Robert L. Ferris, MD, PhD, FACS
University of Pittsburgh Cancer Institute
Contact Principal Investigator, SPORE
Co-Leader, Project 3 and Co-Director, Core A, and DRP
Utilizing my busy clinical practice in head and neck surgical oncology and my NIH R01 funded basic/translational immunology laboratory, we investigate mechanisms of anti-tumor immunity in the microenvironment, as well as immune escape mechanisms developed by tumor cells to evade NK and T cells elimination. My lab also studies immune checkpoint receptors and cellular immune mechanisms of anti-tumor responses and immunotherapy in phase I and phase II clinical trials, as well as correlative studies of immune markers in the serum and tumor microenvironment. I am UPCI Associate Director for Translational Research, Co-Leader of the UPCI Cancer Immunology Program, and the Tumor Microenvironment Center. In these capacities, my goals are to facilitate and enhance development of new targets and therapeutic agents through collaborative, trans-disciplinary preclinical research and clinical application. These include immunosuppressive effects which inhibit clinical activity of cetuximab, including suppressive immunologic effects and immune escape mechanisms by tumor cells in cetuximab treated patients. I am pleased to serve as contact PI of our NCI P50 Head and Neck SPORE, to further facilitate preclinical and clinical investigations, and to stimulate new collaborations. Of note, I also was elected as surgical oncology Co-Chair of the NCI Head and Neck Steering committee, which provides additional opportunities to leverage translational and clinical oncology research. As co-chair of the ECOG H&N committee, I am leading two prospective randomized trials. ECOG 3311 investigates the potential for surgical deintensification through reduced radiation dose in HPV+ oropharyngeal cancer patients treated with transoral robotic or laser surgery. More recently ECOG-ACRIN 3132 compares adjuvant radiation alone vs. cisplation-radiation in patients with disruptive or nondisruptive p53 alteration, using a molecular biomarker of "high risk" status.