BAF Complex Maintains Glioma Stem Cells in Pediatric H3K27M Glioma.
Eshini PanditharatnaJoana G MarquesTingjian WangMaria C TrissalIlon LiuLi JiangAlexander BeckAndrew GrovesNeekesh V DhariaDeyao LiSamantha E HoffmanGuillaume KugenerMcKenzie L ShawHafsa M MireOlivia A HackJoshua M DempsterCaleb A LareauLingling DaiLogan H SiguaMichael A QuezadaAnn-Catherine J StantonMeghan WyattZohra KalaniAmy GoodaleFrancisca VazquezFrederica PiccioniJohn G DoenchDavid E RootJamie N AnastasKristen L JonesAmy Saur ConwaySylwia A StopkaMichael S ReganYu LiangHyuk-Soo SeoKijun SongPuspalata BashyalWilliam P JeromeNathan D MathewsonSirano Dhe-PaganonMario L SuvàAngel Montero CarcabosoCinzia LavarinoJaume Catala-MoraQuang-De NguyenKeith L LigonYang ShiSameer AgnihotriNathalie Y R AgarKimberly StegmaierCharles D StilesMichelle MonjeTodd R GolubJun QiMariella G FilbinPublished in: Cancer discovery (2022)
Epigenetic dysregulation is at the core of H3K27M-glioma tumorigenesis. Here, we identify the BRG1-BAF complex as a critical regulator of enhancer and transcription factor landscapes, which maintain H3K27M glioma in their progenitor state, precluding glial differentiation, and establish pharmacologic targeting of the BAF complex as a novel treatment strategy for pediatric H3K27M glioma. See related commentary by Beytagh and Weiss, p. 2730. See related article by Mo et al., p. 2906.