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However, there is a need to elucidate targetable pathways driving growth and metastasis in SMARCB1-deficient tumors. Here, we demonstrate that SMARCB1 deficiency, defined as genomic SMARCB1 copy number loss associated with reduced mRNA, drives disease progression in patients with bladder cancer by engaging STAT3. SMARCB1 loss increases the chromatin accessibility of the STAT3 locus in vitro. Orthotopically implanted SMARCB1 knockout (KO) cell lines exhibit increased tumor growth and metastasis. SMARCB1-deficient tumors show an increased IL6\/JAK\/STAT3 signaling axis in in vivo models and patients. Furthermore, a pSTAT3 selective inhibitor, TTI-101, reduces tumor growth in SMARCB1 KO orthotopic cell line-derived xenografts and a SMARCB1-deficient patient derived xenograft model. We have identified a gene signature generated from SMARCB1 KO tumors that predicts SMARCB1 deficiency in patients. 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P.M. has received honoraria for service on a Scientific Advisory Board for Mirati Therapeutics, Bristol Myers Squibb, and Exelixis; consulting for Axiom Healthcare Strategies; non-branded educational programs supported by Exelixis and Pfizer; and research funding for clinical trials from Takeda, Bristol Myers Squibb, Mirati Therapeutics, Gateway for Cancer Research, and The University of Texas MD Anderson Cancer Center. M.J.E. reports grants from CPRIT and McNair Medical Foundation during the conduct of the study; personal fees from AstraZeneca outside the submitted work; in addition, M.J.E. has a patent for PAM50 issued, licensed, and with royalties paid from Veracyte. M.J.E. is current employee of AstraZeneca. H.C.H. is a consultant for Avenge Bio, Inc. A.S.K. is Scientific Advisor to Karkinos Health Care Pvt Ltd, India\u00a0and unpaid visiting faculty\u00a0to Sri Sathya Sai Institute for Higher Learning, India.\u00a0The other authors declare that they have no competing interests.","order":1,"name":"Ethics","group":{"name":"EthicsHeading","label":"Competing interests"}}],"article-number":"1373"}}