Evidence map›Paper›PMID 22178590›Full record

ArticleGastroenterology2012

Field cancerization in the intestinal epithelium of patients with Crohn's ileocolitis.

Susan Galandiuk, Manuel Rodriguez-Justo, Rosemary Jeffery, Anna M Nicholson, Yong Cheng, Dahmane Oukrif, George Elia, Simon J Leedham, Stuart A C McDonald, Nicholas A Wright and 1 more

Abstract read
In one paragraph

Article in Gastroenterology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 papers.

0numbers the graph read from it
0cells of the map it votes in
71citing papers in PubMed
2.8field-weighted citation impact, top 10% 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

71 citing papers in PubMed, 123 citations in OpenAlex.

  1. Article
  2. Pathophysiology of colitis-associated colorectal cancer.Nature reviews. Gastroenterology & hepatology · 2026
    Review
  3. Review
  4. Article
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  8. Article
  9. Article
  10. Review
  11. Review
  12. Article
  13. Article
  14. Review
  15. Review
  16. Focal Cancer in Colitis.Clinics in colon and rectal surgery · 2024
    Review
  17. Article
  18. Review
  19. Article
  20. A computational model for the cancer field effect.Frontiers in artificial intelligence · 2023
    Article

11 more citing papers are in PubMed but not listed here.

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 at 6 institutions in 3 countries.

Susan GalandiukHistopathology Laboratory, Cancer Research UK London Research Institute, London, England. s0gala01@louisville.edu
Manuel Rodriguez-Justo
Rosemary Jeffery
Anna M Nicholson
Yong Cheng
Dahmane Oukrif
George Elia
Simon J Leedham
Stuart A C McDonald
Nicholas A Wright
Trevor A Graham
Cancer Research UK · GBQueen Mary University of London · GBUniversity College Hospital · GBFirst Affiliated Hospital of Chongqing Medical University · CNUniversity of Louisville · USUniversity of Oxford · GB

Funding

Strategic Vision & Impact on Environmental HealthP30ES014443 · NIEHS · UNIVERSITY OF LOUISVILLE · PI LI, YONG · 2007 to 2010
$4.4M
Cancer Research UKNIEHS NIH HHS 1P30ES014443-01A1NIEHS NIH HHS P30 ES014443Wellcome Trust 090532
6 · The paper itself

Abstract

BACKGROUND &

aimsTumors that develop in patients with Crohn's disease tend be multifocal, so field cancerization (the replacement of normal cells with nondysplastic but tumorigenic clones) might contribute to intestinal carcinogenesis. We investigated patterns of tumor development from pretumor intestinal cell clones.

methodsWe performed genetic analyses of multiple areas of intestine from 10 patients with Crohn's disease and intestinal neoplasia. Two patients had multifocal neoplasia; longitudinal sections were collected from 3 patients. Individual crypts were microdissected and genotyped; clonal dependency analysis was used to determine the order and timing of mutations that led to tumor development.

resultsThe same mutations in KRAS, CDKN2A(p16), and TP53 that were observed in neoplasias were also present in nontumor, nondysplastic, and dysplastic epithelium. In 2 patients, carcinogenic mutations were detected in nontumor epithelium 4 years before tumors developed. The same mutation (TP53 p.R248W) was detected at multiple sites along the entire length of the colon from 1 patient; it was the apparent founder mutation for synchronous tumors and multiple dysplastic areas. Disruption of TP53, CDKN2A, and KRAS were all seen as possible initial events in tumorigenesis; the sequence of mutations (the tumor development pathway) differed among lesions.

conclusionsPretumor clones can grow extensively in the intestinal epithelium of patients with Crohn's disease. Segmental resections for neoplasia in patients with Crohn's disease might therefore leave residual pretumor disease, and dysplasia might be an unreliable biomarker for cancer risk. Characterization of the behavior of pretumor clones might be used to predict the development of intestinal neoplasia.

Indexed as

Point MutationAdultAgedBiomarkers, TumorCell Transformation, NeoplasticChildClone CellsColitisCrohn DiseaseCyclin-Dependent Kinase Inhibitor p16DNA Mutational AnalysisGenetic Predisposition to DiseaseHumansIleitisImmunohistochemistryIntestinal NeoplasmsBiomarkers, TumorCyclin-Dependent Kinase Inhibitor p16KRAS protein, humanProto-Oncogene ProteinsProto-Oncogene Proteins p21(ras)ras ProteinsTP53 protein, humanTumor Suppressor Protein p53

Identifiers

PMID22178590
PMCPMC4446968
OpenAlexW2064051662

What OpenQuestion holds

Textmetadata
LicenceTDM
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.