David Bhatt

David Bhatt investigates focal adhesion kinase (FAK) as a central mediator of ECM-driven cancer progression, demonstrating that FAK functions not only as a cytoplasmic kinase linking integrins to survival signaling but also as a nuclear scaffold that regulates gene transcription to promote immune evasion. His research on FAK inhibitors including defactinib (VS-6063) has advanced clinical trials in mesothelioma and other solid tumors. He has shown that FAK inhibition in the tumor microenvironment enhances anti-tumor immunity by reducing immunosuppressive cytokine production. His work connects ECM mechanosignaling with cancer immune regulation.