Evidence map›Paper›PMID 25278673›Full record

ReviewWorld journal of gastroenterology2014

Contribution of TLR signaling to the pathogenesis of colitis-associated cancer in inflammatory bowel disease.

Ferenc Sipos, István Fűri, Miklós Constantinovits, Zsolt Tulassay, Györgyi Műzes

Open access · hybridAbstract readEditorialReview
In one paragraph

Review in World journal of gastroenterology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
3.5field-weighted citation impact, top 7% 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

21 citing papers in PubMed, 39 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Article
  5. Review
  6. Article
  7. Review
  8. Anti-Inflammatory and Chemopreventive Effects ofFrontiers in pharmacology · 2020
    Article
  9. Article
  10. Review
  11. Article
  12. Regulation of Tumor Progression by Programmed Necrosis.Oxidative medicine and cellular longevity · 2018
    Review
  13. Profile of gene expression of TLR-signaling pathways in colorectal cancer tissues.International journal of immunopathology and pharmacology · 2017
    Article
  14. Article
  15. Review
  16. Microbiota, Inflammation and Colorectal Cancer.International journal of molecular sciences · 2017
    Review
  17. Article
  18. Article
  19. Article
  20. Review
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

5 authors at 1 institution in 1 country.

Ferenc SiposFerenc Sipos, István Fűri, Miklós Constantinovits, Györgyi Műzes, 2 Department of Internal Medicine, Semmelweis University, 1088 Budapest, Hungary.
István FűriFerenc Sipos, István Fűri, Miklós Constantinovits, Györgyi Műzes, 2 Department of Internal Medicine, Semmelweis University, 1088 Budapest, Hungary.
Miklós ConstantinovitsFerenc Sipos, István Fűri, Miklós Constantinovits, Györgyi Műzes, 2 Department of Internal Medicine, Semmelweis University, 1088 Budapest, Hungary.
Zsolt TulassayFerenc Sipos, István Fűri, Miklós Constantinovits, Györgyi Műzes, 2 Department of Internal Medicine, Semmelweis University, 1088 Budapest, Hungary.
Györgyi MűzesFerenc Sipos, István Fűri, Miklós Constantinovits, Györgyi Műzes, 2 Department of Internal Medicine, Semmelweis University, 1088 Budapest, Hungary.
Semmelweis University · HU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In the intestine a balance between proinflammatory and repair signals of the immune system is essential for the maintenance of intestinal homeostasis. The innate immunity ensures a primary host response to microbial invasion, which induces an inflammatory process to localize the infection and prevent systemic dissemination of pathogens. The key elements of this process are the germline encoded pattern recognition receptors including Toll-like receptors (TLRs). If pathogens cannot be eliminated, they may elicit chronic inflammation, which may be partly mediated via TLRs. Additionally, chronic inflammation has long been suggested to trigger tissue tumorous transformation. Inflammation, the seventh hallmark of cancer, may affect all phases of tumor development, and evade the immune system. Inflammation acts as a cellular stressor and may trigger DNA damage or genetic instability. Furthermore, chronic inflammation can provoke genetic mutations and epigenetic mechanisms that promote malignant cell transformation. Colorectal cancers in inflammatory bowel disease patients are considered typical examples of inflammation-related cancers. Although data regarding the role of TLRs in the pathomechanism of cancer-associated colitis are rather conflicting, functionally these molecules can be classified as "largely antitumorigenic" and "largely pro-tumorigenic" with the caveat that the underlying signaling pathways are mainly context (i.e., organ-, tissue-, cell-) and ligand-dependent.

Indexed as

Signal TransductionAnimalsCell Transformation, NeoplasticColitisColonColonic NeoplasmsHumansImmunity, InnateInflammation MediatorsIntestinal MucosaToll-Like ReceptorsInflammation MediatorsToll-Like ReceptorsCarcinogenesisColitis-associated cancerImmunoregulationInflammationInflammatory bowel diseaseTissue repairToll-like receptor

Identifiers

PMID25278673
PMCPMC4177458
OpenAlexW2322508098

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.