Turning Negatives into Positives: Re-expressing Receptors in Receptor Negative Breast Cancer

Clinical Trial

Summary: It is estimated that 20% of women diagnosed with breast cancer in the state of California will have hormone receptor-negative (HRN) invasive breast cancer, an aggressive subtype of breast cancer that also disproportionately affects young women, African American women, and Hispanic women. HRN breast cancers are characterized by the failure of these tumors to make proteins (called receptors) that allow the tumors to respond to anticancer medications that are normally given to treat cancers that make the estrogen receptor and progesterone receptor proteins. Recent experiments in the laboratory indicate that a class of drugs called histone deacetylase (HDAC) inhibitors are able to cause HRN breast cancer cells to make the estrogen and/or progesterone receptor proteins. It is widely accepted that by treating hormone receptor-producing breast cancer with anti-hormone drugs, the risk of cancer recurrence and death are significantly reduced. Laboratory experiments also show that HRN breast cancer cells will respond for the first time to drugs that are normally effective against breast cancer cells that produce hormone receptors, which means that the cancer cells become effectively hormone receptor-positive. One of the ways that HDAC inhibitors may achieve this effect is by "turning on" genes that are "turned off" by enzymes called HDACs. Blockage of HDACs by HDAC inhibitors appears to be the mechanism by which HDAC inhibitors are able to turn on estrogen and progesterone receptor production in HRN breast cancer cells and make these newly hormone receptor-producing breast cancer cells responsive to anti-cancer medications that target the estrogen and/or progesterone receptor.

The question(s) or central hypotheses of the research: The observation that HDAC inhibitors are capable of making HRN breast cancer cells behave like hormone receptor-positive breast cancer cells raises the possibility that women with HRN breast cancer may someday be effectively treated with anti-cancer medications that are normally ineffective against HRN breast cancer. However, while these laboratory experiments are promising, a key question is whether or not HDAC inhibitors are able to turn HRN breast cancers into hormone receptor-positive breast cancers in humans. In this proposed investigation, we seek to answer this question by determining if, and to what degree, HDAC inhibitors are capable of stimulating production of the estrogen and progesterone receptor proteins in women with HRN invasive breast cancer.

Eligibility: Women with newly diagnosed triple negative breast cancer measuring 2cm or more who have not yet undergone surgery.

Location: University of Southern California (USC).

Contact: For more information about this clinical trial, please contact Jacqueline Major, R.N. at 323-226-6354.

Funding: Funded by the California Breast Cancer Research Program.

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