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New Breast Cancer Therapies
September 17, 2007 at 9:18 PM
Cancer News
Estrogen causes hormone-responsive breast cancer cells to grow and divide by interacting with estrogen receptors made by cancer cells. Interfering with estrogen signaling is the basis of two common breast cancer therapies -- tamoxifen, which blocks estrogen's interaction with a primary estrogen receptor called ER-alpha, and aromatase inhibitors that reduce the amount of estrogen the body makes and therefore affect any pathway that uses estrogen.
The study, led by Ronald Weigel, M.D., Ph.D., professor and head of surgery at the University of Iowa Roy J. and Lucille A. Carver College of Medicine, reveals a central role for transcription factor AP2C (TFAP2C) in controlling multiple pathways of estrogen signaling. The findings are published in the Sept. 15 issue of Cancer Research.
"Estrogen binds to estrogen receptors and triggers a cascade of events including gene regulation," said Weigel, who also is a member of the Holden Comprehensive Cancer Center at the UI. "We found that elimination of the TFAP2C from the cell causes all of those cascades that we associate with estrogen to go away. The treated cancer cells were not able to respond to estrogen by any normal pathway."
The researchers found that silencing expression of TFAP2C in hormone-responsive breast cancer cells significantly decreased the amount of ER-alpha made by the cancer cell. This reduction in ER-alpha (down to 16 percent of the level normally made by breast cancer cells) also affected production of other "downstream" genes involved in cancer growth.
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More News on: Women and Cancer, Breast Biopsy, Pagets disease of the breast, Mastitis, Cancer and Homeopathy, Breast Cancer Facts, Cancer Facts, Cancer, Breasts - Structures and Types, Breast Lumps
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