Evidence map›Paper›PMID 27295313›Full record

ReviewBrain tumor pathology2016

Cancer metabolism as a central driving force of glioma pathogenesis.

Kenta Masui, Webster K Cavenee, Paul S Mischel

Open access · greenAbstract readReview
In one paragraph

Review in Brain tumor pathology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
4.4field-weighted citation impact, top 5% 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

26 citing papers in PubMed, 42 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Review
  8. Article
  9. Frontiers in oncology · 2022
    Review
  10. Article
  11. Review
  12. The Sociobiology of Brain Tumors.Advances in experimental medicine and biology · 2020
    Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. mTOR Complexes as a Nutrient Sensor for Driving Cancer Progression.International journal of molecular sciences · 2018
    Review
  18. Article
  19. Review
  20. 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

3 authors at 2 institutions in 2 countries.

Kenta MasuiDepartment of Pathology, Tokyo Women's Medical University, Tokyo, 162-8666, Japan. masui-kn@research.twmu.ac.jp.
Webster K CaveneeLudwig Institute for Cancer Research, University of California San Diego, La Jolla, CA, 92093, USA.
Paul S MischelLudwig Institute for Cancer Research, University of California San Diego, La Jolla, CA, 92093, USA. pmischel@ucsd.edu.
Ludwig Cancer Research · USTokyo Women's Medical University · JP

Funding

QUANTITATIVE IMAGE ANALYSIS SPECIALIZED RESOURCE COREU54CA119347 · NCI · CALIFORNIA INSTITUTE OF TECHNOLOGY · PI ROUKES, MICHAEL L · 2005 to 2009
$17.8M
The role of mTORC2 in reprogramming cancer cell metabolismR01NS073831 · NINDS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI MISCHEL, PAUL S · 2011 to 2020
$3.4M
NCI NIH HHS U54 CA119347NINDS NIH HHS R01 NS073831
6 · The paper itself

Abstract

The recent identification of distinct genetic and epigenetic features in each glioma entity is leading to a multilayered, integrated diagnostic approach combining histologic features with molecular genetic information. Somatic mutations in isocitrate dehydrogenase (IDH) and receptor tyrosine kinase (RTK) pathways are key oncogenic events in diffuse gliomas, including lower grade (grade II and III) gliomas (LGG) and the highly lethal brain tumor glioblastoma (GBM), respectively, where they reprogram the epigenome, transcriptome, and metabolome to drive tumor growth. However, the mechanisms by which these genetic aberrations are translated into the aggressive nature of gliomas through metabolic reprogramming have just begun to be unraveled. The intricate interactions between the oncogenic signaling and cancer metabolism have also been recently demonstrated. Here, we describe a set of recent discoveries on cancer metabolism driven by IDH mutation and mutations in RTK pathways, highlighting the integration of genetic mutations, metabolic reprogramming, and epigenetic shifts, potentially providing new therapeutic opportunities.

Indexed as

Epigenesis, GeneticBrain NeoplasmsGliomaHumansIsocitrate DehydrogenaseMolecular Targeted TherapyMutationReceptor Protein-Tyrosine KinasesSignal TransductionIsocitrate DehydrogenaseReceptor Protein-Tyrosine KinasesGenetic-metabolism interactionGliomaIDHMetabolic reprogrammingMolecular geneticsRTK

Identifiers

PMID27295313
PMCPMC5488809
OpenAlexW2427654690

What OpenQuestion holds

Textmetadata
LicenceTDM
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.