Evidence map›Paper›PMID 30194083›Full record

ReviewCancer genomics & proteomics

Bridging Cancer Biology with the Clinic: Comprehending and Exploiting IDH Gene Mutations in Gliomas.

Ourania Romanidou, Vassiliki Kotoula, George Fountzilas

Open access · diamondAbstract readReview
In one paragraph

Review in Cancer genomics & proteomics. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
0.7field-weighted citation impact, top 27% 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

13 citing papers in PubMed, 14 citations in OpenAlex.

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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 1 institution in 1 country.

Ourania RomanidouDepartment of Medical Oncology, Papageorgiou Hospital, Aristotle University of Thessaloniki, School of Health Sciences, Faculty of Medicine, Thessaloniki, Greece.
Vassiliki KotoulaDepartment of Pathology, Aristotle University of Thessaloniki, School of Health Sciences, Faculty of Medicine, Thessaloniki, Greece.
George FountzilasLaboratory of Molecular Oncology, Hellenic Foundation for Cancer Research/Aristotle University of Thessaloniki, Thessaloniki, Greece fountzil@auth.gr.
Aristotle University of Thessaloniki · GR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Isocitrate dehydrogenases 1 and 2 (IDH1/2) are enzymes that play a major role in the Krebs cycle. Mutations in these enzymes are found in the majority of lower gliomas and secondary glioblastomas, but also in myeloid malignancies and other cancers. IDH1 and IDH2 mutations are restricted to specific arginine residues in the active site of the enzymes and are gain-of-function, i.e. they confer a neomorphic enzyme activity resulting in the accumulation of D-2-hydroxyglutarate (2-HG). 2-HG is an oncometabolite causing profound metabolic dysregulation which, among others, results in methylator phenotypes and in defects in homologous recombination repair. In this review, we summarize current knowledge regarding the function of normal and mutated IDH, explain the possible mechanisms through which these mutations might drive malignant transformation of progenitor cells in the central nervous system, and provide a comprehensive review of potential treatment strategies for IDH-mutated malignancies, focusing on gliomas.

Indexed as

ArginineCatalytic DomainCell Transformation, NeoplasticGliomaHumansIsocitrate DehydrogenaseMutationArginineIDH1 protein, humanIDH2 protein, humanIsocitrate DehydrogenaseBCL2-inhibitorGliomasIDH1IDH2IDH-inhibitorIsocitrate dehydrogenases 1 and 2myeloid leukemiareviewsynthetic lethality

Identifiers

PMID30194083
PMCPMC6199574
OpenAlexW2890163667

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.