Jonathan Chernoff, MD, PhD
Senior Vice President
Chief Scientific Officer
Stanley P. Reimann Chair in Oncology Research
Co-Leader, Cancer Biology
As Chief Scientific Officer, Dr. Chernoff coordinates and charts the future course of research at Fox Chase.
Chernoff joined the staff in 1991 as an associate member and was promoted to member with tenure in 1996. In 2002 he was promoted to be a senior member in Fox Chase Cancer Center's Basic Science division, the equivalent of a full professor in a university.
A molecular oncologist as well as a board-certified medical oncologist, Chernoff has a special interest in factors that control cell growth and movement, including oncogenes and anticancer or tumor-suppressor genes, and has made fundamental contributions in this research.
Chernoff earned his MD and his PhD in biochemistry in 1984 at Mount Sinai School of Medicine in New York City. 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.
In recognition of his national reputation in molecular oncology and biochemistry, Chernoff also holds the Stanley P. Reimann Chair in Oncology.
- 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)
- 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)
- Proliferative signal transduction
- Regulation of neoplastic growth by protein kinases and phosphatases
- Regulation and role of p21-activated kinases in cancer
- Hippo tumor suppressor pathway
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.
Effects of p21-activated kinase 1 inhibition on 11q13-amplified ovarian cancer cells. Prudnikova TY, Villamar-Cruz O, Rawat SJ, Cai KQ, Chernoff J. Oncogene. 2015 Aug 10. doi: 10.1038/onc.2015.278. PMID:26257058
Kosoff RE, Aslan JE, Kostyak JC, Dulaimi E, Chow HY, Prudnikova TY, Radu M, Kunapuli SP, McCarty OJ, Chernoff J. Pak2 restrains endomitosis during megakaryopoiesis and alters cytoskeleton organization. Blood. 2015 May 7;125(19):2995-3005. doi: 10.1182/blood-2014-10-604504. Epub 2015 Mar 30. PubMed PMID: 25824689; PubMed Central PMCID: PMC4424419.
Regulation of mammalian Ste20 (Mst) kinases. Rawat SJ, Chernoff J. Trends in biochemical sciences. 2015; 40(3):149-56. NIHMSID: NIHMS655499 PubMed PMID: 25665457 PMCID:PMC4340714.
Chow HY, Dong B, Duron SG, Campbell DA, Ong CC, Hoeflich KP, Chang LS, Welling DB, Yang ZJ, Chernoff J. Group I Paks as therapeutic targets in NF2-deficient meningioma. Oncotarget. 2015 Feb 10;6(4):1981-94. PubMed PMID: 25596744; PubMed Central PMCID: PMC4385830.
Kelly ML, Astsaturov A, Rhodes J, Chernoff J. A Pak1/Erk signaling module acts through Gata6 to regulate cardiovascular development in zebrafish. Dev Cell. 2014 May 12;29(3):350-9. doi: 10.1016/j.devcel.2014.04.003. PubMed PMID: 24823378; PubMed Central PMCID: PMC4073496.
PAK signalling during the development and progression of cancer. Radu M, Semenova G, Kosoff R, Chernoff J. Nature reviews. Cancer. 2014; 14(1):13-25. NIHMSID: NIHMS556174 PubMed PMID: 24505617 PMCID: PMC4115244.
Pak1 kinase links ErbB2 to β-catenin in transformation of breast epithelial cells. Arias-Romero LE, Villamar-Cruz O, Huang M, Hoeflich KP, Chernoff J. Cancer research. 2013; 73(12):3671-82. NIHMSID: NIHMS464433 PubMed PMID: 23576562 PMCID: PMC3687032.
ArhGAP15, a Rac-specific GTPase-activating protein, plays a dual role in inhibiting small GTPase signaling. Radu M, Rawat SJ, Beeser A, Iliuk A, Tao WA, et al. The Journal of biological chemistry. 2013; 288(29):21117-25. PubMed PMID:23760270 PMCID: PMC3774378.
The tumor suppressor Mst1 promotes changes in the cellular redox state by phosphorylation and inactivation of peroxiredoxin-1 protein. Rawat SJ, Creasy CL, Peterson JR, Chernoff J. The Journal of biological chemistry. 2013; 288(12):8762-71.PubMed PMID:23386615 PMCID:PMC3605693.
p21-Activated kinase 1 is required for efficient tumor formation and progression in a Ras-mediated skin cancer model. Chow HY, Jubb AM, Koch JN, Jaffer ZM, Stepanova D, et al. Cancer research. 2012; 72(22):5966-75. NIHMSID: NIHMS407835 PubMed PMID: 22983922 PMCID: PMC3500416.
Sumoylated protein tyrosine phosphatase 1B localizes to the inner nuclear membrane and regulates the tyrosine phosphorylation of emerin. Yip SC, Cotteret S, Chernoff J. Journal of cell science. 2012; 125(Pt 2):310-6. PubMed PMID: 22266903 PMCID: PMC3283870.
Identification of the atypical MAPK Erk3 as a novel substrate for p21-activated kinase (Pak) activity. De la Mota-Peynado A, Chernoff J, Beeser A. The Journal of biological chemistry. 2011; 286(15):13603-11. PubMed PMID:21317288 PMCID:PMC3075705.