"Our struggle to fully understand the the pathophysiology of cancer continually challenges our understanding of cellular proccesses. Oncology is the area where the synergy between my training in science and medicine is apparent."

- Dr. Raj Rohatgi

View CV

Academic Appointment 

  • Associate Professor of Biochemistry and Medicine at Stanford University School of Medicine

About DSA-Funded Research

One of the major challenges in cancer treatment today is the development of strategies for the durable eradication of tumors. My research program is based on the premise that this important problem in cancer biology can be solved by understanding how molecular mechanisms that sculpt our organs during development are hijacked by cancer cells. I study the Hedgehog pathway, a cellular communication system that normally organizes embryonic development. Several cancers such as medulloblastoma, the most common pediatric brain tumor, can appropriate this powerful pathway to drive unchecked growth, invasion and spread. I propose to understand how the final executioners of this pathway, known as the Gli proteins, are unleashed in tumor cells by a chemical tag called phosphorylation. This understanding will allow the rational development of methods to monitor and eventually block the action of this phosphorylation event. As a practicing oncologist, I am committed to extending this work to uncover diagnostic and therapeutic strategies against medulloblastoma and other Hedgehog-driven cancers.


"As a scientist, Rajat combines the attributes of a deeply innovative and intrepid thinker and an exceptional experimentalist. As a practicing oncologist, he has an intimate understanding of the clinical aspects of cancer and how it affects the lives of patients. His ability to integrate these two worlds has put him in a unique position to make strides against this devastating disease."

Ronald Levy, M.D.
Stanford University School of Medicine

"Rajat Rohatgi is a rare and extraordinarily talented scientist and teacher and person. He will surely continue to have a powerful impact on the fields of signal transduction and molecular oncology."

Matthew P. Scott, Ph.D.
Stanford University School of Medicine


  • Dorn K, Hughes C and Rohatgi R. A Smoothened-Evc2 complex transduces the Hedgehog signal at primary cilia. Developmental Cell 23(4):823-35 (2012).
  • Niewiadomski P*, Kong JH, Ahrends R, Ma Y, Humke EW, Khan S, Teruel MN, Novitch BG, Rohatgi R*. Gli protein activity is controlled by multi-site phosphorylation in vertebrate Hedgehog signaling. Cell Reports 6(1):168-81 (2014).
  • Pusapati GV, Hughes CE, Dorn KV, Zhang D, Sugianto P, Aravind L*, and Rohatgi R*. EFCAB7 and IQCE regulate Hedgehog signaling by tethering the EVC-EVC2 complex to the base of primary cilia. Developmental Cell 28(5):483-496 (2014).
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