Evidence map›Paper›PMID 27141887›Full record

ReviewNature reviews. Clinical oncology2017

Cancer metabolism: a therapeutic perspective.

Ubaldo E Martinez-Outschoorn, Maria Peiris-Pagés, Richard G Pestell, Federica Sotgia, Michael P Lisanti

Erratum issuedOpen access · greenAbstract readReview
PubMed Publisher
In one paragraph

Review in Nature reviews. Clinical oncology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 750 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
750citing papers in PubMed, 2 pooled it
55.1field-weighted citation impact, top 1% 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

750 citing papers in PubMed, 2 syntheses or guidelines pooled it, 1,467 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Review
  4. Glutamine metabolism in health and disease.Signal transduction and targeted therapy · 2026
    Review
  5. CD112 Lactylation Drives Dual Immune Evasion From CD8+ T Cells and NK Cells.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
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690 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

5 authors at 4 institutions in 2 countries.

Ubaldo E Martinez-OutschoornThe Sidney Kimmel Cancer Center, Thomas Jefferson University, 233 South 10th Street, Philadelphia, Pennsylvania 19107, USA.
Maria Peiris-PagésThe Breast Cancer Now Manchester Research Unit, Institute of Cancer Sciences, Cancer Research UK Manchester Institute, University of Manchester, Paterson Building, Wilmslow Road, Manchester M20 4BX, UK.
Richard G PestellThe Sidney Kimmel Cancer Center, Thomas Jefferson University, 233 South 10th Street, Philadelphia, Pennsylvania 19107, USA.
Federica SotgiaThe Breast Cancer Now Manchester Research Unit, Institute of Cancer Sciences, Cancer Research UK Manchester Institute, University of Manchester, Paterson Building, Wilmslow Road, Manchester M20 4BX, UK.
Michael P LisantiThe Breast Cancer Now Manchester Research Unit, Institute of Cancer Sciences, Cancer Research UK Manchester Institute, University of Manchester, Paterson Building, Wilmslow Road, Manchester M20 4BX, UK.
Breast Cancer Now · GBCancer Research UK Manchester Institute · GBSidney Kimmel Cancer Center · USThomas Jefferson University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Awareness that the metabolic phenotype of cells within tumours is heterogeneous - and distinct from that of their normal counterparts - is growing. In general, tumour cells metabolize glucose, lactate, pyruvate, hydroxybutyrate, acetate, glutamine, and fatty acids at much higher rates than their nontumour equivalents; however, the metabolic ecology of tumours is complex because they contain multiple metabolic compartments, which are linked by the transfer of these catabolites. This metabolic variability and flexibility enables tumour cells to generate ATP as an energy source, while maintaining the reduction-oxidation (redox) balance and committing resources to biosynthesis - processes that are essential for cell survival, growth, and proliferation. Importantly, experimental evidence indicates that metabolic coupling between cell populations with different, complementary metabolic profiles can induce cancer progression. Thus, targeting the metabolic differences between tumour and normal cells holds promise as a novel anticancer strategy. In this Review, we discuss how cancer cells reprogramme their metabolism and that of other cells within the tumour microenvironment in order to survive and propagate, thus driving disease progression; in particular, we highlight potential metabolic vulnerabilities that might be targeted therapeutically.

Indexed as

Acetyl Coenzyme AAdaptation, PhysiologicalAmino AcidsAntineoplastic AgentsAntioxidantsAutophagyBlood GlucoseEnergy MetabolismEpigenomicsFatty AcidsGenetic HeterogeneityGlutamic AcidGlutamineHumansKetone BodiesLactic AcidAcetyl Coenzyme AAmino AcidsAntineoplastic AgentsAntioxidantsBlood GlucoseFatty AcidsGlutamic AcidGlutamineKetone BodiesLactic AcidLipidsMTOR protein, humanNucleic AcidsPyruvic AcidTOR Serine-Threonine KinasesTranscription Factors

Identifiers

PMID27141887
OpenAlexW2345381093

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.