Targeting MYC as a Therapeutic Intervention for Anaplastic Thyroid Cancer
Author(s) -
Keisuke Enomoto,
Xuguang Zhu,
SunMi Park,
Li Zhao,
Yuelin J. Zhu,
Mark C. Willingham,
Jun Qi,
John A. Copland,
Paul S. Meltzer,
Sheue-yann Cheng
Publication year - 2017
Publication title -
the journal of clinical endocrinology and metabolism
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.206
H-Index - 353
eISSN - 1945-7197
pISSN - 0021-972X
DOI - 10.1210/jc.2016-3771
Subject(s) - bromodomain , cancer research , cell growth , brd4 , anaplastic thyroid cancer , bet inhibitor , cell cycle , chromatin , biology , thyroid cancer , acetylation , transcription factor , cancer , gene , genetics
Recent studies showed that transcription of the MYC gene is driven by the interaction of bromodomain and extraterminal domain (BET) proteins with acetylated histones on chromatin. JQ1, a potent inhibitor that effectively disrupts the interaction of BET proteins with acetylated histones, preferentially suppresses transcription of the MYC gene. We recently reported that JQ1 decreased thyroid tumor growth and improved survival in a mouse model of anaplastic thyroid cancer (ATC) by targeting MYC transcription. The role of MYC in human ATC and whether JQ1 can effectively target MYC as a treatment modality have not been elucidated.
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