Gender	Male
E-mail	stuart.aaronson@mssm.edu
Education and Training	M.D., University of California, San Francisco School of Medicine
	B.S., University of California, Berkeley
	Internship, Moffitt Hospital
	Fellowship, University of Cambridge
Awards	1991 Chirone Prize
	1991 Harvey Lecture
	1990 Milken Award
	1989 PHS Distinguished Service Medal
	1989 Paul Ehrlich Prize
	1982 Rhoads Memorial Award
	1982 PHS Meritorious Service Medal
	1966 Alpha Omega Alpha
	1962 Phi BetaKappa

Dr. Aaronson is an internationally recognized cancer biologist, who in early studies established the transformation-competent but replication defective nature of mammalian sarcoma viruses and molecularly cloned many of their oncogenes. He and colleagues implicated retroviral-related oncogenes in human cancer through investigations including the initial detection of their expression in human tumors and critical contributions to the demonstration of their involvement in human cancer. His investigations of the v-sis oncogene established the first normal function of an oncogene and the role of oncogenes in growth factor signaling. His discovery of erbB2 as a v-erbB-related gene amplified in a human breast carcinoma and demonstration of its transforming properties paved the way for targeted therapies directed against its product.

He isolated KGF (FGF7), a growth factor with novel epithelial cell specificity and demonstrated its involvement in wound repair. Its successful phase III clinical trial by Amgen for treatment of mucositis, recently led the FDA to approve Kepivance (KGF) for treatment of this debilitating side effect of many cancer therapies. Thus, Dr. Aaronson's pioneering discoveries have directly led to new therapies for cancer patients.

His development and application of stable expression cDNA cloning technology resulted in his identification of new human oncogenes, growth factor receptors, and other genes, which induce transformation or drug resistance. He and colleagues identified the protooncogene product, MET, as the receptor for HGF/Scatter Factor and LRP5/6 as the receptor for a novel Wnt antagonist, Dkk1. This latter discovery paved the way for his recent demonstration with colleagues of a Wnt autocrine transforming mechanism in human malignancies.

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 1994 and is the Jack and Jane B. Aron Professor and Chairman 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 Rhoads Memorial Award from the American Association of Cancer Research, and the Paul Erhlich Prize from Germany. He is the author of over 530 publications, an inventor on more than 50 patents, and serves on numerous editorial boards and scientific advisory committees.

Education and Training	M.D., University of California, San Francisco School of Medicine
	B.S., University of California, Berkeley
	Internship, Moffitt Hospital
	Fellowship, University of Cambridge

The laboratory of Stuart A. Aaronson, M.D., focuses on cancer gene discovery. His current research includes investigations into the mechanisms by which tumor suppressor genes induce permanent growth arrest/senescence and the signaling pathways involved. He is examining the role of reactive oxygen species (ROS), which accumulate in response to p53 induction in determining cell fate decisions concerning growth arrest and apoptosis. He has also identified a novel p53 effector pathway involving sustained MAPK activation and identified growth factors and receptors, which are induced in a p53 dependent manner and contribute to activation of this signaling pathway. The lab is also investigating other known and novel p53 response genes with respect to their involvement in cellular senescence.

Other projects include investigations of autocrine and paracrine acting growth factors PDGF, KGF, HGF, and Wnt ligands. In particular, the lab is investigating the mechanisms of activation of Wnt co- receptors, frizzled and LRP5/6, and the specific contributions of each receptor to canonical signaling through B-catenin upregulation. Another major goal is to elucidate mechanisms of transformation by up-regulated Wnt signaling and novel mechanisms activating this pathway in cancer cells. Finally, the laboratory is applying cDNA cloning technology and other functional genomic strategies to the discovery of novel targets for cancer intervention.

Graduate Students:
Erica Benson, Martina Kracikova

Postdoctoral Fellows:
Gal Akiri, Luca Grumolato, Sapna Vijayakumar,  Satish Kumar Mungamuri, Zhongwei Cao, Igotz Delgado Balzategui

New York Academy of Sciences eBriefing: Digging for Therapeutic Gold

Ide T, Ongusaha P, Raj L, Ohtsuka T, Aaronson S, Lee S. GMAT, a p53-Inducible Modulator of Apoptosis, Is Critical for the Adaptive Response to Nutrient Stress. Molcular Cell 2009 Nov;.

Akiri G, Cherian M, Vijayakumar S, Liu G, Bafico A, Aaronson S. Wnt pathway aberrations including autocrine Wnt activation occur at high frequency in human non-small-cell lung carcinoma. Oncogene 2009; 28: 2163-2172.

Liu G, Grumolato L, Arroyave R, Qiao H, Akiri G, Aaronson S. Canonical Wnts function as potent regulators of osteogenesis by human mesenchymal stem cells. Journal of Cell Biology 2009 April; 185(1): 67-75.

Zhao B, Benson E, Qiao R, Wang X, Kim S, Manfredi J, Lee S, Aaronson S. Cellular senescence and organismal ageing in the absence of p21 CIP1/WAF1 in ku80-/-mice . EMBO 2009;: 71-78.

Ongusaha PP, Qi HH, Raj L, Kim YB, Aaronson SA, Davis R, Shi Y, Liao J, Lee SW. Identification of ROCK1 as an Upstream Activator of the JIP-3 to JNK Signaling Axis in Response to UVB Damage [PMID: 19036714]. Sci Signal 2008 Nov 25; 1(47): ra14.

Munoz-Fontella C, Macip S, Martinez-Sobrido L, Brown L, Ashour J, Garcia-Sastre A, Lee SW, Aaronson SA. Transcriptional role of p53 in Interferon-mediated antiviral immunity [PMID: 18663127]. Journal of Exp. Med 2008 July;: 1-10.

Mahale A, Khan Z, Igarashi M, Nanjangud G, Qiao RF, Yao S, Lee SW, Aaronson SA. Clonal Selection in Malignant Transformation of Human Fibroblasts Transduces with Defined Cellualr Oncogenes [PMID: 18316605]. Cancer Research 2008; 68(5): 1417-1426.

Brown L, Ongusaha P, Kim H, Nuti S, Mandinova A, Lee J, Khosravi-Far R, Aaronson SA, Lee S. CDIP, a novel pro-apoptotic gene, regulates TNFalpha-mediated apoptosis in a p53-dependent manner [PMID: 17599062]. The EMBO Journal 2007; 26(14): 3410-3422.

Das S, Raj L, Zhao B, Bernstein A, Aaronson SA, Lee SA. Hzf, a key modulator of p53 mediated transcription, functions as a critical determinant of cell survival and death upon genotoxic stress [PMID: 17719541]. Cell 2007; 130: 624-637.

Lopez Bergami P, Huang C, Goydos J, Yip D, Bar-Eli M, Herlyn M, Smalley K, Mahale A, Eroshkin A, Aaronson S, Ronai Z. Re-wired ERK-JNK signaling pathways in melanoma. Cancer Cell 2007;.