Evidence map›Paper›PMID 30158439›Full record

ReviewCells2018

Inflammation and NF-κB Signaling in Prostate Cancer: Mechanisms and Clinical Implications.

Jens Staal, Rudi Beyaert

Open access · goldAbstract readReview
In one paragraph

Review in Cells, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
75citing papers in PubMed, 3 pooled it
2.4field-weighted citation impact, top 11% 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

75 citing papers in PubMed, 3 syntheses or guidelines pooled it, 99 citations in OpenAlex.

  1. Pooled it
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  4. Article
  5. Differential Effects of a First-in-Class IKKCalcified tissue international · 2026
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15 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.

Jens StaalVIB-UGent Center for Inflammation Research, Unit of Molecular Signal Transduction in Inflammation, VIB, 9052 Ghent, Belgium.ORCID 0000-0003-2664-3357
Rudi BeyaertVIB-UGent Center for Inflammation Research, Unit of Molecular Signal Transduction in Inflammation, VIB, 9052 Ghent, Belgium. rudi.beyaert@irc.vib-ugent.be.ORCID 0000-0002-5704-582X
Ghent University · BE

Funding

Stichting Tegen Kanker FAF-F/2016/812
6 · The paper itself

Abstract

Prostate cancer is a highly prevalent form of cancer that is usually slow-developing and benign. Due to its high prevalence, it is, however, still the second most common cause of death by cancer in men in the West. The higher prevalence of prostate cancer in the West might be due to elevated inflammation from metabolic syndrome or associated comorbidities. NF-κB activation and many other signals associated with inflammation are known to contribute to prostate cancer malignancy. Inflammatory signals have also been associated with the development of castration resistance and resistance against other androgen depletion strategies, which is a major therapeutic challenge. Here, we review the role of inflammation and its link with androgen signaling in prostate cancer. We further describe the role of NF-κB in prostate cancer cell survival and proliferation, major NF-κB signaling pathways in prostate cancer, and the crosstalk between NF-κB and androgen receptor signaling. Several NF-κB-induced risk factors in prostate cancer and their potential for therapeutic targeting in the clinic are described. A better understanding of the inflammatory mechanisms that control the development of prostate cancer and resistance to androgen-deprivation therapy will eventually lead to novel treatment options for patients.

Indexed as

androgencancercastrationclinicalcytokinesinflammationNF-κBprostateprotein kinase Csignaling

Identifiers

PMID30158439
PMCPMC6162478
OpenAlexW2889483924

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.