Evidence map›Paper›PMID 41731118›Full record

ArticleBritish journal of cancer2026

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

Lochlan Fennell, Cheng Liu, Alexandra Kane, Simon Tria, Jennifer Borowsky, Lu Chai, Sarron Randall-Demllo, Diane McKeone, Catherine Bond, Barbara Leggett and 1 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in British journal of cancer, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

1 citing paper in PubMed.

  1. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

11 authors.

Lochlan FennellSchool of Health, University of Sunshine Coast, Birtinya, QLD, Australia. lfennell@usc.edu.au.ORCID http://orcid.org/0000-0003-3214-3527
Cheng LiuConjoint Gastroenterology Laboratory; Cancer Faculty, QIMR Berghofer Medical Research Institute, Herston, QLD, Australia.
Alexandra KaneConjoint Gastroenterology Laboratory; Cancer Faculty, QIMR Berghofer Medical Research Institute, Herston, QLD, Australia.ORCID http://orcid.org/0000-0002-3414-8455
Simon TriaConjoint Gastroenterology Laboratory; Cancer Faculty, QIMR Berghofer Medical Research Institute, Herston, QLD, Australia.
Jennifer BorowskyConjoint Gastroenterology Laboratory; Cancer Faculty, QIMR Berghofer Medical Research Institute, Herston, QLD, Australia.
Lu ChaiOncogenic Aging Laboratory, Biomedicine Discovery Institute, Monash University, Clayton, VIC, Australia.
Sarron Randall-DemlloOncogenic Aging Laboratory, Biomedicine Discovery Institute, Monash University, Clayton, VIC, Australia.
Diane McKeoneConjoint Gastroenterology Laboratory; Cancer Faculty, QIMR Berghofer Medical Research Institute, Herston, QLD, Australia.
Catherine BondConjoint Gastroenterology Laboratory; Cancer Faculty, QIMR Berghofer Medical Research Institute, Herston, QLD, Australia.
Barbara LeggettConjoint Gastroenterology Laboratory; Cancer Faculty, QIMR Berghofer Medical Research Institute, Herston, QLD, Australia.
Vicki WhitehallConjoint Gastroenterology Laboratory; Cancer Faculty, QIMR Berghofer Medical Research Institute, Herston, QLD, Australia.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundSerrated 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.

methodsTemporospatial activation of oncogenic Braf

resultsProlonged exposure to oncogenic Braf is associated with a time-dependent accumulation of murine serrated precursors (mSP, P = 3 × 10

conclusionKras mutation can induce serrated neoplasia, but with significantly greater latency period and lower penetrance compared to Braf. Kras-mutant neoplasms display an attenuated CIMP-like phenotype, rarely developing aberrant WNT signalling. These data refine our understanding of MAPK-induced intestinal neoplasia.

Indexed as

CpG IslandsDNA MethylationIntestinal NeoplasmsProto-Oncogene Proteins p21(ras)Wnt Signaling PathwayAnimalsGene Expression Regulation, NeoplasticMiceMutationPhenotypeProto-Oncogene Proteins B-rafBraf protein, mouseHras protein, mouseProto-Oncogene Proteins B-rafProto-Oncogene Proteins p21(ras)

Identifiers

PMID41731118
PMCPMC13035823

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.