Evidence map›Paper›PMID 28621843›Full record

ReviewImmunology2017

Metabolic reprogramming in the tumour microenvironment: a hallmark shared by cancer cells and T lymphocytes.

Katrina E Allison, Brenda L Coomber, Byram W Bridle

Abstract readReview
In one paragraph

Review in Immunology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 papers.

0numbers the graph read from it
0cells of the map it votes in
71citing papers in PubMed
–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

71 citing papers in PubMed.

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11 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

3 authors.

Katrina E AllisonDepartment of Pathobiology, Ontario Veterinary College, University of Guelph, Guelph, ON, Canada.
Brenda L CoomberDepartment of Biomedical Sciences, Ontario Veterinary College, University of Guelph, Guelph, ON, Canada.
Byram W BridleDepartment of Pathobiology, Ontario Veterinary College, University of Guelph, Guelph, ON, Canada.ORCID 0000-0002-8335-1118

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Altered metabolism is a hallmark of cancers, including shifting oxidative phosphorylation to glycolysis and up-regulating glutaminolysis to divert carbon sources into biosynthetic pathways that promote proliferation and survival. Therefore, metabolic inhibitors represent promising anti-cancer drugs. However, T cells must rapidly divide and survive in harsh microenvironments to mediate anti-cancer effects. Metabolic profiles of cancer cells and activated T lymphocytes are similar, raising the risk of metabolic inhibitors impairing the immune system. Immune checkpoint blockade provides an example of how metabolism can be differentially impacted to impair cancer cells but support T cells. Implications for research with metabolic inhibitors are discussed.

Indexed as

Cellular ReprogrammingEnergy MetabolismTumor MicroenvironmentAnimalsAntineoplastic AgentsCell ProliferationGlycolysisHumansHydrogen-Ion ConcentrationLymphocyte ActivationLymphocytes, Tumor-InfiltratingMolecular Targeted TherapyNeoplasmsOxidative PhosphorylationPhenotypeSignal TransductionAntineoplastic AgentscancerT cellstumour immunology

Identifiers

PMID28621843
PMCPMC5588769

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.