Department of Pediatrics
Section of Hematology/Oncology
Committee on Cancer Biology
M.D., Cornell University, 1996
Ph.D., Cornell University, 1995
Phone: (773) 702-4919
The University of Chicago
KCBD 5220-A (5th floor)
900 East 57th Street
Chicago, Illinois 60637
Related Research Interests:
Susceptibility to Cancer
Kenan Onel, M.D., Ph.D.
Pathways of Apoptosis and DNA Repair; Genetic
Susceptibility to Cancer
Dr. Kenan Onel is an expert in cancer genetics and cancer biology. His research is aimed at identifying and studying functionally the genetic basis of cancer susceptibility by identifying genes and genetic markers that alter cancer risk in both inherited and sporadic cancers. His work is largely directed towards developing studies minimizing inter-individual heterogeneity in order to improve the detection of genetic risk variants with large effects and gene x exposure interactions. By understanding the genetic contribution to cancer in the context of exposures, he is then able to perform hypothesis-driven laboratory studies to investigate the role of these variants.
Timothy Best (CCB graduate student)
Sapana Vora (CCB graduate student)
Kate Wolak (CCB graduate student)
Imge Hülür (GGSB graduate student)
Mark Sasaki (Post-doc)
Cozen W, Li D, Best T, Van Den Berg DJ, Gourraud P-A, Cortessis VK, Skol AD, Mack TM, Glaser SL, Weiss LM, Nathwani BN, Bhatia S, Schumacher FR, Edlund CK, Hwang AE, Slager SL, Fredericksen ZS, Strong LC, Habermann TM, Link BK, Cerhan JR, Robison LL, Conti DV, and Onel K. 2011. A genome-wide meta-analysis of Nodular Sclerosis Hodgkin Lymphoma identifies risk loci at 6p21.32. Blood: In press. PMID: 22086417.
Best T, Li D, Skol AD, Kirchhoff T, Jackson SA, Yasui Y, Bhatia S, Strong LC, Domchek SM, Nathanson KL, Olopade O, Mack TM, Conti DV, Offit K, Cozen W, Robison LL, and Onel K. 2011. Variants at 6q21 implicate PRDM1 in the etiology of therapy-induced second malignancies after Hodgkin lymphoma. Nat Med 17(8): 941-3. PMID: 21785431.
Best T, Skol AD, and Onel K. 2011. The translational potential of genomics in cancer. ASCO Educational Book. In press.
Sucheston L, Witonsky DB, Hastings D, Yildiz O, Clark VJ, Di Rienzo A, and Onel K. 2011. Natural selection and functional genetic variation in the p53 pathway. Hum Mol Genet. 20(8): 1502-8. PMID: 21266458.
Godley LA, Cunningham J, Dolan ME, Huang RS, Gurbuxani S, McNerney ME, Larson RA, Leong H, Lussier Y, Onel K, Odenike O, Stock W, White KP, and Le Beau MM. 2011. An integrated genomic approach to the assessment and treatment of acute myeloid leukemia. Semin Oncol 38(2): 215-24. PMID: 21421111.
Knight JA, Skol AD, Shinde A, Hastings D, Walgren RA, Shao J, Tennant TR, Banerjee M, Allan JM, Le Beau MM, Larson RA, Graubert TA, Cox NJ, and Onel K. 2009. A genome-wide association study to identify novel loci associated with therapy-related myeloid leukemia susceptibility. Blood 113(22): 5575-82. PMID: 19299336.
Ellis NA, Huo D, Yildiz O, Worrillow LJ, Banerjee M, Le Beau MM, Larson RA, Allan JM, and Onel K. 2008. MDM2 SNP309 and TP53 Arg72Prointeract to alter therapy-related acute myeloid leukemia susceptibility. Blood. 112(3): 741-9. PMID: 18426989.
Bond GL, Hu W, Bond EE, Robins H, Lutzker SG, Arva NC, Bargonetti J, Bartel F, Taubert H, Wuerl P, Onel K, Yip L, Hwang SJ, Strong LC, Lozano G, and Levine AJ. 2004. A single nucleotide polymorphism in the MDM2 promoter attenuates the p53 tumor suppressor pathway and accelerates tumor formation in humans. Cell 119: 591-602. PMID: 15550242
Faculty and Research