Evidence map›Paper›PMID 33624450›Full record

ReviewCancer medicine2020

Metabolic dysfunction and early-onset colorectal cancer - how macrophages build the bridge.

Katharina M Scheurlen, Adrian T Billeter, Stephen J O'Brien, Susan Galandiuk

Open access · goldAbstract readReview
In one paragraph

Review in Cancer medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
1.6field-weighted citation impact, top 16% 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

31 citing papers in PubMed, 42 citations in OpenAlex.

  1. Review
  2. Article
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  5. Microbiome of Young and Later-Onset Colorectal Cancer.The Surgical clinics of North America · 2025
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  8. The role of adipogenic niche resident cells in colorectal cancer progression in relation to obesity.Obesity reviews : an official journal of the International Association for the Study of Obesity · 2025
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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

4 authors at 2 institutions in 2 countries.

Katharina M ScheurlenPrice Institute of Surgical Research, Department of Surgery, University of Louisville, Louisville, KY, USA.ORCID 0000-0003-4169-9041
Adrian T BilleterDepartment of General, Visceral, and Transplantation Surgery, University Hospital Heidelberg, Heidelberg, Baden-Wuerttemberg, Germany.
Stephen J O'BrienPrice Institute of Surgical Research, Department of Surgery, University of Louisville, Louisville, KY, USA.ORCID 0000-0003-2686-0300
Susan GalandiukPrice Institute of Surgical Research, Department of Surgery, University of Louisville, Louisville, KY, USA.ORCID 0000-0001-9994-5263
University of Louisville · USHeidelberg University · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe incidence of colorectal cancer (CRC) among patients <50 years of age has increased dramatically over the last decades. At the same time, the growing proportion of obese children and adolescents and the increasing proportion of young and obese patients with CRC suggests an association between metabolic dysfunction and carcinogenesis. Tumor-associated macrophages (TAMs) are able to orchestrate tumor promoting and suppressing mechanisms in CRC. The aim of this review was to discuss the different roles of TAMs in CRC and their phenotype-specific metabolic pathways to identify potential new targets for CRC treatment.

methodsA literature search was performed using PubMed, Cochrane and Embase to identify studies on TAMs and their metabolism in CRC. The following search terms were used in various combinations: (obesity OR adiposity OR obese) AND (macrophage OR polarization OR macrophage metabolism) AND ((colon cancer*) OR (colon carcinoma) OR (colonic tumor*) OR (colonic neoplasm[MeSH]) OR (rectal cancer*) OR (rectal carcinoma) OR (rectal tumor*) OR (rectal neoplasm[MeSH]) OR (colorectal cancer*) OR (colorectal carcinoma) OR (colorectal tumor*) OR (colorectal neoplasm[MeSH])). Studies including data on the phenotype and metabolism of TAMs in CRC were analyzed.

resultsEvidence for the prognostic utility of macrophage markers in CRC is currently evolving, with a particular role of stage-dependent cellular metabolism profiles of TAMs. Itaconate is one of the metabolites produced by proinflammatory subtypes of TAMs and it is known to have tumor promoting effects. Metabolic pathways that are involved in macrophage activation and reprogramming play a role in a chronic inflammatory setting, consequently affecting the onset and development of CRC.

conclusionsTumor-promoting metabolites, such as itaconate, are directly regulating these mechanisms, thereby triggering carcinogenesis. Metabolic reprogramming in TAMs can build a bridge between metabolic dysfunction and the onset and progression of CRC through inflammatory pathways, particularly in younger patients with early-onset CRC.

Indexed as

AdiposityAdolescentAdultCell PolarityCellular ReprogrammingChildColonic NeoplasmsHumansInflammationMacrophage ActivationMiddle AgedObesityPediatric ObesityPhenotypePrognosisRectal Neoplasmsitaconic acidSuccinatesadipositycolonic neoplasmscolorectal neoplasmsobesityrectal neoplasmstumor‐associated macrophages

Identifiers

PMID33624450
PMCPMC7520341
OpenAlexW3043837093

What OpenQuestion holds

Textmetadata
LicenceCC BY
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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.