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Article

STAT3 sustains tumorigenicity following mutant KRAS ablation.

EMBO reports - 1 Oct 2025

D'Amico Stephen, Kirillov Varvara, Liu Jingxuan, Qiu Zhijuan, Lei Xinyuan, Qin Hong, Sheridan Brian S, Reich Nancy C

Abstract excerpt

Oncogenic KRAS mutations underlie some of the deadliest human cancers. Genetic or pharmacological KRAS inactivation produces mixed outcomes and frequent relapse. Mechanisms of tumor resistance to KRAS inhibition remain poorly understood. We present evidence that STAT3 supports tumor growth following KRAS depletion. Using a conceptual framework of pancreatic ductal adenocarcinoma, we show that cancer cells that...

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Topics

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Share to Carcinogenesis
Share to Carcinoma, Pancreatic Ductal

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Cell Line, Tumor

Share to Cell Transformation, Neoplastic

Share to Gene Expression Regulation, Neoplastic

Share to Pancreatic Neoplasms

Share to Proto-Oncogene Proteins p21(ras)

Share to STAT3 Transcription Factor

Source

Open in PubMed Open full text

Identifiers

PMID: 40859018
DOI: 10.1038/s44319-025-00563-w
PMCID: PMC12549880

Genes

KRAS
STAT3

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026.

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STAT3 sustains tumorigenicity following mutant KRAS ablation.PMID 40859018Read ↗

STAT3 Sustains Tumorigenicity Following Mutant KRAS AblationSemantic proximity Read ↗

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