Xiaofeng Wang

TL;DR: It is found that loss of ARID1B in AR ID1A-deficient backgrounds destabilizes SWI/SNF and impairs proliferation in both cancer cells and primary cells, and is identified as a potential therapeutic target for ARID 1A-mutant cancers.

TL;DR: It is demonstrated how environmental signals acting via FOS/JUN and BAF coordinate with cell-type-specific TFs to select enhancer repertoires that enable differentiation during development.

TL;DR: It is shown via ChIP-seq and biochemical assays that SWI/SNF complexes are preferentially targeted to distal lineage specific enhancers and interact with p300 to modulate histone H3 lysine 27 acetylation, establishingSWI/ SNF complexes as regulators of the enhancer landscape and providing insight into the roles of SWI-SNF in cellular fate control.

TL;DR: It is demonstrated that Arid1a functions as a tumor suppressor in the mouse colon, but not the small intestine, and that invasive ARID1A-deficient adenocarcinomas resemble human colorectal cancer (CRC).

TL;DR: It is shown that, despite having indistinguishable mutational landscapes, human rhabdoid tumors exhibit distinct enhancer H3K27ac signatures, which identify remnants of differentiation programs, and that these retained super-enhancers are essential for rhabDoid tumor survival.