Evidence map›Paper›PMID 36260158›Full record

ReviewJournal of cancer research and clinical oncology2023

Cancer-associated inflammation: pathophysiology and clinical significance.

Piotr Pęczek, Monika Gajda, Kacper Rutkowski, Marta Fudalej, Andrzej Deptała, Anna M Badowska-Kozakiewicz

Abstract readReview
In one paragraph

Review in Journal of cancer research and clinical oncology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed, 1 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

36 citing papers in PubMed, 1 synthesis or guideline pooled it.

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  9. Cervicovaginal microbiome alterations across HPV infection.Frontiers in cellular and infection microbiology · 2026
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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.

Piotr Pęczek *Department of Cancer Prevention, Students' Scientific Organization of Cancer Cell Biology, Medical University of Warsaw, Warsaw, Poland.
Monika Gajda *Department of Cancer Prevention, Students' Scientific Organization of Cancer Cell Biology, Medical University of Warsaw, Warsaw, Poland.
Kacper Rutkowski *Department of Cancer Prevention, Students' Scientific Organization of Cancer Cell Biology, Medical University of Warsaw, Warsaw, Poland.
Marta FudalejDepartment of Cancer Prevention, Medical University of Warsaw, Erazma Ciołka 27, Warsaw, Poland.
Andrzej DeptałaDepartment of Cancer Prevention, Medical University of Warsaw, Erazma Ciołka 27, Warsaw, Poland.
Anna M Badowska-KozakiewiczDepartment of Cancer Prevention, Medical University of Warsaw, Erazma Ciołka 27, Warsaw, Poland. abadowska@wum.edu.pl.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeCancer cells, despite stemming from the own cells of their host, usually elicit an immune response. This response usually enables elimination of cancer at its earliest stages. However, some tumors develop mechanisms of escaping immune destruction and even profiting from tumor-derived inflammation.

methodsWe summarized the roles of different immune cell populations in various processes associated with cancer progression and possible methods of reshaping tumor-associated inflammation to increase the efficacy of cancer therapy.

resultsChanges in various signaling pathways result in attraction of immunosuppressive, pro-tumorigenic cells, such as myeloid-derived suppressor cells, tumor-associated macrophages, and neutrophils, while at the same time suppressing the activity of lymphocytes, which have the potential of destroying cancer cells. These changes promote tumor progression by increasing angiogenesis and growth, accelerating metastasis, and impairing drug delivery to the tumor site.

conclusionDue to its multi-faceted role in cancer, tumor-associated inflammation can serve as a valuable therapy target. By increasing it, whether through decreasing overall immunosuppression with immune checkpoint inhibitor therapy or through more specific methods, such as cancer vaccines, oncolytic viruses, or chimeric antigen receptor T cells, cancer-derived immunosuppression can be overcome, resulting in immune system destroying cancer cells. Even changes occurring in the microbiota can influence the shape of antitumor response, which could provide new attractive diagnostic or therapeutic methods. Interestingly, also decreasing the distorted tumor-associated inflammation with non-steroidal anti-inflammatory drugs can lead to positive outcomes.

Indexed as

NeoplasmsOncolytic VirusesClinical RelevanceHumansImmunotherapyInflammationTumor MicroenvironmentCancerImmunotherapyInflammationOncology

Identifiers

PMID36260158
PMCPMC9579684

What OpenQuestion holds

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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.