Elda Grabocka, PhD

Assistant Professor

Elda Grabocka


233 South 10th Street
BLSB 1002
Philadelphia, PA 19107

Email Elda Grabocka


Elda Grabocka, PhD

Assistant Professor


PhD, Structural Biology and Molecular Pharmacology, 2007
BS, Biology, Washington College

Most Recent Peer-Reviewed Publications

Research Interests

Research in the Grabocka lab is centered on uncovering unique vulnerabilities of RAS-driven cancers and how to exploit them for the development of novel therapeutic targeting strategies.

Activating mutations in one of the RAS genes (KRAS, NRAS, or HRAS) drive the development of approximately 30% of all human cancers including cancers of the pancreas, colon, and lung. A major focus of the Grabocka laboratory is to decipher the contribution of aberrant RAS signaling to the development of pancreatic cancer. ~ 90% of pancreatic cancer patients present activating mutations in the KRAS gene. Unfortunately for patients, these tumors are very aggressive and highly resistant to standard chemotherapy. Additionally, targeted therapy options are completely lacking. We are interested in defining how mutant RAS coerces stress adaptation mechanisms of cancer cells and the tumor microenvironment to promote tumor progression and drug resistance. To this end, significant effort in the Grabocka laboratory is dedicated to understanding how mutant RAS regulates the formation of stress granules, a cellular process we have linked to the drug resistance of KRAS-driven tumors. Ongoing studies in the lab include the establishment of 3D cell culture models and mouse models to study the role of stress granules in the drug resistance of KRAS tumors, the elucidation of the molecular pathways that drive stress granule formation in cancer, and the identification of molecular targets that are candidates for therapeutic intervention. Additional research interests include the cooperation of oncogenic signaling and stress stimuli to promote the acquisition of pro-tumorigenic properties, as well as the reprogramming of the DNA damage response signaling pathways in RAS-driven cancers.