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Article

Attenuation of the CpG island methylator phenotype and lack of WNT signalling activation restrains Kras mutant intestinal neoplasia.

British journal of cancer - 1 Apr 2026

Fennell Lochlan, Liu Cheng, Kane Alexandra, Tria Simon, Borowsky Jennifer, Chai Lu, Randall-Demllo Sarron, McKeone Diane, Bond Catherine, Leggett Barbara, Whitehall Vicki

Abstract excerpt

BACKGROUND: Serrated neoplasia arises from serrated precursor lesions. Hyperplastic polyps commonly activate MAPK signalling, initiated by BRAF or KRAS mutation, but premalignant KRAS-mutant sessile serrated lesions are rare. Here, we model Kras- and Braf-mutant neoplasia in vivo comparing histological, transcriptomic, and epigenetic changes. METHODS: Temporospatial activation of oncogenic BrafV637 or KrasG12D...

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Share to CpG Islands
Share to DNA Methylation

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Gene Expression Regulation, Neoplastic

Share to Intestinal Neoplasms

Share to Proto-Oncogene Proteins B-raf

Share to Proto-Oncogene Proteins p21(ras)

Share to Wnt Signaling Pathway

Source

Open in PubMed Open full text

Identifiers

PMID: 41731118
DOI: 10.1038/s41416-025-03271-3
PMCID: PMC13035823

Genes

KRAS
BRAF

Provenance

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

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