Evidence map›Paper›PMID 35416564›Full record

ReviewCancer metastasis reviews2022

Inflammatory bowel disease and carcinogenesis.

Hiroko Nagao-Kitamoto, Sho Kitamoto, Nobuhiko Kamada

Abstract readReview
PubMed Publisher
In one paragraph

Review in Cancer metastasis reviews, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
54citing papers in PubMed, 1 pooled it
11.0field-weighted citation impact, top 1% 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

54 citing papers in PubMed, 1 synthesis or guideline pooled it, 63 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Review
  5. Review
  6. Biomedicines · 2026
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  8. Synergistic effects ofmSystems · 2026
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  9. Review
  10. Review
  11. Article
  12. Review
  13. Embryonic Signaling Pathways Shape Colorectal Cancer Subtypes: Linking Gut Development to Tumor Biology.Pathophysiology : the official journal of the International Society for Pathophysiology · 2025
    Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. The role ofFrontiers in immunology · 2025
    Review
  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

3 authors at 1 institution in 2 countries.

Hiroko Nagao-KitamotoDivision of Gastroenterology and Hepatology, Department of Internal Medicine, University of Michigan, 1150 W. Medical Center Drive, Ann Arbor, MI, 48109, USA. khiroko@umich.edu.
Sho KitamotoDivision of Gastroenterology and Hepatology, Department of Internal Medicine, University of Michigan, 1150 W. Medical Center Drive, Ann Arbor, MI, 48109, USA.
Nobuhiko KamadaDivision of Gastroenterology and Hepatology, Department of Internal Medicine, University of Michigan, 1150 W. Medical Center Drive, Ann Arbor, MI, 48109, USA. nkamada@umich.edu.ORCID 0000-0002-1980-4178
University of Michigan · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Colorectal cancer (CRC) is the third most common cancer and the fourth most common cause of cancer mortality worldwide. Colitis-associated colorectal cancer (CAC) is a subtype of CRC associated with inflammatory bowel disease (IBD). It is well known that individuals with IBD have a 2-3 times higher risk of developing CRC than those who do not, rendering CAC a major cause of death in this group. Although the etiology and pathogenesis of CAC are incompletely understood, animal models of chronic inflammation and human cohort data indicate that changes in the intestinal environment, including host response dysregulation and gut microbiota perturbations, may contribute to the development of CAC. Genomic alterations are a hallmark of CAC, with patterns that are distinct from those in sporadic CRC. The discovery of the biological changes that underlie the development of CAC is ongoing; however, current data suggest that chronic inflammation in IBD increases the risk of developing CAC. Therefore, a deeper understanding of the precise mechanisms by which inflammation triggers genetic alterations and disrupts intestinal homeostasis may provide insight into novel therapeutic strategies for the prevention of CAC.

Indexed as

Colorectal NeoplasmsInflammatory Bowel DiseasesAnimalsCarcinogenesisHumansInflammationIntestinesCACIBDInflammationMicrobiota

Identifiers

PMID35416564
OpenAlexW4223629158

What OpenQuestion holds

Textmetadata
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.