Evidence map›Paper›PMID 23170831›Full record

ReviewCurrent molecular medicine2013

Potential association between TLR4 and chitinase 3-like 1 (CHI3L1/YKL-40) signaling on colonic epithelial cells in inflammatory bowel disease and colitis-associated cancer.

A Kamba, I-A Lee, E Mizoguchi

Open access · greenAbstract readReview
In one paragraph

Review in Current molecular medicine, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
1.3field-weighted citation impact, top 19% 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

30 citing papers in PubMed, 46 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. Edaravone in Digestive Diseases - A Narrative Review.Drug design, development and therapy · 2025
    Review
  7. Article
  8. Review
  9. Review
  10. Review
  11. Article
  12. Review
  13. Review
  14. Article
  15. Review
  16. Review
  17. Review
  18. Chitinase-3 like-protein-1 function and its role in diseases.Signal transduction and targeted therapy · 2020
    Review
  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

3 authors at 1 institution in 1 country.

A KambaGastrointestinal Unit, Department of Medicine, Massachusetts General Hospital, Harvard Medical School, Boston, MA 02114, USA.
I-A Lee
E Mizoguchi
Massachusetts General Hospital · 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 inflammatory disorders in the small and large intestines. Several studies have proved that persistent and disregulated host/microbial interactions are required for the development of IBD. It is well known that chronic IBD is strongly associated with an increased risk of developing colorectal cancer by 0.5-1% annually, 8-10 years after the initial diagnosis. To detect the tiny dysplasia or early stage of cancer in chronic IBD patients, a tremendous amount of effort is currently directed for improving colonoscopic technology and noninvasive serological marker development. However, there is only a limited amount of data available to understand the exact mechanism of how long term chronic colitis is connected to the development of colorectal tumors. Recently, our group has identified significantly increased expression of chitinase 3-like 1 (CHI3L1) molecule in non-dysplastic mucosa from patients with IBD and remote dysplasia/cancer, compared to patients with IBD without dysplasia or healthy controls. CHI3L1 seems to contribute to the proliferation, migration, and neoplastic progression of colonic epithelial cells (CECs) under inflammatory conditions. Furthermore, the TLR4-mediated intracellular signaling cascade is likely to interact with CHI3L1 signaling in CECs. In this review article, we have concisely summarized the cellular and molecular mechanisms underlining the development of IBD and colitis-associated cancer, with particular focus on the TLR4- and CHI3L1-signaling pathways in CECs.

Indexed as

AdipokinesCarcinogenesisCell MovementCell ProliferationChitinase-3-Like Protein 1ColitisColonic NeoplasmsEpithelial CellsHumansInflammatory Bowel DiseasesLectinsSignal TransductionToll-Like Receptor 4AdipokinesCHI3L1 protein, humanChitinase-3-Like Protein 1LectinsTLR4 protein, humanToll-Like Receptor 4

Identifiers

PMID23170831
PMCPMC3661706
OpenAlexW2104358541

What OpenQuestion holds

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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.