Jonathan Chernoff, MD, PhD

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This Fox Chase professor participates in the Undergraduate Summer Research Fellowship. 
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Cancer Center Director

Senior Vice President

Stanley P. Reimann Chair in Oncology Research

Research Program

Lab Overview

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. 

 

Bio

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

Educational Background

  • 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)
  • ACS Research Scholar (1993-1998)
  • W.W. Smith Charitable Trust Fellowship 1993-1996
  • Pfizer Traveling Fellow (1996)
  • B.S. cum laude, Yale University (1978)

People

Research Interests

  • Rac1 signaling in malignant melanoma
  • Regulation and role of p21-activated kinases in cancer
  • Hippo tumor suppressor pathway
  • Kras isoform-specific signaling

Lab Overview

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. 

 

  • Blocking Pak function restores normal development in Rac1P29S zebrafish. Embryos were injected with Phenol red or Phenol red + RAC1P29S mRNA during the one-cell stage. 1 μM inhibitors were added at 4 hpf, then removed after 1 h. Embryonic morphology was scored at 24 hpf. (a) Representative images of developmental abnormalities. (b) Embryo phenotypes were scored as normal if they presented an elongated body axis, eye and heart development.

  • Role of Pakl1 in EMT in colorectal cancer epithelia

  • Hippo pathway regulation: Role of Mst homo- and heterodimers. In their homodimeric form, Mst1 and Mst2 are highly active and promote cell cycle delay, apoptosis, and tumor suppression. Mst1 and Mst2 can also heterodimerize with additional proteins, some of which containing SARAH domains (WW45, Rassf; SARAH domain indicated by extension from rectangle), and some which do not (c-Raf, Abl, Pdx1, and mTORC2 (via Rictor). Such heterodimers are inactive, and the Hippo pathway is suppressed.

    Selected Publications

    Karchugina S., Benton D.,Chernoff J., Regulation of mst complexes and activity via sarah domain modifications. Biochem Soc Trans. 49(2): 675-683, 2021. https://www.ncbi.nlm.nih.gov/pubmed/33860801.

    Benton D.,Chernoff J., A new rho(d) map to diffuse gastric cancer. Cancer Discov. 10(2): 182-184, 2020. PMC7079203. https://www.ncbi.nlm.nih.gov/pubmed/32024682.

    Cannon A.C., Uribe-Alvarez C.,Chernoff J., Rac1 as a therapeutic target in malignant melanoma. Trends Cancer. 6(6): 478-488, 2020. PMC7380552. https://www.ncbi.nlm.nih.gov/pubmed/32460002.

    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

    Additional Publications

    My NCBI

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