Evidence map›Paper›PMID 21247378›Full record

ReviewCurrent cancer drug targets2011

Cytokines, inflammation and colon cancer.

Lidija Klampfer

Open access · bronzeAbstract readReview
In one paragraph

Review in Current cancer drug targets, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 163 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
163citing papers in PubMed, 2 pooled it
6.8field-weighted citation impact, top 2% 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

163 citing papers in PubMed, 2 syntheses or guidelines pooled it, 290 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Trial
  4. Article
  5. Article
  6. Review
  7. Review
  8. Article
  9. Article
  10. Review
  11. Review
  12. Promising immunotherapeutic treatments for colon cancer.Medical oncology (Northwood, London, England) · 2025
    Review
  13. Gut Microbiota and Colorectal Cancer: A Balance Between Risk and Protection.International journal of molecular sciences · 2025
    Review
  14. Review
  15. Review
  16. Immunomodulatory effects of live and UV-killedIranian journal of microbiology · 2024
    Article
  17. Review
  18. Review
  19. Review
  20. Article

103 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

1 author at 1 institution in 1 country.

Lidija KlampferAlbert Einstein Cancer Center, Montefiore Medical Center, Department of Oncology, Bronx, NY 10467, USA. lidija.klampfer@einstein.yu.edu
Albert Einstein College of Medicine · US

Funding

Oncogenic Ras, STAT1 and ChemopreventionR01CA111361 · NCI · MONTEFIORE MEDICAL CENTER (BRONX, NY) · PI KLAMPFER, LIDIJA · 2005 to 2009
$1.1M
NCI NIH HHS CA 111361NCI NIH HHS R01 CA111361
6 · The paper itself

Abstract

Patients with inflammatory bowel diseases, such as ulcerative colitis and Crohn's disease, are at increased risk of developing colon cancer, confirming that chronic inflammation predisposes to development of tumors. Moreover, it appears that colon cancers that do not develop as a complication of inflammatory bowel disease are also driven by inflammation, because it has been shown that regular use of nonsteroidal anti-inflammatory drugs (NSAIDs) lowers the mortality from sporadic colon cancer and results in regression of adenomas in familial adenomatous polyposis (FAP) patients, who inherit a mutation in the Apc gene. Colorectal cancer therefore represents a paradigm for the link between inflammation and cancer. Inflammation is driven by soluble factors, cytokines and chemokines, which can be produced by tumor cells themselves or, more often, by the cells recruited to the tumor microenvironment. Inflammatory cytokines and chemokines promote growth of tumor cells, perturb their differentiation, and support the survival of cancer cells. Tumor cells become addicted to inflammatory stroma, suggesting that the tumor microenvironment represents an attractive target for preventive and therapeutic strategies. Proinflammatory cytokines, such as TNFα, IL-6 and IL-1β, or transcription factors that are required for signaling by these cytokines, including NF-κB and STATs, are indeed emerging as potential targets for anticancer therapy. TNFα antagonists are in phase I/II clinical trials and have been shown to be well tolerated in patients with solid tumors, and IL-1β antagonists that ameliorate several inflammatory disorders characterized by excessive IL-1β production, will likely follow. Therefore, development of drugs that normalize the tumor microenvironment or interrupt the crosstalk between the tumor and the tumor microenvironment is an important approach to the management of cancer.

Indexed as

AnimalsColonic NeoplasmsCytokinesHumansInflammatory Bowel DiseasesCytokines

Identifiers

PMID21247378
PMCPMC3540985
OpenAlexW1967595513

What OpenQuestion holds

Textmetadata
LicenceTDM
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.