Dr. Tiki Hayes’s research program broadly focuses on basic and pre-clinical mechanisms surrounding oncogene dependency, signal transduction, and therapeutic strategies. Identifying and understanding of variants of unknown significance (VUS) and development of resistance to targeted therapies represent two significant challenges facing current cancer care. Dr. Hayes is particularly interested in 1) interrogating oncogenic dependency and signal transduction networks, 2) assessing mechanisms driving therapeutic sensitivity/resistance, and 3) characterizing somatic variants of unknown significance. She addresses these questions using a combination of high-throughput genetic screening and molecular biology and pharmacology.
Persky NS, Hernandez D, Do Carmo M, Brenan L, Cohen O, Kitajima S, Nayar U, Walker A, Pantel S, Lee Y, Cordova J, Sathappa M, Zhu C, Hayes TK, Ram P, Pancholi P, Mikkelsen TS, Barbie DA, Yang X, Haq R, Piccioni F, Root DE, Johannessen CM. Defining the landscape of ATP-competitive inhibitor resistance residues in protein kinases. Nat Struct Mol Biol 27(1), 92–104 (2020). PMID: 31925410
Hayes TK, Luo F, Cohen O, Goodale AB, Lee Y, Pantel S, Bagul M, Piccioni F, Root DE, Garraway LA, Meyerson M, Johannessen CM. A Functional Landscape of Resistance to MEK1/2 and CDK4/6 Inhibition in NRAS-Mutant Melanoma. Cancer Res. May 1;79(9):2352-2366. PMID: 30819666
Hayes TK, Neel NF, Hu C, Gautam P, Chenard M, Long B, Aziz M, Kassner M, Bryant KL, Pierobon M, Marayati R, Kher S, George SD, Xu M, Wang-Gillam A, Samatar AA, Maitra A, Wennerberg K, Petricoin EF 3rd, Yin HH, Nelkin B, Cox AD, Yeh JJ, Der CJ. Long-Term ERK Inhibition in KRAS Mutant Pancreatic Cancer Is Associated with MYC Degradation and Senescence-like Growth Suppression. Cancer Cell. 2016 Jan 11;29 (1):75-89. PMCID: PMC4816652