Sandi Radko-Juettner, Hong Yue, Jacquelyn A Myers, Raymond D Carter, Alexis N Robertson, Priya Mittal, Zhexin Zhu, Baranda S Hansen, Katherine A Donovan, Moritz Hunkeler, Wojciech Rosikiewicz, Zhiping Wu, Meghan G McReynolds, Shourya S Roy Burman, Anna M Schmoker, Nada Mageed, Scott A Brown, Robert J Mobley, Janet F Partridge, Elizabeth A Stewart, Shondra M Pruett-Miller, Behnam Nabet, Junmin Peng, Nathanael S Gray, Eric S Fischer, Charles W M Roberts
Whereas oncogenes can potentially be inhibited with small molecules, the loss of tumour suppressors is more common and is problematic because the tumour-suppressor proteins are no longer present to be targeted. Notable examples include SMARCB1-mutant cancers, which are highly lethal malignancies driven by the inactivation of a subunit of SWI/SNF (also known as BAF) chromatin-remodelling complexes. Here, to generate mechanistic insights into the consequences of SMARCB1 mutation and to identify vulnerabilities, we contributed 14 SMARCB1-mutant cell lines to a near genome-wide CRISPR screen as part of the Cancer Dependency Map Project1-3 ...
March 27, 2024: Nature