Evidence map›Paper›PMID 20885960›Full record

ArticlePloS one2010

Toll-like receptor 2 signaling protects mice from tumor development in a mouse model of colitis-induced cancer.

Emily L Lowe, Timothy R Crother, Shervin Rabizadeh, Bing Hu, Hanlin Wang, Shuang Chen, Kenichi Shimada, Michelle H Wong, Kathrin S Michelsen, Moshe Arditi

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 83 papers.

0numbers the graph read from it
0cells of the map it votes in
83citing papers in PubMed
4.6field-weighted citation impact, top 4% 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

83 citing papers in PubMed, 145 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Review
  5. Gut Microbiota and Colorectal Cancer: A Balance Between Risk and Protection.International journal of molecular sciences · 2025
    Review
  6. Role of Innate Immunity in Cancer.Advances in experimental medicine and biology · 2025
    Review
  7. Article
  8. Review
  9. Review
  10. Review
  11. Article
  12. Review
  13. Inflammatory bowel disease and carcinogenesis.Cancer metastasis reviews · 2022
    Review
  14. Sodium houttuyfonate effectively treats acute pulmonary infection ofFrontiers in cellular and infection microbiology · 2022
    Article
  15. Review
  16. Article
  17. Review
  18. Review
  19. Review
  20. Review

23 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

10 authors at 2 institutions in 1 country.

Emily L LoweDivision of Pediatric Infectious Diseases and Immunology, Cedars-Sinai Medical Center and David Geffen School of Medicine at University of California Los Angeles, Los Angeles, California, United States of America.
Timothy R Crother
Shervin Rabizadeh
Bing Hu
Hanlin Wang
Shuang Chen
Kenichi Shimada
Michelle H Wong
Kathrin S Michelsen
Moshe Arditi
Cedars-Sinai Medical Center · USUniversity of California, Los Angeles · US

Funding

MD2 signaling in LPS/TLR4 induced cellular responsesR01AI058128 · NIAID · CEDARS-SINAI MEDICAL CENTER · PI ARDITI, MOSHE · 2004 to 2009
$2.4M
Role of Innate Immunity and Stat3 Activation in Colitis Mouse ModelK08DK089076 · NIDDK · CEDARS-SINAI MEDICAL CENTER · PI RABIZADEH, SHERVIN · 2010 to 2014
$850k
NIAID NIH HHS AI-058128NIAID NIH HHS R01 AI058128NIDDK NIH HHS K08 DK089076
6 · The paper itself

Abstract

Inflammatory bowel disease (IBD) is a disorder of chronic inflammation with increased susceptibility to colorectal cancer. The etiology of IBD is unclear but thought to result from a dysregulated adaptive and innate immune response to microbial products in a genetically susceptible host. Toll-like receptor (TLR) signaling induced by intestinal commensal bacteria plays a crucial role in maintaining intestinal homeostasis, innate immunity and the enhancement of intestinal epithelial cell (IEC) integrity. However, the role of TLR2 in the development of colorectal cancer has not been studied. We utilized the AOM-DSS model for colitis-associated colorectal cancer (CAC) in wild type (WT) and TLR2(-/-) mice. Colons harvested from WT and TLR2(-/-) mice were used for histopathology, immunohistochemistry, immunofluorescence and cytokine analysis. Mice deficient in TLR2 developed significantly more and larger colorectal tumors than their WT controls. We provide evidence that colonic epithelium of TLR2(-/-) mice have altered immune responses and dysregulated proliferation under steady-state conditions and during colitis, which lead to inflammatory growth signals and predisposition to accelerated neoplastic growth. At the earliest time-points assessed, TLR2(-/-) colons exhibited a significant increase in aberrant crypt foci (ACF), resulting in tumors that developed earlier and grew larger. In addition, the intestinal microenvironment revealed significantly higher levels of IL-6 and IL-17A concomitant with increased phospho-STAT3 within ACF. These observations indicate that in colitis, TLR2 plays a protective role against the development of CAC.

Indexed as

Signal TransductionAberrant Crypt FociAnimalsColitisColorectal NeoplasmsDisease Models, AnimalFemaleHumansImmunity, InnateInterleukin-6MaleMiceMice, Inbred C57BLMice, KnockoutNeoplastic ProcessesToll-Like Receptor 2Interleukin-6Toll-Like Receptor 2

Identifiers

PMID20885960
PMCPMC2946405
OpenAlexW2011753823

What OpenQuestion 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 OpenQuestion graph.