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This review aims to explore the molecular mechanisms underlying KMT2C alterations in gastrointestinal cancers and their clinical significance.

Molecular mechanisms of KMT2C alterations in gastrointestinal cancers: enhancer network destabilization, lineage plasticity, and clinical translation

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Review examines KMT2C impacts on enhancer networks and clinical implications in gastrointestinal cancers, suggesting vulnerabilities.

This review aims to explore the molecular mechanisms underlying KMT2C alterations in gastrointestinal cancers and their clinical significance.
Integration of evidence from various cancer types including hepatocellular carcinoma and colorectal cancer.
Analysis of KMT2C's role in enhancer network destabilization and tumor complexity.
Discussion of therapeutic strategies linked to KMT2C alterations.
KMT2C alterations destabilize enhancer and super-enhancer networks, promoting large-scale transcriptional changes.
KMT2C dysfunction is associated with increased tumor mutational burden and altered immune response.
KMT2C-related genomic instability presents therapeutic vulnerabilities, including potential effectiveness of PARP inhibitors.

Zeng et al. (2026) studied this question.

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