Gain of function of ASXL1 truncating protein in the pathogenesis of myeloid malignancies
Hui Yang(Sylvester Comprehensive Cancer Center), Stefan Kurtenbach(The California Eye Institute), Ying Guo(Sylvester Comprehensive Cancer Center), Ines Lohse(Center for Innovation), Michael Durante(The California Eye Institute), Jianping Li(Sylvester Comprehensive Cancer Center), Zhaomin Li(Sylvester Comprehensive Cancer Center), Hassan Al‐Ali(Sylvester Comprehensive Cancer Center), Lingxiao Li(University of Miami), Zizhen Chen(Chinese Academy of Medical Sciences & Peking Union Medical College), Matthew G. Field(The California Eye Institute), Peng Zhang(Sylvester Comprehensive Cancer Center), Shi Chen(Sylvester Comprehensive Cancer Center), Shohei Yamamoto(Sylvester Comprehensive Cancer Center), Zhuo Li(Sylvester Comprehensive Cancer Center), Yuan Zhou(Chinese Academy of Medical Sciences & Peking Union Medical College), Stephen D. Nimer(University of Miami), J. William Harbour(The California Eye Institute), Claes Wahlestedt(Center for Innovation), Mingjiang Xu(Sylvester Comprehensive Cancer Center), Feng‐Chun Yang(Sylvester Comprehensive Cancer Center)
Cited by 167Open Access
Abstract
Key Points Transgenic expression of ASXL1aa1-587 truncating protein in the hematopoietic system leads to diverse myeloid malignancies in mice. ASXL1aa1-587 gains an interaction with BRD4 and Asxl1Y588XTg hematopoietic stem/progenitor cells are hypersensitive to BET bromodomain inhibitors.
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