Authors
Zheng Yang, Zixuan Tian, Renji Liang, Yi Lu, Tengfei Zhu, Ya-Nan Wang, Wei Zhang
Published in
Journal of cellular and molecular medicine. Volume 30. Issue 16. Pages e71290.
Abstract
Chromatin remodelling SWI/SNF complexes are recurrently altered in malignancies, and some members were found to be associated with immune checkpoint blockade (ICB) response. However, it is unclear whether SWI/SNF complex genes as a collective factor have clinical relevance. Through pan-cancer analysis of 8507 tumours across 26 types from The Cancer Genome Atlas, we demonstrate that SWI/SNF loss-of-function (LOF) mutations correlate with elevated immunogenicity markers, such as higher tumour mutational burden (TMB), neoantigen load, and microsatellite instability. SWI/SNF-LOF tumours exhibited enriched CD8+ T cell and M1-like macrophage infiltration, upregulation of major histocompatibility complex class genes, and increased expression of immunostimulators, immunoinhibitors, and chemokines. Crucially, in ICB-treated patients across discovery (n = 750) and validation (n = 562) cohorts encompassing nine cancer types, SWI/SNF-LOF status consistently predicted superior clinical outcomes, including prolonged overall survival, progression-free survival, and higher objective response rates compared to non-mutated tumours. Multivariate analysis confirmed SWI/SNF-LOF as an independent ICB response predictor independent of TMB, age, sex, or cancer type. These findings identify SWI/SNF LOF mutations as promising biomarkers of an inflamed tumour microenvironment and favourable responses to ICB across multiple solid tumours.
PMID:
42642869
Bibliographic data and abstract were imported from PubMed on 26 Aug 2026.
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