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Article

Molecular dynamics driving phenotypic divergence among KRAS mutants in pancreatic tumorigenesis.

Developmental cell - 12 Aug 2026

Grimont Adrien, Falvo David J, Sisso Whitney J, Santos Francisco, Chan Christopher W, Zumbo Paul, Fall William B, Ferrick Katherine, Pan Grace, Cleveland Megan, Yaron-Barir Tomer M, Osterhoudt Alexa, Meng Yinuo, Zafra Maria Paz, Rendeiro Andre F, Hissong Erika, Yantiss Rhonda K, Betel Doron, Magnuson Mark A, Leach Steven D, Rustgi Anil K, Dow Lukas E, Chandwani Rohit

Abstract excerpt

Inflammation in the pancreas drives acinar-to-ductal metaplasia (ADM), a progenitor-like state that can be hijacked by mutant Kras in the formation of pancreatic ductal adenocarcinoma. How these cell fate decisions vary according to KRAS mutation remains poorly understood. To define mutation-specific lineage reversion and tumor initiation, we implement Ptf1a-tdTomato mice and multiple KRAS mutants across several...

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Share to Carcinogenesis
Share to Carcinoma, Pancreatic Ductal

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

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Share to Cell Transformation, Neoplastic

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Share to Pancreatic Neoplasms

Share to Proto-Oncogene Proteins c-akt

Share to Proto-Oncogene Proteins p21(ras)

Source

Open in PubMed Open full text

Identifiers

PMID: 42480541
DOI: 10.1016/j.devcel.2026.06.016
PMCID: PMC13404274

Genes

KRAS
ADM
EGFR
RAC1
VAV1

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 6 Sept 2026.

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