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Linchpin Gene May Be Useful Target For Breast Cancer Therapies

University of Iowa researchers have discovered a gene that plays a linchpin role in the ability of breast cancer cells to respond to estrogen. The finding may lead to improved therapies for hormone responsive breast cancers and may explain differences in the effectiveness of current treatments.

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."

Click here to see the rest of this article in Medical News Today

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