Evidence map›Paper›PMID 20233436›Full record

ArticleBMC cancer2010

Dietary, lifestyle and clinicopathological factors associated with BRAF and K-ras mutations arising in distinct subsets of colorectal cancers in the EPIC Norfolk study.

Adam Naguib, Panagiota N Mitrou, Laura J Gay, James C Cooke, Robert N Luben, Richard Y Ball, Alison McTaggart, Mark J Arends, Sheila A Rodwell

Open access · goldAbstract read
In one paragraph

Article in BMC cancer, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed, 2 pooled it
2.9field-weighted citation impact, top 9% of its field
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

34 citing papers in PubMed, 2 syntheses or guidelines pooled it, 70 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Predictive and prognostic roles of BRAF mutation in stage III colon cancer: results from intergroup trial CALGB 89803.Clinical cancer research : an official journal of the American Association for Cancer Research · 2012
    Trial
  4. Review
  5. Article
  6. Observational
  7. Article
  8. Article
  9. Article
  10. Dietary Fat Intake andNutrients · 2022
    Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Clinicopathological Significance ofJournal of Cancer · 2019
    Article
  16. Main Risk Factors Association with Proto-Oncogene Mutations in Colorectal CancerAsian Pacific journal of cancer prevention : APJCP · 2018
    Article
  17. Article
  18. Article
  19. Article
  20. 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

9 authors at 5 institutions in 1 country.

Adam NaguibDepartment of Pathology, University of Cambridge, Addenbrooke's Hospital, Cambridge CB22QQ, UK.
Panagiota N Mitrou
Laura J Gay
James C Cooke
Robert N Luben
Richard Y Ball
Alison McTaggart
Mark J Arends
Sheila A Rodwell
Medical Research Council · GBUniversity of Cambridge · GBAddenbrooke's Hospital · GBNorfolk and Norwich University Hospitals NHS Foundation Trust · GBWellcome Trust · GB

Funding

Cancer Research UKMedical Research Council MC_U105630924
6 · The paper itself

Abstract

backgroundBRAF and K-ras proto-oncogenes encode components of the ERK signalling pathway and are frequently mutated in colorectal cancer. This study investigates the associations between BRAF and K-ras mutations and clinicopathological, lifestyle and dietary factors in colorectal cancers.

methods186 adenocarcinomas and 16 adenomas from the EPIC Norfolk study were tested for BRAF and K-ras mutations. Diet and lifestyle data were collected prospectively using seven day food diaries.

resultsBRAF V600E mutation was found in 15.6% of colorectal cancers but at higher frequencies in cancers with proximal location, poor differentiation and microsatellite instability (MSI) (all p < 0.001). K-ras mutation (mostly in codons 12 and 13) was found in 22.0% of colorectal cancers but at higher frequencies in cancers of more advanced Dukes' stage (p = 0.001), microsatellite stable (MSS) status (p = 0.002) and in individuals with lower blood high-density lipoprotein concentrations (p = 0.04). Analysis of dietary factors demonstrated no link between BRAF mutation and any specific dietary constituent, however, K-ras mutation was found at higher frequencies in individuals with higher white meat consumption (p < 0.001). Further analysis of specific mutation type demonstrated that G to A transitions in K-ras were observed at higher frequencies in individuals consuming lower amounts of fruit (p = 0.02).

conclusionThese data support the model of BRAF and K-ras mutations arising in distinct colorectal cancer subsets associated with different clinicopathological and dietary factors, acting as mutually exclusive mechanisms of activation of the same signalling pathway.

Indexed as

DietGenes, rasLife StyleMutationAdenocarcinomaAdenomaAgedColorectal NeoplasmsEnglandFemaleHumansMaleMiddle AgedProspective StudiesProto-Oncogene Proteins B-rafBRAF protein, humanProto-Oncogene Proteins B-raf

Identifiers

PMID20233436
PMCPMC2847960
OpenAlexW2082522931

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.