Evidence map›Paper›PMID 21274454›Full record

ReviewJournal of biomedicine & biotechnology2011

Animal models of colitis-associated carcinogenesis.

Manasa Kanneganti, Mari Mino-Kenudson, Emiko Mizoguchi

Open access · hybridAbstract readReview
In one paragraph

Review in Journal of biomedicine & biotechnology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.

0numbers the graph read from it
0cells of the map it votes in
59citing papers in PubMed
7.2field-weighted citation impact, top 3% 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

59 citing papers in PubMed, 103 citations in OpenAlex.

  1. A Review on the Molecular Dynamics of EnterotypeInternational journal of molecular sciences · 2026
    Review
  2. Article
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  4. Review
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  6. CHI3L1 enhances melanoma lung metastasisFrontiers in immunology · 2022
    Article
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  8. Review
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  11. Review
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  14. American journal of respiratory cell and molecular biology · 2020
    Article
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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

3 authors at 1 institution in 1 country.

Manasa KannegantiGastrointestinal Unit, Department of Medicine, Harvard Medical School, Massachusetts General Hospital GRJ702, 55 Fruit Street, Boston, MA 02114, USA.
Mari Mino-Kenudson
Emiko Mizoguchi
Harvard University · US

Funding

Pilot & Feasibility ProgramP30DK043351 · NIDDK · MASSACHUSETTS GENERAL HOSPITAL · PI Ramnik J Xavier · 1991 to 2026
$35.3M
Role of Mammalian Chitinases in Inflammatory Bowel DiseaseR01DK080070 · NIDDK · MASSACHUSETTS GENERAL HOSPITAL · PI MIZOGUCHI, EMIKO · 2009 to 2013
$1.6M
TNF Receptors of Colonic Epithelial Cells in IBDK08DK064289 · NIDDK · MASSACHUSETTS GENERAL HOSPITAL · PI MIZOGUCHI, EMIKO · 2003 to 2007
$637k
Regulatory Role of TNFR1 in Inflammatory Bowel DiseaseR03DK074454 · NIDDK · MASSACHUSETTS GENERAL HOSPITAL · PI MIZOGUCHI, EMIKO · 2006 to 2007
$172k
NIDDK NIH HHS DK43351NIDDK NIH HHS DK64289NIDDK NIH HHS DK74454NIDDK NIH HHS DK 80070NIDDK NIH HHS K08 DK064289NIDDK NIH HHS P30 DK043351NIDDK NIH HHS R01 DK080070NIDDK NIH HHS R03 DK074454
6 · The paper itself

Abstract

Inflammatory bowel disease (IBD) is a group of chronic inflammatory disorders that affect individuals throughout life. Although the etiology and pathogenesis of IBD are largely unknown, studies with animal models of colitis indicate that dysregulation of host/microbial interactions are requisite for the development of IBD. Patients with long-standing IBD have an increased risk for developing colitis-associated cancer (CAC), especially 10 years after the initial diagnosis of colitis, although the absolute number of CAC cases is relatively small. The cancer risk seems to be not directly related to disease activity, but is related to disease duration/extent, complication of primary sclerosing cholangitis, and family history of colon cancer. In particular, high levels and continuous production of inflammatory mediators, including cytokines and chemokines, by colonic epithelial cells (CECs) and immune cells in lamina propria may be strongly associated with the pathogenesis of CAC. In this article, we have summarized animal models of CAC and have reviewed the cellular and molecular mechanisms underlining the development of carcinogenic changes in CECs secondary to the chronic inflammatory conditions in the intestine. It may provide us some clues in developing a new class of therapeutic agents for the treatment of IBD and CAC in the near future.

Indexed as

Disease Models, AnimalAnimalsAnimals, Genetically ModifiedCallitrichinaeColonic NeoplasmsHumansInflammatory Bowel DiseasesMice

Identifiers

PMID21274454
PMCPMC3025384
OpenAlexW2020098501

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.