Evidence map›Paper›PMID 31833906›Full record

ArticleChinese medical journal2019

Clinico-neuropathological features of isocitrate dehydrogenase 2 gene mutations in lower-grade gliomas.

Lei-Ming Wang, Zhuo Li, Yue-Shan Piao, Yan-Ning Cai, Li-Yan Zhang, Hai-Jing Ge, Wei-Wei Xu, De-Hong Lu

Abstract read
In one paragraph

Article in Chinese medical journal, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed, 1 pooled it
–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

6 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Review
  3. Isocitrate Dehydrogenase Mutant Grade II and III Glial Neoplasms.Hematology/oncology clinics of North America · 2022
    Review
  4. Article
  5. Article
  6. 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

8 authors.

Lei-Ming WangDepartment of Pathology, Xuanwu Hospital, Capital Medical University, Key Laboratory for Neurodegenerative Diseases, Ministry of Education, Beijing 100053, China.
Zhuo LiDepartment of Pathology, Xuanwu Hospital, Capital Medical University, Key Laboratory for Neurodegenerative Diseases, Ministry of Education, Beijing 100053, China.
Yue-Shan PiaoDepartment of Pathology, Xuanwu Hospital, Capital Medical University, Key Laboratory for Neurodegenerative Diseases, Ministry of Education, Beijing 100053, China.
Yan-Ning CaiDepartment of Neurobiology, Xuanwu Hospital, Capital Medical University, Key Laboratory for Neurodegenerative Diseases, Ministry of Education, Beijing 100053, China.
Li-Yan ZhangDepartment of Pathology, Xuanwu Hospital, Capital Medical University, Key Laboratory for Neurodegenerative Diseases, Ministry of Education, Beijing 100053, China.
Hai-Jing GeDepartment of Pathology, Xuanwu Hospital, Capital Medical University, Key Laboratory for Neurodegenerative Diseases, Ministry of Education, Beijing 100053, China.
Wei-Wei XuDepartment of Pathology, Xuanwu Hospital, Capital Medical University, Key Laboratory for Neurodegenerative Diseases, Ministry of Education, Beijing 100053, China.
De-Hong LuDepartment of Pathology, Xuanwu Hospital, Capital Medical University, Key Laboratory for Neurodegenerative Diseases, Ministry of Education, Beijing 100053, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundMutations in the isocitrate dehydrogenase 1 (IDH1) and IDH2 genes are important for both the integrated diagnosis and the prognosis of diffuse gliomas. The p.R132H mutation of IDH1 is the most frequently observed IDH mutation, while IDH2 mutations were relatively rarely studied. The aim of the study was to determine the pathological and genetic characteristics of lower-grade gliomas that carry IDH2 mutations.

methodsData from 238 adult patients with lower-grade gliomas were retrospectively analyzed. The status of IDH1/2 gene mutations, telomerase reverse transcriptase (TERT) promoter mutations, O-methylguanine-DNA-methyltransferase (MGMT) promoter methylation, 1p/19q co-deletion and the expressions of IDH1 R132H, alpha-thalassemia X-linked mental retardation, and p53 were evaluated. Progression-free survival (PFS) and overall survival (OS) were calculated via Kaplan-Meier estimation using the log-rank test.

resultsTotally, 71% (169/238) of patients were positive for IDH mutations, including 12 patients harboring mutations in IDH2. Among the 12 patients with IDH2 mutations, ten patients harbored the R172K mutation, one patient harbored the R172S mutation and one harbored the R172W mutation. Of these, 11 tumors occurred in the frontal lobe and showed morphology typical of oligodendroglioma. The proportion of grade II tumors was higher than that of grade III tumors in IDH2 mutant-gliomas. IDH2 mutations were frequently associated with TERT promoter mutations, 1p/19q co-deletion and MGMT promoter methylation. IDH2 mutations were associated with better outcomes compared with IDH wild-type gliomas (P < 0.05). However, the PFS and OS did not differ from that of IDH1 mutant patients (P = 0.95 and P = 0.60, respectively).

conclusionsIDH2 mutations are more frequent in oligodendrogliomas and associated with a better prognosis. IDH2 mutations may segregate in distinct clinico-pathological and genetic subtypes of gliomas, and therefore may merit routine investigation.

Indexed as

MutationBrain NeoplasmsGliomaHumansIsocitrate DehydrogenaseRetrospective StudiesIDH2 protein, humanIsocitrate Dehydrogenase

Identifiers

PMID31833906
PMCPMC6964951

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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.