|MIT Department: Biological Engineering
Faculty Mentor: Prof. Forest White
Undergraduate Institution: University of Puerto Rico – Mayagüez
My name is Andrea S. Flores Pérez and I am a Biotechnology major at the University of Puerto Rico at Mayagüez, where I specialize in statistics and biochemistry. My research interests include tissue engineering, biomaterials, and cancer biology. I am pursuing a Ph.D. in bioengineering, where I hope to study disease progression and develop novel treatments. At MSRP, I am working in the White Laboratory where I’m studying tyrosine phosphorylation in triple negative breast cancer in response to multiple chemotherapy treatments. Outside of the lab, I love to watch movies and bake!
Characterization of Tyrosine Phosphorylation in Response to Chemotherapy Drugs in Triple Negative Breast Cancer
Andrea S. Flores Pérez1, Jason E. Conage-Pough2 and Forest M. White2
1Department of Industrial Biotechnology, University of Puerto Rico – Mayagüez
2Department of Biological Engineering, Massachusetts Institute of Technology
Triple negative breast cancer (TNBC) is an aggressive subtype characterized by the absence of receptors commonly found in the disease. Due to the lack of critical biomarkers, there are no effective targeted therapies for TNBC and as a result, cases tend to have poorer prognosis and shorter relapse-free survival than other types of breast cancer. Among the most well-established therapeutic targets in breast cancers are receptor tyrosine kinases (RTKs). In TNBC, about half of the cases overexpress a subtype of RTKs called the epidermal growth factor receptor (EGFR) family. However, EGFR-targeted therapies have demonstrated poor efficacy in TNBC patients. Thus, there exists a critical need to better understand dysregulated signaling in TNBC tumors to improve treatment options for patients. In this study, we use liquid chromatography tandem mass spectrometry (LC-MS/MS) to measure signaling changes in TNBC in response to the genotoxic chemotherapy treatment Taxol and the EGFR inhibitor Erlotinib. We also evaluated the viability of TNBC cells in-vitro in response to both drugs. Interestingly, Erlotinib appeared to prevent the Taxol-induced phosphorylation of several proteins without inhibiting EGFR phosphorylation. These results could reveal novel insights into intrinsic and acquired resistance to therapy in TNBC.