Evidence map›Paper›PMID 30914826›Full record

ReviewNature reviews. Clinical oncology2019

Navigating metabolic pathways to enhance antitumour immunity and immunotherapy.

Xiaoyun Li, Mathias Wenes, Pedro Romero, Stanley Ching-Cheng Huang, Sarah-Maria Fendt, Ping-Chih Ho

Open access · greenAbstract readReview
PubMed Publisher
In one paragraph

Review in Nature reviews. Clinical oncology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 428 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
428citing papers in PubMed, 2 pooled it
39.9field-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

428 citing papers in PubMed, 2 syntheses or guidelines pooled it, 764 citations in OpenAlex.

  1. Multilevel Mechanisms of Cancer Drug Resistance.International journal of molecular sciences · 2024
    Pooled it
  2. Pooled it
  3. Effect ofCancer science · 2023
    Trial
  4. Trial
  5. Review
  6. Review
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Review
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. Article

368 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

6 authors at 3 institutions in 3 countries.

Xiaoyun LiDepartment of Fundamental Oncology, University of Lausanne, Lausanne, Vaud, Switzerland.
Mathias WenesDepartment of Fundamental Oncology, University of Lausanne, Lausanne, Vaud, Switzerland.
Pedro RomeroDepartment of Fundamental Oncology, University of Lausanne, Lausanne, Vaud, Switzerland.
Stanley Ching-Cheng HuangDepartment of Pathology, Case Western Reserve University School of Medicine, Cleveland, OH, USA.ORCID http://orcid.org/0000-0002-6557-3737
Sarah-Maria FendtLaboratory of Cellular Metabolism and Metabolic Regulation, Vlaams Instituut voor Biotechnologie (VIB)-Katholieke Universiteit (KU) Leuven Center for Cancer Biology, VIB, Leuven, Belgium.
Ping-Chih HoDepartment of Fundamental Oncology, University of Lausanne, Lausanne, Vaud, Switzerland. ping-chih.ho@unil.ch.ORCID http://orcid.org/0000-0003-3078-3774
Ludwig Cancer Research · CHRega Institute for Medical Research · BEUniversity School · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The development of immunotherapies over the past decade has resulted in a paradigm shift in the treatment of cancer. However, the majority of patients do not benefit from immunotherapy, presumably owing to insufficient reprogramming of the immunosuppressive tumour microenvironment (TME) and thus limited reinvigoration of antitumour immunity. Various metabolic machineries and nutrient-sensing mechanisms orchestrate the behaviour of immune cells in response to nutrient availability in the TME. Notably, tumour-infiltrating immune cells typically experience metabolic stress as a result of the dysregulated metabolic activity of tumour cells, leading to impaired antitumour immune responses. Moreover, the immune checkpoints that are often exploited by tumour cells to evade immunosurveillance have emerging roles in modulating the metabolic and functional activity of T cells. Thus, repurposing of drugs targeting cancer metabolism might synergistically enhance immunotherapy via metabolic reprogramming of the TME. In addition, interventions targeting the metabolic circuits that impede antitumour immunity have been developed, with several clinical trials underway. Herein, we discuss how these metabolic circuits regulate antitumour immunity and the possible approaches to targeting these pathways in the context of anticancer immunotherapy. We also describe hypothetical combination treatments that could be used to better unleash the potential of adoptive cell therapies by enhancing T cell metabolism.

Indexed as

Antineoplastic AgentsCombined Modality TherapyDrug RepositioningDrug SynergismHumansImmunotherapyMetabolic Networks and PathwaysNeoplasmsTumor MicroenvironmentAntineoplastic Agents

Identifiers

PMID30914826
OpenAlexW2924849767

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.