Evidence map›Paper›PMID 27549311›Full record

ReviewCold Spring Harbor perspectives in medicine2016

p53 and the Carcinogenicity of Chronic Inflammation.

Andrei V Gudkov, Elena A Komarova

Open access · bronzeAbstract readReview
In one paragraph

Review in Cold Spring Harbor perspectives in medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
64citing papers in PubMed, 2 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

64 citing papers in PubMed, 2 syntheses or guidelines pooled it, 110 citations in OpenAlex.

  1. Pooled it
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  8. Frontiers in immunology · 2026
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4 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

2 authors at 1 institution in 1 country.

Andrei V GudkovDepartment of Cell Stress Biology, Roswell Park Cancer Institute, Buffalo, New York 14263.
Elena A KomarovaDepartment of Cell Stress Biology, Roswell Park Cancer Institute, Buffalo, New York 14263.
Roswell Park Comprehensive Cancer Center · US

Funding

Mechanisms of mitigation of radiation damage of GI tract by Protectan CBLB502RC2AI087616 · NIAID · CLEVELAND BIOLABS, INC. · PI GUDKOV, ANDREI V · 2009 to 2010
$5.3M
MODULATORS OF P53 EXPRESSION AND FUNCTIONR01CA075179 · NCI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI GUDKOV, ANDREI V · 1997 to 2007
$1.9M
Controlling Radiation Injury by TLR5 AgonistsR01AI080446 · NIAID · ROSWELL PARK CANCER INSTITUTE CORP · PI GUDKOV, ANDREI V · 2008 to 2012
$1.7M
An intercross between the circadian and NFkB pathwaysR01GM095874 · NIGMS · ROSWELL PARK CANCER INSTITUTE CORP · PI ANTOCH, MARINA, GUDKOV, ANDREI V · 2011 to 2014
$1.4M
NCI NIH HHS R01 CA075179NIAID NIH HHS R01 AI080446NIAID NIH HHS RC2 AI087616NIGMS NIH HHS R01 GM095874
6 · The paper itself

Abstract

Chronic inflammation is a major cancer predisposition factor. Constitutive activation of the inflammation-driving NF-κB pathway commonly observed in cancer or developed in normal tissues because of persistent infections or endogenous tissue irritating factors, including products of secretion by senescent cells accumulating with age, markedly represses p53 functions. In its turn, p53 acts as a suppressor of inflammation helping to keep it within safe limits. The antagonistic relationship between p53 and NF-κB is controlled by multiple mechanisms and reflects cardinal differences in organismal responses to intrinsic and extrinsic cell stresses driven by these two transcription factors, respectively. This provides an opportunity for developing drugs to treat diseases associated with inappropriate activity of either p53 or NF-κB through targeting the opposing pathway. Several drug candidates of this kind are currently in clinical testing. These include anticancer small molecules capable of simultaneous suppression of p53 and activation of NF-κB and NF-κB-activating biologics that counteract p53-mediated pathologies associated with systemic genotoxic stresses such as acute radiation syndrome and side effects of cancer treatment.

Indexed as

Cellular SenescenceDNA DamageGenetic Predisposition to DiseaseHumansInflammationNeoplasmsNF-kappa BSignal TransductionTumor Suppressor Protein p53NF-kappa BTumor Suppressor Protein p53

Identifiers

PMID27549311
PMCPMC5088512
OpenAlexW2511025182

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.