Evidence map›Paper›PMID 27653961›Full record

ReviewInflammation research : official journal of the European Histamine Research Society ... [et al.]2017

Prolonged inflammatory microenvironment is crucial for pro-neoplastic growth and genome instability: a detailed review.

Kumari Anuja, Souvick Roy, Chinmoy Ghosh, Priya Gupta, Surajit Bhattacharjee, Birendranath Banerjee

Abstract readReview
PubMed Publisher
In one paragraph

Review in Inflammation research : official journal of the European Histamine Research Society ... [et al.], 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
2.8field-weighted citation impact, top 8% 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

27 citing papers in PubMed, 53 citations in OpenAlex.

  1. Determinants of cancer mortality in patients after acute myocardial infarction.International journal of cardiology. Heart & vasculature · 2026
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  20. Human microbial ecology and the rising new medicine.Annals of translational medicine · 2019
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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

6 authors at 2 institutions in 1 country.

Kumari AnujaMolecular Stress and Stem Cell Biology Group, School of Biotechnology, KIIT University, Bhubaneshwar, Odisha, 751024, India.
Souvick RoyMolecular Stress and Stem Cell Biology Group, School of Biotechnology, KIIT University, Bhubaneshwar, Odisha, 751024, India.
Chinmoy GhoshMolecular Stress and Stem Cell Biology Group, School of Biotechnology, KIIT University, Bhubaneshwar, Odisha, 751024, India.
Priya GuptaDepartment of Molecular Biology and Bioinformatics, Tripura University (A Central University), Suryamaninagar, Agartala, Tripura, 799022, India.
Surajit BhattacharjeeDepartment of Molecular Biology and Bioinformatics, Tripura University (A Central University), Suryamaninagar, Agartala, Tripura, 799022, India. surajit77@tripurauniv.in.
Birendranath BanerjeeMolecular Stress and Stem Cell Biology Group, School of Biotechnology, KIIT University, Bhubaneshwar, Odisha, 751024, India. bnbanerjee@kiitbiotech.ac.in.
KIIT University · INTripura University · IN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionChronic inflammation can affect the normal cell homeostasis and metabolism by rendering the cells susceptible to genomic instability that may lead to uncontrolled cellular growth and proliferation ensuing tumorigenesis. The causal agents for inflammation may be pathogenic infections like microbial agents ranging from viruses to bacteria. These infections lead to DNA damage or disruption of normal cell metabolism and alter the genome integrity.

findingsIn this review, we have highlighted the role of recurrent infections in tumor microenvironment can lead to recruitment of pro-inflammatory cells, cytokines and growth factors to the site of inflammation. This makes the environment rich in cytokines, chemokines, DNA-damaging agents (ROS, RNS) and growth factors which activate DNA damage response pathway and help in sustained proliferation of the tumor cells. In any inflammatory response, the production of cytokines and related signaling molecules is self-regulating and limiting. But in case of neoplastic risk, deregulation of these factors may lead to abnormalities and related pathogenesis.

conclusionThe scope of the present review is to explore the probable mechanistic link and factors responsible for chronic inflammation. The relation between chronic inflammation and DNA damage response was further elucidated to understand the mechanism by which it makes the cells susceptible to carcinogenesis.

Indexed as

AnimalsDNA DamageGenomic InstabilityHumansInfectionsInflammationNeoplasmsOxidative StressTumor MicroenvironmentCarcinogenesisChronic inflammationDNA damage responseGenomic instabilityImmune responseOxidative stress

Identifiers

PMID27653961
OpenAlexW2522669510

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.