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Maria J Costa, PhD
Maria Jose Costa is a Principal Scientist at Rinat Research and Development, part of Pfizer’s Oncology Research and Development Group. Since joining Pfizer in 2014, she has been focused on developing targeted therapies for types of hematological malignancies that still have an unmet need and, more recently, on researching new strategies to counteract the immunosuppressive microenvironment of solid tumors and improve the efficacy of immunotherapies.
Dr. Costa received her BS degree in Biochemistry from University of Coimbra, Portugal. As an undergraduate student, she trained with Prof. Sobrinho-Simoes in thyroid pathology and cancer biology. She then moved to Brussels, Belgium, to pursue her PhD studies in Human (Cell) Biology in a joint program between University of Porto and Free University of Brussels, under the supervision of Prof. Jacques Dumont. Dr. Costa’s PhD thesis focused on the role of plasma membrane microdomains in the regulation of signal transduction downstream thyrotropin and hormone production in human thyroid cells. She uncovered that plasma membrane microdomains named “caveolae” at the apex of thyroid cells are critical for the formation of the “thyroxisome,” a multi-enzyme complex responsible for the safe and efficient production of H2O2 and thyroid pro-hormone iodination.
Prior to joining Pfizer, Dr. Costa moved to the San Francisco Bay Area, where she completed two postdocs at University of California San Francisco. First, with Prof. Wang, she discovered the cancer-promoting role of host Notch4 in the breast tumor microenvironment and angiogenesis. Then, in the laboratory of Prof. Ruggero, Maria used genetic and small molecule inhibitor approaches to demonstrate the key oncogenic role of eIF4E on translation control of anti-apoptotic factors downstream hyper-activated AKT-mTOR pathway in lymphoma. She then joined the Stanford University Institute for Stem Cell Biology and Regenerative Medicine in the laboratory of Prof. Feldman, where she studied the effects of glucocorticoid hormone and circadian clock disruption on the fate of adipose tissue-derived progenitor cells.