Article
Frequent mutation of receptor protein tyrosine phosphatases provides a mechanism for STAT3 hyperactivation in head and neck cancer.
Proceedings of the National Academy of Sciences of the United States of America - 21 Jan 2014
Lui Vivian Wai Yan, Peyser Noah D, Ng Patrick Kwok-Shing, Hritz Jozef, Zeng Yan, Lu Yiling, Li Hua, Wang Lin, Gilbert Breean R, General Ignacio J, Bahar Ivet, Ju Zhenlin, Wang Zhenghe, Pendleton Kelsey P, Xiao Xiao, Du Yu, Vries John K, Hammerman Peter S, Garraway Levi A, Mills Gordon B, Johnson Daniel E, Grandis Jennifer R
Abstract excerpt
The underpinnings of STAT3 hyperphosphorylation resulting in enhanced signaling and cancer progression are incompletely understood. Loss-of-function mutations of enzymes that dephosphorylate STAT3, such as receptor protein tyrosine phosphatases, which are encoded by the PTPR gene family, represent a plausible mechanism of STAT3 hyperactivation. We analyzed whole exome sequencing (n = 374) and reverse-phase...
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