ArticleCellular and molecular life sciences : CMLS2025
Mutant p53 regulates reversible subtype plasticity in pancreatic cancer.
Article in Cellular and molecular life sciences : CMLS, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
- Revisiting tumor immunogenicity through the lens of mutant p53: Implications for cancer immunotherapy.Apoptosis : an international journal on programmed cell death · 2026Review
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3 authors.
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Abstract
Loss-of-function mutations in the TP53 gene are the most frequent genetic events in human malignancies. However, the extent to which missense TP53 mutations confer oncogenic gain-of-function (GOF) properties remains incompletely understood. Using genetically defined pancreatic cancer organoid models, we demonstrated that mutant p53 provides a selective growth advantage under acute environmental stress and drives molecular transition toward a basal-like state. Transcriptomic analyses showed that under stress conditions, organoids expressing mutant p53 adopted a basal-like gene expression program, a characteristic of a poor prognosis subtype of pancreatic cancer. Furthermore, the molecular subtype was reversed to the classical subtype once it returned to normal growth conditions, suggesting that transcriptional plasticity arises from acute changes in the tissue microenvironment. Given these context-dependent oncogenic properties, our findings suggest that targeting mutant p53 may be a promising therapeutic strategy for pancreatic cancer.
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