded that the presence of circulating tumor cells accurately predicted outcomes.

Nexavar® May Overcome Resistance to Arimidex® in Breast Cancer

October 9, 2008

By CancerConsultants.com

The addition of Nexavar® (sorafenib) to Arimidex® (anastrozole) helps restore sensitivity to Arimidex among women with breast cancer. These results were recently presented at the 2008 annual American Society of Clinical Oncology (ASCO) breast cancer symposium.The majority of breast cancers are hormone positive, meaning that the cancer cells are stimulated to grow from exposure to the female hormones estrogen and/or progesterone. Women with hormone-positive breast cancer receive hormone therapy, which prevents estrogen from forming in the body or blocks the exposure of cancer cells to estrogen. 

Arimidex is a hormone therapy that prevents the formation of estrogen in the body. It is commonly used among postmenopausal women with hormone-positive breast cancer. Unfortunately, some women can become resistant to Arimidex, meaning that their cancer continues to grow despite treatment, whereas others may never respond to Arimidex. Reasons for this lack of response are not clear. Researchers continue to evaluate ways to work around this resistance, such as targeting other biologic pathways associated with cancer.

Nexavar is an agent that has multiple targets involved in several biologic pathways associated with cancer. Used alone, Nexavar has not demonstrated anticancer responses in the treatment of breast cancer; however, researchers have speculated that Nexavar may aid in reversing the resistance to Arimidex or other hormone agents.

Scientists Identify a Molecule That Coordinates the Movement of Cells

October 5, 2008

By Rockefeller University

Even cells commute. To get from their birthplace to their work site, they sequentially attach to and detach from an elaborate track of exceptionally strong proteins known as the extracellular matrix. Now, in research to appear in the October 3 issue of Cell, scientists at Rockefeller University show that a molecule, called ACF7, helps regulate and power this movement from the inside — findings that could have implications for understanding how cancer cells