Welcome to the Kazanietz lab

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Dr. Marcelo Kazanietz

Marcelo Kazanietz, PhD.

Professor of Pharmacology


Dr. Marcelo G. Kazanietz received his Ph.D. from University of Buenos Aires and completed a postdoctoral training at the National Cancer Institute (NCI, Bethesda, MD). In 1995, he joined the Department of Systems Pharmacology and Translational Therapeutics (SPATT), University of Pennsylvania Perelman School of Medicine, and became an established leader in the field of cancer signaling and therapeutics.

Dr. Kazanietz trained more to 60 post-doctoral fellows and students, many of whom took leadership positions in academia and the pharmaceutical industry around the world. His laboratory has been mainly funded by the NIH, the Department of Defense and the American Cancer Society. He received more than 20 million dollars from federal funding sources throughout his career. Dr. Kazanietz served as editor of multiple scientific journals and was appointed as member of the NCI Board of Scientific Counselors (Basic Sciences). He published more than 180 articles in peer-reviewed journals. He also served as Chair of the Graduate Group of Pharmacology and directed several courses on pharmacology and cancer signaling at UPenn.

Latest publications

  • Characterization of Novel Derivatives of MBQ-167, an inhibitor of the GTP-binding proteins Rac/Cdc42 Thursday, March 2, 2023

    Rac and Cdc42, are homologous GTPases that regulate cell migration, invasion, and cell cycle progression; thus, representing key targets for metastasis therapy. We previously reported on the efficacy of MBQ-167, which blocks both Rac1 and Cdc42 in breast cancer cells and mouse models of metastasis. To identify compounds with increased activity, a panel of MBQ-167 derivatives was synthesized, maintaining its 9-ethyl-3-(1H-1,2,3-triazol-1-yl)-9H-carbazole core. Similar to MBQ-167, MBQ-168 and...


    Aberrant expression of protein kinase C (PKC) isozymes is a hallmark of cancer. The different members of the PKC family control cellular events associated with cancer development and progression. Whereas the classical/conventional PKCα isozyme has been linked to tumor suppression in most cancer types, here we demonstrate that this kinase is required for the mitogenic activity of aggressive human prostate cancer cells displaying aberrantly high PKCα expression. Immunohistochemical analysis showed...

  • Germline intergenic duplications at Xq26.1 underlie Bazex-Dupré-Christol basal cell carcinoma susceptibility syndrome Saturday, August 20, 2022

    CONCLUSIONS: Noncoding Xq26.1 duplications cause BDCS. The BDCS duplications most likely lead to dysregulation of ARHGAP36. ARHGAP36 is a potential therapeutic target for both inherited and sporadic BCCs. What is already known about this topic? Bazex-Dupré-Christol syndrome (BDCS) is a rare X-linked basal cell carcinoma susceptibility syndrome linked to an 11·4-Mb interval on chromosome Xq25-q27.1. Loss-of-function variants in ACTRT1 and its regulatory elements were suggested to cause BDCS. What...

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