While the mortality rate in breast cancer has decreased in the past few decades, some subsets still have poor outlooks. With the advent of targeted therapy, particularly endocrine and anti-human epidermal growth factor receptor 2 (HER2) therapies, the outcome of breast cancer has changed dramatically. Nevertheless, approximately 15 to 20 percent of breast cancers lack expression of all three constructive cell surface receptors, namely estrogen receptor (ER), progesterone receptor (PR) and HER2, hence the term "triple negative" breast cancer (TNBC). Due to an absence of ER and/or PR, these tumors typically do not respond to endocrine therapy like tamoxifen and aromatase inhibitors, which have minimal toxicities and are generally well tolerated. For that reason, the treatment option for these tumors is solely chemotherapy.

It has been demonstrated in multiple studies that the loss of ER protein expression is a result of epigenetic changes such as aberrant DNA methylation and recruitment of histone modifying enzymes to the ER promoter in the tumors. Targeting such changes with epigenetic treatments has been validated as a successful strategy in other cancer indications and the data being published suggest that it may be effective as a therapeutic intervention in the treatment of ER-negative breast cancers.

"Triple negative breast cancer is a particularly challenging form of breast cancer that is normally unresponsive to hormone therapy as well as many forms of chemotherapy," said Joanna Horobin, M.D., president and chief executive officer of Syndax. "The pre-clinical research provides us with a provocative question. Can we turn some of these tumors into estrogen receptor positive breast cancer and extend the benefit of well tolerated hormone therapy to this otherwise underserved patient population? The clinical study is designed to address this issue."

This multi-center trial sponsored by NCI is being coordinated through the University of Chicago Consortium.

SOURCE Syndax Pharmaceuticals, Inc.