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Mechanisms by which cancers initiate/progress and develop resistance to targeted therapies parallels those that prevent many tissues/organs from fully regenerating - these biomedical hurdles are at the center of our research efforts. In fact, many solid tumors undergo changes that mirror those in tissues during natural wound healing events. By understanding what drives cancer proegression/relapse and what prevents complete tissue regeneration, we aim to develop novels strategies to diagnose/treat malignancies and degenerative disorders.


Jonathan Kelber trained as a doctoral student under Wylie Vale at the Salk Institute where he made important contributions to understanding how TGFbeta signaling is regulated at the surface of tumor and stem cells. Several years later, as a postdoctoral fellow at UCSD with Richard Klemke, he discovered a novel kinase called PEAK1 that regulates the cytoskeleton and cancer progression. Since starting his laboratory at CSUN, his group has bridged these two areas to establish a role for PEAK1 function in TGFbeta-mediated cancer progression. Most recently, Dr. Kelber worked as a Visiting Professor at Harvard Medical School with Joan Brugge's group to establish methods for interrogating the role of stromal cell populations in driving targeted therapy resistance in breast cancer. Current work in the Kelber Lab is focused on understanding how upstream regulators and downstream targets of PEAK1 influence TGFbeta signaling and function in cell and animal models. Additional efforts are focused on how regulators of TGFbeta signaling function during tissue regeneration in model organisms that have the potential to fully regenerate tissue structure and function after injury.