Evidence mapPaperPMID 40277893Full record

ReviewCells2025

Inflammation-Associated Carcinogenesis in Inflammatory Bowel Disease: Clinical Features and Molecular Mechanisms.

Tadakazu Hisamatsu, Jun Miyoshi, Noriaki Oguri, Hiromu Morikubo, Daisuke Saito, Akimasa Hayashi, Teppei Omori, Minoru Matsuura

Abstract readReview
In one paragraph

Review in Cells, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing 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

17 citing papers in PubMed.

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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

8 authors.

Tadakazu HisamatsuDepartment of Gastroenterology and Hepatology, Kyorin University School of Medicine, Tokyo 181-8611, Japan.ORCID 0000-0002-1178-3536
Jun MiyoshiDepartment of Gastroenterology and Hepatology, Kyorin University School of Medicine, Tokyo 181-8611, Japan.
Noriaki OguriDepartment of Gastroenterology and Hepatology, Kyorin University School of Medicine, Tokyo 181-8611, Japan.
Hiromu MorikuboDepartment of Gastroenterology and Hepatology, Kyorin University School of Medicine, Tokyo 181-8611, Japan.ORCID 0000-0002-1232-5879
Daisuke SaitoDepartment of Gastroenterology and Hepatology, Kyorin University School of Medicine, Tokyo 181-8611, Japan.
Akimasa HayashiDepartment of Pathology, Kyorin University School of Medicine, Tokyo181-8611, Japan.
Teppei OmoriDepartment of Gastroenterology and Hepatology, Kyorin University School of Medicine, Tokyo 181-8611, Japan.
Minoru MatsuuraDepartment of Gastroenterology and Hepatology, Kyorin University School of Medicine, Tokyo 181-8611, Japan.ORCID 0000-0001-9590-2370

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Inflammatory bowel disease (IBD), comprising ulcerative colitis (UC) and Crohn's disease (CD), is a chronic condition marked by persistent intestinal inflammation of unknown etiology. Disease onset involves genetic predisposition and environmental factors that disrupt the intestinal immune homeostasis. The intestinal microbiome and immune response play pivotal roles in disease progression. Advances in molecular therapies and early interventions have reduced surgery rates; however, colorectal cancer (CRC) remains a significant concern, driven by chronic inflammation. In UC, the risk of UC-associated neoplasia (UCAN) increases with disease duration, while CD patients face elevated risks of small intestine, anal fistula, and anal canal cancers. Endoscopic surveillance is advised for UCAN, but optimal screening intervals remain undefined, and no established guidelines exist for CD-associated cancers. UCAN morphology often complicates detection due to its flat, inflammation-blended appearance, which differs pathologically from sporadic CRC (sCRC). UCAN is frequently surrounded by dysplasia, with p53 mutations evident at the dysplasia stage. IBD-associated gastrointestinal cancers exemplify inflammation-driven carcinogenesis with distinct molecular mechanisms from the adenoma-carcinoma sequence. This review explores the epidemiology, risk factors, clinical and pathological features, current surveillance practices, and molecular pathways underlying inflammation-associated cancers in IBD.

Indexed as

CarcinogenesisInflammationInflammatory Bowel DiseasesColorectal NeoplasmsHumansRisk FactorsCrohn’s diseasedysplasiainflammatory bowel diseasep53ulcerative colitis-associated neoplasia (UCAN)

Identifiers

PMID40277893
PMCPMC12025475

What Socratic 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 Socratic graph.