Dr. Aaronson received his M.D. from UCSF in 1966. He joined the National Institutes of Health in 1967 and became Chief of the Laboratory of Cellular and Molecular Biology at the National Cancer Institute in 1977. He joined Mount Sinai in 1993 and is the Jack and Jane B. Aron Professor and Founding Chair, Emeritus of the Department of Oncological Sciences. He is the recipient of numerous awards including the Distinguished Service Medal from the U.S. Public Health Service, the AACR Outstanding Achievement in Cancer Research Award , and the Paul Erhlich Prize from Germany. He is the author of over 550 publications, an inventor on more than 40 patents, and serves on numerous editorial boards and scientific advisory committees.
Aging, Cancer, Growth Factors and Receptors, Oncogenes, Signal Transduction
Cancer Biology [CAB]
BS, University of California, Berkeley
MD, University of California, San Francisco School of Medicine
, Moffitt Hospital
, National Cancer Institute
Italian National Academy of Sciences, Foreign Member
Accademia Nazionale Dei Lincei
National FLC Award for Excellence in Technology Transfer
Kepivance: Improving the Quality of Life for Cancer Patients
PHS Distinguished Service Medal
Paul Ehrlich and Ludwig Darmstaedter Prize
PHS Meritorious Service Medal
AACR - Outstanding Achievement in Cancer Research Award
American Association for Cancer Research
Alpha Omega Alpha
The Aaronson laboratory is involved in cancer gene discovery and function with the goal of identifying novel targets for therapy. Topics currently under investigation include growth factors and receptors, Wnt and Hippo developmental pathways deregulated in cancer as well as the p53 tumor suppressor gene. Past discoveries include ErbB2, initially identified by his lab as an amplified erbB related gene in a primary human breast cancer. The lab has also discovered and characterized genes for a number of other growth factor signaling molecules activated as oncogenes in human malignancies. This research has contributed to novel cancer drugs including Herceptin, which targets ERBB2, and KGF/FGF7, which became Kepivance, for treatment of cancer therapy associated mucositis. Other discoveries including erbB3, PDGFR alpha, and HGF as the ligand for MET, have also led to agents currently in clinical development as cancer therapeutics. More recent accomplishments include identification of a Wnt autocrine mechanism that contributes to the transformed phenotypes of several major human tumors and novel homeostatic stress responses involving the p53 tumor suppressor gene.
Eva A, Robbins KC, Andersen PR, Srinivasan A, Tronick SR, Reddy EP, Ellmore NW, Galen AT, Lautenberger JA, Papas TS, Westin EH, Wong-Staal F, Gallo RC, Aaronson SA. Cellular genes analogous to retroviral onc genes are transcribed in human tumour cells. Nature 1982 Jan; 295(5845).
Taub R, Kirsch I, Morton C, Lenoir G, Swan D, Tronick S, Aaronson S, Leder P. Translocation of the c-myc gene into the immunoglobulin heavy chain locus in human Burkitt lymphoma and murine plasmacytoma cells. Proceedings of the National Academy of Sciences of the United States of America 1982 Dec; 79(24).
Pulciani S, Santos E, Lauver AV, Long LK, Aaronson SA, Barbacid M. Oncogenes in solid human tumours. Nature 1982 Dec; 300(5892).
Devare SG, Reddy EP, Law JD, Robbins KC, Aaronson SA. Nucleotide sequence of the simian sarcoma virus genome: demonstration that its acquired cellular sequences encode the transforming gene product p28sis. Proceedings of the National Academy of Sciences of the United States of America 1983 Feb; 80(3).
Doolittle RF, Hunkapiller MW, Hood LE, Devare SG, Robbins KC, Aaronson SA, Antoniades HN. Simian sarcoma virus onc gene, v-sis, is derived from the gene (or genes) encoding a platelet-derived growth factor. Science (New York, N.Y.) 1983 Jul; 221(4607).
Robbins KC, Antoniades HN, Devare SG, Hunkapiller MW, Aaronson SA. Structural and immunological similarities between simian sarcoma virus gene product(s) and human platelet-derived growth factor. Nature; 305(5935).
King CR, Kraus MH, Aaronson SA. Amplification of a novel v-erbB-related gene in a human mammary carcinoma. Science (New York, N.Y.) 1985 Sep; 229(4717).
Di Fiore PP, Pierce JH, Kraus MH, Segatto O, King CR, Aaronson SA. erbB-2 is a potent oncogene when overexpressed in NIH/3T3 cells. Science (New York, N.Y.) 1987 Jul; 237(4811).
Kraus MH, Issing W, Miki T, Popescu NC, Aaronson SA. Isolation and characterization of ERBB3, a third member of the ERBB/epidermal growth factor receptor family: evidence for overexpression in a subset of human mammary tumors. Proceedings of the National Academy of Sciences of the United States of America 1989 Dec; 86(23).
Matsui T, Heidaran M, Miki T, Popescu N, La Rochelle W, Kraus M, Pierce J, Aaronson S. Isolation of a novel receptor cDNA establishes the existence of two PDGF receptor genes. Science (New York, N.Y.) 1989 Feb; 243(4892).
Finch PW, Rubin JS, Miki T, Ron D, Aaronson SA. Human KGF is FGF-related with properties of a paracrine effector of epithelial cell growth. Science (New York, N.Y.) 1989 Aug; 245(4919).
Miki T, Fleming TP, Bottaro DP, Rubin JS, Ron D, Aaronson SA. Expression cDNA cloning of the KGF receptor by creation of a transforming autocrine loop. Science (New York, N.Y.) 1991 Jan; 251(4989).
Bottaro DP, Rubin JS, Faletto DL, Chan AM, Kmiecik TE, Vande Woude GF, Aaronson SA. Identification of the hepatocyte growth factor receptor as the c-met proto-oncogene product. Science (New York, N.Y.) 1991 Feb; 251(4995).
Sugrue MM, Shin DY, Lee SW, Aaronson SA. Wild-type p53 triggers a rapid senescence program in human tumor cells lacking functional p53. Proceedings of the National Academy of Sciences of the United States of America 1997 Sep; 94(18).
Bafico A, Liu G, Yaniv A, Gazit A, Aaronson SA. Novel mechanism of Wnt signalling inhibition mediated by Dickkopf-1 interaction with LRP6/Arrow. Nature cell biology 2001 Jul; 3(7).
Bafico A, Liu G, Goldin L, Harris V, Aaronson SA. An autocrine mechanism for constitutive Wnt pathway activation in human cancer cells. Cancer cell 2004 Nov; 6(5).
Muñoz-Fontela C, Macip S, Martínez-Sobrido L, Brown L, Ashour J, García-Sastre A, Lee SW, Aaronson SA. Transcriptional role of p53 in interferon-mediated antiviral immunity. The Journal of experimental medicine 2008 Aug; 205(8).
Akiri G, Cherian MM, Vijayakumar S, Liu G, Bafico A, Aaronson SA. Wnt pathway aberrations including autocrine Wnt activation occur at high frequency in human non-small-cell lung carcinoma. Oncogene 2009 May; 28(21).
Vijayakumar S, Liu G, Rus IA, Yao S, Chen Y, Akiri G, Grumolato L, Aaronson SA. High-frequency canonical Wnt activation in multiple sarcoma subtypes drives proliferation through a TCF/β-catenin target gene, CDC25A. Cancer cell 2011 May; 19(5).
Muñoz-Fontela C, Pazos M, Delgado I, Murk W, Mungamuri SK, Lee SW, García-Sastre A, Moran TM, Aaronson SA. p53 serves as a host antiviral factor that enhances innate and adaptive immune responses to influenza A virus. Journal of immunology (Baltimore, Md. : 1950) 2011 Dec; 187(12).
Mungamuri SK, Benson EK, Wang S, Gu W, Lee SW, Aaronson SA. p53-mediated heterochromatin reorganization regulates its cell fate decisions. Nature structural & molecular biology 2012 May; 19(5).
Grumolato L, Liu G, Haremaki T, Mungamuri SK, Mong P, Akiri G, Lopez-Bergami P, Arita A, Anouar Y, Mlodzik M, Ronai ZA, Brody J, Weinstein DC, Aaronson SA. β-Catenin-independent activation of TCF1/LEF1 in human hematopoietic tumor cells through interaction with ATF2 transcription factors. PLoS genetics 2013; 9(8).
Mungamuri SK, Murk W, Grumolato L, Bernstein E, Aaronson SA. Chromatin modifications sequentially enhance ErbB2 expression in ErbB2-positive breast cancers. Cell reports 2013 Oct; 5(2).
Mungamuri SK, Wang S, Manfredi JJ, Gu W, Aaronson SA. Ash2L enables P53-dependent apoptosis by favoring stable transcription pre-initiation complex formation on its pro-apoptotic target promoters. Oncogene 2015 May; 34(19).
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Below are financial relationships with industry reported by Dr. Aaronson during 2016 and/or 2017. Please note that this information may differ from information posted on corporate sites due to timing or classification differences.
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