Albert Einstein College of Medicine
New York, New York
Associate Professor, Department of Medicine (Oncology)
Associate Professor, Department of Molecular Pharmacology
Identifying targeted therapies and novel combination approaches to decrease drug resistance and improve outcomes for patients with triple-negative breast cancer.
Therapeutics such as Taxol are indicated for first-line treatment of patients with triple-negative breast cancer (TNBC) and other types of breast cancer. While many patients experience good outcomes to this treatment, some patients experience drug resistance, or relapse after a period of remission. In addition, some patients develop toxicities or experience long-term, debilitating side effects. The BCRF research led by Dr. McDaid is focused on characterizing cancer cells that survive anti-cancer therapy, specifically investigating the causes of resistance after therapy with drugs like Taxol. Her team has synthesized novel molecules that work like Taxol but are more effective at killing breast cancer cells in laboratory models. They are investigating the therapeutic efficacy of these molecules with the long-term goal of developing potent, less toxic Taxol-like drugs for use in advanced disease.
One of the candidate drugs has shown promising anti-tumor efficacy and a low toxicity profile and Dr. McDaid’s team is now evaluating its mechanism of action. They demonstrated it has distinct structural differences from taxol and this may account for its unique properties. In related studies, they are examining cellular senescence—an underlying cause of relapse after chemotherapy. They showed that while senescent cancer cells do not divide, they do produce inflammatory proteins that can promote the growth of neighboring tumor cells thereby leading to recurrence, or metastasis. In the last year, Dr. McDaid discovered circulating senescence-associated proteins after treatment with chemotherapy and believes they may serve as a biomarker for the presence of senescent tumor cells.
Dr. McDaid will continue investigating potential drug candidates for treatment of TNBC that are both strongly toxic to tumor cells and have a low risk of inducing cellular senescence. Her team will investigate the mechanism of action of these candidate drugs to determine the potential for resistance. In the next year, her team will also examine whether senescent cells acquire genetic alterations that could cause them to become oncogenic and whether these alterations are transmitted to daughter cells in senescent cells that resume proliferation.
Hayley McDaid, PhD received her degree 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. With her colleagues, she is interested in defining chemical-biological approaches to minimize the risk of developing senescence during treatment.
The David Yurman Award
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