Why the study?
To explore the common mutational mechanisms affecting SWI/SNF complex subunits, their impact on gastrointestinal tumors, and emerging therapeutic approaches to provide a foundation for clinical research.
This review highlights the role of SWI/SNF complex mutations in driving aggressive gastrointestinal tumors and explores emerging therapeutic approaches based on synthetic lethality.
SWI/SNF mutations mark dedifferentiated, aggressive GI tumors; leaves open targeted epigenetic therapies pending prospective validation.
The ATP‑dependent switch/sucrose non-fermentable (SWI/SNF) complex serves a crucial role in systematically modifying chromatin structure and regulating cellular epigenetics. A decreased expression or mutations in the SWI/SNF complex can lead to a series of physiological and pathological changes. Several gene sequencing studies have identified diverse mutations in the SWI/SNF subunits across gastrointestinal cancers. Tumor cells with these mutations are dedifferentiated and more aggressive, with early metastases, including to lymph nodes, often associated with poor prognosis. At present, for tumors with SWI/SNF mutations, the main treatment regimen is based on the phenomenon of synthetic lethality. The present review explores the common mutational mechanisms that affect these subunits and their impact on gastrointestinal tumors, as well as the emerging therapeutic approaches, thereby providing a substantive foundation for further clinical research in this field.
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Xue et al. (2025) studied this question.
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