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Hayley McDaid, PhD
Assistant Professor, Medicine (Oncology)
Albert Einstein College of Medicine
Bronx, New York
- Seeking to identify new therapeutic options for triple negative and BRCA-driven breast cancers.
- Laboratory studies are ongoing to test new drug candidates in models of triple negative breast cancer and to understand how tumors become drug resistant.
- These studies may lead to targeted therapies and new combination approaches to counter drug resistance and improve outcomes for patients with aggressive breast cancer.
Triple negative breast cancer (TNBC) is an aggressive form of breast cancer. TNBC tumors are frequently resistant or become resistant to a variety of drugs, increasing their potential to spread to other tissues–a process called metastasis. Dr. McDaid and Horwitz are conducting laboratory studies to identify more effective and less toxic drugs for patients with TNBC.
Full Research Summary
Triple negative breast cancer (TNBC) comprises approximately 15-20 percent of all breast cancers. These aggressive tumors are treated with a cocktail of chemotherapy drugs. Although many patients have excellent survival following treatment, some patients with specific types of TNBC have an incomplete response, and/or relapse after a period of remission. In particular, patients who have hereditary gene mutations in pathways that control DNA damage, such as BRCA, often have a high risk of relapse following treatment.
To address these challenges, Drs. McDaid and Horwitz have screened novel chemotherapy drugs against TNBC cells to identify those with superior activity and less toxicity than conventional therapy.
The team has made steady progress in identifying a series of molecules that are similar to the common chemotherapy drug Taxol but with a reduced risk of promoting therapy-mediated tumor dormancy.
Dormancy is a state in which cancer cells do not divide. They do however, produce vast quantities of inflammatory proteins that can make tumor cells migratory, leading to metastatic disease. Dormant cells are frequently enriched in tumors following completion of chemotherapy, implying an association with therapeutic resistance.
Drs. McDaid and Horwitz will thus rank potential drug candidates on their ability to strongly induce tumor cell death coupled with low risk of inducing dormancy. These efforts may lead to the development of a novel chemotherapy drug with potent tumor cell killing activity in TNBC.
Complementing this work, they are also studying how tumor cells interact with immune cells to promote a chemo resistant tumor microenvironment and enhance cancer cell survival. They have identified a component of the cytoskeleton (the cellular scaffolding) that facilitates transport of these proteins and have shown that this process is overactive in cancer cells and may be therapeutically targetable.
Future studies will elucidate the relevance of this transport mechanism to cancer cell survival by generating TNBC cell lines that are missing the transport protein.
Dr. Hayley McDaid received her PhD from the Queens University of Belfast, where she characterized the role of the cAMP-dependent protein kinase A signaling pathway in breast and ovarian cancer. These studies pioneered her present-day interest in targeted therapies, pharmacogenomics and rationally designed drug combinations.
Dr. McDaid's broad research theme in breast cancer is focused on investigating molecular mechanisms of action and resistance to novel therapeutics. She is interested in defining the ‘circuitry’ of breast cancer in the different molecular subtypes of triple negative tumors; and mechanisms by which tumors counteract the effects of therapy. As part of this focus, Dr. McDaid has been studying chemotherapy-mediated senescence, a type of growth arrest that is increasingly perceived as a deleterious outcome of treatment. Together with colleagues, she is interested in chemical-biological approaches to minimize the risk of developing senescence during treatment.