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The process of neoplastic transformation can be conceptually divided into two components. The first of these, proliferative transformation, refers to the ability of transformed cells to bypass growth suppression signals, suriviving and dividing when normal cells would not. The second, morphologic transformation, refers to loss of normal cytoskeletal architecture, often accompanied by decreased adhesion and acquisition of the ability to invade surrounding tissues. These two fundamental properties are intimately linked to one another, although experimentally they can be dissected apart through the use of gain-of-function and loss-of-function manupulation of signaling molecules. The overall focus this research is in uncovering the roles of protein phosphorylation in governing these two fundamental aspects of cancer biology.
As Cancer Center Director at Fox Chase Cancer Center, Jonathan Chernoff works with Temple University Health System and Temple University peers to lead Fox Chase into the future of cancer care. With decades of research expertise, Chernoff has helped Fox Chase focus on the areas that best leverage the institution’s enhanced strengths in scientific development: translational research, precision medicine, epigenetics, signaling reprograming, immunotherapy, hematologic malignancies, and cancer disparities.
A molecular oncologist and board-certified medical oncologist, Chernoff joined Fox Chase in 1991. In addition to helping define the strategic direction for Fox Chase research, he has made fundamental contributions in his own laboratory, which focuses on factors that control cell growth and movement, including oncogenes and anticancer or tumor-suppressor genes. He currently holds the Stanley P. Reimann Chair in Oncology Research...Expand
Chernoff has trained dozens of postdoctoral and graduate students at Fox Chase. He serves as an adjunct professor for the Drexel University School of Medicine and for the University of Pennsylvania, and is a member of the Cancer Signaling and Epigenetics research program at Fox Chase.
In addition to these roles, Chernoff has served on multiple external advisory boards, including the Scientific Advisory Board for Nexgenix Pharmaceuticals, as well as advisory boards for Genentech, Novartis Pharmaceuticals, and the New York University (Perlmutter) Cancer Center, among others. He has also taken on roles for multiple committees and programs within Fox Chase.
Chernoff earned his bachelor’s degree in molecular biophysics and biochemistry from Yale College and his medical degree and doctorate from the Mount Sinai School of Medicine in New York. He completed his residency in internal medicine at the University Health Center of Pittsburgh and a clinical fellowship in medical oncology at Johns Hopkins Oncology Center. He then held a postdoctoral fellowship in cellular and developmental biology at Harvard University before coming to Fox Chase. Collapse
PhD, Biochemistry, Mt. Sinai School of Medcine, New York, NY, 1984
MD, Biochemistry, Mt. Sinai School of Medcine, New York, NY, 1984
BA, Molecular Biophysics and Biochemistry, Yale College, New Haven, CT, 1978
Honors & Awards
Faculty of 1000 (2007-present)
Stanley P. Reimann Chair in Oncology research (2008-present)
Fellow, American Association for the Advancement of Science (AAAS) (2017)
AACR, Educational Session Leader (2014)
Pennsylvania Drug Discovery Institute, Drug Discovery Award (2013)
Senior Fellow, American Asthma Assn (2008-2011)
Chair: NF2 Preclinical Consortium (2011-2012)
American Cancer Society, Southeast PA division, Scientific Research Award (2010)
Vice-Chair, FASEB “Small GTPases” (2008)
Chair, GRC “Mechanisms of Cell Signaling (2007)
Dozor Lecturer, Ben-Gurion University, Israel (2007)
Leukemia Society of America Scholar Award, (1997-2002)
Regulation and role of p21-activated kinases in cancer
Hippo tumor suppressor pathway
Kras isoform-specific signaling
The process of neoplastic transformation can be conceptually divided into two components. The first of these, proliferative transformation, refers to the ability of transformed cells to bypass growth suppression signals, surviving and dividing when normal cells would not. The second, morphologic transformation, refers to loss of normal cytoskeletal architecture, often accompanied by decreased adhesion and acquisition of the ability to invade surrounding tissues. These two fundamental properties are intimately linked to one another, although experimentally they can be dissected apart through the use of gain-of-function and loss-of-function manipulation of signaling molecules. The overall focus this research is in uncovering the roles of key protein kinases that govern these two fundamental aspects of cancer biology.
Binder P., Wang S., Radu M., Zin M., Collins L., Khan S., Li Y., Sekeres K., Humphreys N., Swanton E., Reid A., Pu F., Oceandy D., Guan K., Hille S.S., Frey N., Muller O.J., Cartwright E.J., Chernoff J., Liu W., Wang X., Pak2 as a novel therapeutic target for cardioprotective endoplasmic reticulum stress response. Circ Res. 124(5): 696-711, 2019.PMC6407830. 15.862
Chernoff J., How much is my paper worth? Mol Biol Cell. 30(23): 2878-2879, 2019. PMC6822591. 3.905
Kurimchak A.M., Shelton C., Herrera-Montavez C., Duncan K.E., Chernoff J., Duncan J.S., Intrinsic resistance to mek inhibition through bet protein mediated kinome reprogramming in nf1-deficient ovarian cancer. Mol Cancer Res. 17(8): 1721-1734, 2019. PMC6679760. 4.484
Lu H., Liu S., Zhang G., Wu B., Zhu Y., Frederick D.T., Hu Y., Zhong W., Randell S., Sadek N., Zhang W., Chen G., Cheng C., Zeng J., Wu L.W., Zhang J., Liu X., Xu W., Krepler C., Sproesser K., Xiao M., Miao B., Liu J., Song C.D., Liu J.Y., Karakousis G.C., Schuchter L.M., Lu Y., Mills G., Cong Y., Chernoff J., Guo J., Boland G.M., Sullivan R.J., Wei Z., Field J., Amaravadi R.K., Flaherty K.T., Herlyn M., Xu X. ,Guo W., Author correction: Pak signalling drives acquired drug resistance to mapk inhibitors in braf-mutant melanomas. Nature. 565(7738): E4, 2019. 43.070
Sannai M., Doneddu V., Giri V., Seeholzer S., Nicolas E., Yip S.C., Bassi M.R., Mancuso P., Cortellino S., Cigliano A., Lurie R., Ding H., Chernoff J., Sobol R.W., Yen T.J., Bagella L., Bellacosa A., Modification of the base excision repair enzyme mbd4 by the small ubiquitin-like molecule sumo1. DNA Repair. 82: 102687, 2019.PMC6785017. 3.711
Araiza-Olivera D. ,Chernoff J., Hras helps hippo heterodimerize to evade tumor suppression. Small GTPases. 9(4): 327-331, 2018. PMC5997136.
Chow HY, Dong B, Valencia CA, Zeng CT, Koch JN, Prudnikova TY, Chernoff J. Group I Paks are essential for epithelial- mesenchymal transition in an Apc-driven model of colorectal cancer. Nature communications, 9(1):3473, 2018. PMC6110733...Expand
Karchugina S., Chernoff J., Detection of heterodimerization of protein isoforms using an in situ proximity ligation assay. J Vis Exp, (140)2018. PMC6235567. 1.108
Kim S.M., Nguyen T.T., Ravi A., Kubiniok P., Finicle B.T., Jayashankar V., Malacrida L., Hou J., Robertson J., Gao D., Chernoff J., Digman M.A., Potma E.O., Tromberg B.J., Thibault P.,Edinger A.L., Pten deficiency and ampk activation promote nutrient scavenging and anabolism in prostate cancer cells. Cancer Discov. 8(7): 866-883, 2018. PMC6030497. 26.370
Stepanova D.S., Braun L., Chernoff J., A new concept in nf2 pharmacotherapy: Targeting fatty acid synthesis. Oncoscience. 5(5-6): 126-127, 2018. PMC6049319.
Prudnikova T.Y., Chernoff J., The group i pak inhibitor frax-1036 sensitizes 11q13-amplified ovarian cancer cells to the cytotoxic effects of rottlerin. Small GTPases. 8(4): 193-198, 2017. PMC5680705. 2.048
Semenova G., Stepanova D., Deyev S.M., Chernoff J., Medium throughput biochemical compound screening identifies novel agents for pharmacotherapy of neurofibromatosis type i. Biochimie. 135: 1-5, 2017. PMC5405558. 3.362
Araiza-Olivera D, Feng Y, Semenova G, Prudnikova TY, Rhodes J, Chernoff J. Suppression of RAC1-driven malignant melanoma by group A PAK inhibitors. Oncogene, 37(7):944-52, 2018. PMC5814328Collapse
Semenova G, Stepanova DS, Dubyk C, Handorf E, Deyev SM, Lazar AJ, Chernoff J. Targeting group I p21-activated kinases to control malignant peripheral nerve sheath tumor growth and metastasis. Oncogene, 36(38):5421-31, 2017. PMC5608634
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