Evidence map›Paper›PMID 27913448›Full record

ReviewCancer prevention research (Philadelphia, Pa.)2016

Targeting Inflammation in Cancer Prevention and Therapy.

Jelena Todoric, Laura Antonucci, Michael Karin

Abstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Cancer prevention research (Philadelphia, Pa.), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 194 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
194citing papers in PubMed, 4 pooled it
–field-weighted citation impact
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

194 citing papers in PubMed, 4 syntheses or guidelines pooled it.

  1. Pooled it
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  4. The diagnostic efficacy of platelet-to-lymphocyte ratio and neutrophil-to-lymphocyte ratio in ovarian cancer.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2017
    Pooled it
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  13. UnveilingFrontiers in immunology · 2026
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134 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

3 authors.

Jelena TodoricLaboratory of Gene Regulation and Signal Transduction, Department of Pharmacology, School of Medicine, University of California San Diego, La Jolla, California.
Laura AntonucciLaboratory of Gene Regulation and Signal Transduction, Department of Pharmacology, School of Medicine, University of California San Diego, La Jolla, California.
Michael KarinLaboratory of Gene Regulation and Signal Transduction, Department of Pharmacology, School of Medicine, University of California San Diego, La Jolla, California. karinoffice@ucsd.edu.

Funding

Tumor Assessment CoreP01CA128814 · NCI · SANFORD BURNHAM PREBYS MEDICAL DISCOVERY INSTITUTE · PI OSTERMAN, ANDREI L · 2009 to 2020
$19.1M
Vector and Human Acinar CoreP01DK098108 · NIDDK · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI GUKOVSKAYA, ANNA S. · 2014 to 2018
$8.1M
IKKalpha, autophagy, obesity and injury enhanced pancreatic cancerR01CA163798 · NCI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI KARIN, MICHAEL · 2012 to 2016
$1.9M
NCI NIH HHS P01 CA128814NCI NIH HHS R01 CA163798NIDDK NIH HHS P01 DK098108
6 · The paper itself

Abstract

Inflammation is associated with the development and malignant progression of most cancers. As most of the cell types involved in cancer-associated inflammation are genetically stable and thus are not subjected to rapid emergence of drug resistance, the targeting of inflammation represents an attractive strategy both for cancer prevention and for cancer therapy. Tumor-extrinsic inflammation is caused by many factors, including bacterial and viral infections, autoimmune diseases, obesity, tobacco smoking, asbestos exposure, and excessive alcohol consumption, all of which increase cancer risk and stimulate malignant progression. In contrast, cancer-intrinsic or cancer-elicited inflammation can be triggered by cancer-initiating mutations and can contribute to malignant progression through the recruitment and activation of inflammatory cells. Both extrinsic and intrinsic inflammation can result in immunosuppression, thereby providing a preferred background for tumor development. In clinical trials, lifestyle modifications including healthy diet, exercise, alcohol, and smoking cessation have proven effective in ameliorating inflammation and reducing the risk of cancer-related deaths. In addition, consumption of certain anti-inflammatory drugs, including aspirin, can significantly reduce cancer risk, suggesting that common nonsteroidal anti-inflammatory drugs (NSAID) and more specific COX2 inhibitors can be used in cancer prevention. In addition to being examined for their preventative potential, both NSAIDs and more potent anti-inflammatory antibody-based drugs need to be tested for their ability to augment the efficacy of more conventional therapeutic approaches on the basis of tumor resection, radiation, and cytotoxic chemicals. Cancer Prev Res; 9(12); 895-905. ©2016 AACR.

Indexed as

AlcoholismAnti-Inflammatory Agents, Non-SteroidalCytokinesExerciseHumansHydroxymethylglutaryl-CoA Reductase InhibitorsInflammationMicrobiotaNeoplasmsObesityRisk FactorsTobacco SmokingAnti-Inflammatory Agents, Non-SteroidalCytokinesHydroxymethylglutaryl-CoA Reductase Inhibitors

Identifiers

PMID27913448
PMCPMC5142754

What OpenQuestion holds

Texttitle and abstract
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.