Evidence map›Paper›PMID 35271755›Full record

ReviewCancer science2022

The metabolomic landscape plays a critical role in glioma oncogenesis.

Kenta Masui, Webster K Cavenee, Paul S Mischel, Noriyuki Shibata

Abstract readReview
In one paragraph

Review in Cancer science, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing 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

16 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Review
  8. Interplay between altered metabolism and DNA damage and repair in ovarian cancer.BioEssays : news and reviews in molecular, cellular and developmental biology · 2024
    Review
  9. Article
  10. Review
  11. Article
  12. Effects ofZhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2023
    Article
  13. Article
  14. Article
  15. Review
  16. Article
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.

Kenta MasuiDepartment of Pathology, Tokyo Women's Medical University, Shinjuku, Tokyo, Japan.ORCID https://orcid.org/0000-0002-5824-6690
Webster K CaveneeLudwig Institute for Cancer Research, University of California San Diego, La Jolla, California, USA.
Paul S MischelDepartment of Pathology, Stanford University School of Medicine, Stanford, California, USA.
Noriyuki ShibataDepartment of Pathology, Tokyo Women's Medical University, Shinjuku, Tokyo, Japan.

Funding

Software and algorithms for elucidating the structure, function, and evolution of extrachromosomal DNAU24CA264379 · NCI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI BAFNA, VINEET, MESIROV, JILL P. · 2021 to 2025
$3.5M
The role of mTORC2 in reprogramming cancer cell metabolismR01NS073831 · NINDS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI MISCHEL, PAUL S · 2011 to 2020
$3.4M
Integrated ligand and target discovery by chemical proteomics for glioblastoma treatment.R01CA238249 · NCI · STANFORD UNIVERSITY · PI CRAVATT, BENJAMIN F, MISCHEL, PAUL S · 2021 to 2025
$3.3M
Japan Society for the Promotion of Science JP19K07649NCI NIH HHS R01 CA238249NCI NIH HHS U24 CA264379NIH HHS RO1 CA238249NIH HHS U24 CA264379NINDS NIH HHS R01 NS073831
6 · The paper itself

Abstract

Cancer cells depend on metabolic reprogramming for survival, undergoing profound shifts in nutrient sensing, nutrient uptake and flux through anabolic pathways, in order to drive nucleotide, lipid, and protein synthesis and provide key intermediates needed for those pathways. Although metabolic enzymes themselves can be mutated, including to generate oncometabolites, this is a relatively rare event in cancer. Usually, gene amplification, overexpression, and/or downstream signal transduction upregulate rate-limiting metabolic enzymes and limit feedback loops, to drive persistent tumor growth. Recent molecular-genetic advances have revealed discrete links between oncogenotypes and the resultant metabolic phenotypes. However, more comprehensive approaches are needed to unravel the dynamic spatio-temporal regulatory map of enzymes and metabolites that enable cancer cells to adapt to their microenvironment to maximize tumor growth. Proteomic and metabolomic analyses are powerful tools for analyzing a repertoire of metabolic enzymes as well as intermediary metabolites, and in conjunction with other omics approaches could provide critical information in this regard. Here, we provide an overview of cancer metabolism, especially from an omics perspective and with a particular focus on the genomically well characterized malignant brain tumor, glioblastoma. We further discuss how metabolomics could be leveraged to improve the management of patients, by linking cancer cell genotype, epigenotype, and phenotype through metabolic reprogramming.

Indexed as

Brain NeoplasmsGliomaCarcinogenesisCell Transformation, NeoplasticHumansMetabolomicsProteomicsTumor MicroenvironmentepigeneticsglioblastomametabolomemTOR complexomics

Identifiers

PMID35271755
PMCPMC9128185

What OpenQuestion holds

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LicenceCC BY-NC
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.