Oncogenic Deregulation of EZH2 as an Opportunity for Targeted Therapy in Lung Cancer
Cancer Discovery2016Vol. 6(9), pp. 1006–1021
Citations Over TimeTop 10% of 2016 papers
Haikuo Zhang, Jun Qi, Jaime M. Reyes, Lewyn Li, Prakash K. Rao, Fugen Li, Charles Y. Lin, Jennifer A. Perry, Matthew A. Lawlor, Alexander Federation, Thomas De Raedt, Yvonne Y. Li, Yan Liu, Melissa Duarte, Y. Zhang, Grit S. Herter-Sprie, Eiki Kikuchi, Julián Carretero, Charles M. Perou, Jacob B. Reibel, Joshiawa Paulk, Roderick T. Bronson, Hideo Watanabe, Christine F. Brainson, Carla F. Kim, Peter S. Hammerman, Myles Brown, Karen Cichowski, Henry W. Long, James E. Bradner, Kwok‐Kin Wong
Abstract
EZH2 overexpression induces murine lung cancers that are similar to human NSCLC with high EZH2 expression and low levels of phosphorylated AKT and ERK, implicating biomarkers for EZH2 inhibitor sensitivity. Our EZH2 inhibitor, JQEZ5, promotes regression of these tumors, revealing a potential role for anti-EZH2 therapy in lung cancer. Cancer Discov; 6(9); 1006-21. ©2016 AACR.See related commentary by Frankel et al., p. 949This article is highlighted in the In This Issue feature, p. 932.
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