Evidence map›Paper›PMID 27196377›Full record

ArticleCancer science2016

World Health Organization grade II-III astrocytomas consist of genetically distinct tumor lineages.

Natsuki Hattori, Yuichi Hirose, Hikaru Sasaki, Shunsuke Nakae, Saeko Hayashi, Shigeo Ohba, Kazuhide Adachi, Takuro Hayashi, Yuya Nishiyama, Mitsuhiro Hasegawa and 1 more

Open access · goldAbstract read
In one paragraph

Article in Cancer science, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed, 2 pooled it
2.8field-weighted citation impact, top 9% 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

10 citing papers in PubMed, 2 syntheses or guidelines pooled it, 25 citations in OpenAlex.

  1. Pooled it
  2. Molecular Biomarker Testing for the Diagnosis of Diffuse Gliomas.Archives of pathology & laboratory medicine · 2022
    Guideline
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Whole-exome sequencing identifies germline mutation inCold Spring Harbor molecular case studies · 2018
    Article
  9. Article
  10. 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

11 authors at 2 institutions in 1 country.

Natsuki HattoriDepartment of Neurosurgery, Fujita Health University, Toyoake, Japan.
Yuichi HiroseDepartment of Neurosurgery, Fujita Health University, Toyoake, Japan.
Hikaru SasakiDepartment of Neurosurgery, Keio University School of Medicine, Tokyo, Japan.
Shunsuke NakaeDepartment of Neurosurgery, Fujita Health University, Toyoake, Japan.
Saeko HayashiDepartment of Neurosurgery, Keio University School of Medicine, Tokyo, Japan.
Shigeo OhbaDepartment of Neurosurgery, Fujita Health University, Toyoake, Japan.
Kazuhide AdachiDepartment of Neurosurgery, Fujita Health University, Toyoake, Japan.
Takuro HayashiDepartment of Neurosurgery, Fujita Health University, Toyoake, Japan.
Yuya NishiyamaDepartment of Neurosurgery, Fujita Health University, Toyoake, Japan.
Mitsuhiro HasegawaDepartment of Neurosurgery, Fujita Health University, Toyoake, Japan.
Masato AbeFaculty of Medical Technology, Fujita Health University, Toyoake, Japan.
Fujita Health University · JPKeio University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Recent investigations revealed genetic analysis provides important information in management of gliomas, and we previously reported grade II-III gliomas could be classified into clinically relevant subgroups based on the DNA copy number aberrations (CNAs). To develop more precise genetic subgrouping, we investigated the correlation between CNAs and mutational status of the gene encoding isocitrate dehydrogenase (IDH) of those tumors. We analyzed the IDH status and CNAs of 174 adult supratentorial gliomas of astrocytic or oligodendroglial origin by PCR-based direct sequencing and comparative genomic hybridization, respectively. We analyzed the relationship between genetic subclassification and clinical features. We found the most frequent aberrations in IDH mutant tumors were the combined whole arm-loss of 1p and 19q (1p/19q codeletion) followed by gain on chromosome arm 7q (+7q). The gain of whole chromosome 7 (+7) and loss of 10q (-10q) were detected in IDH wild-type tumors. Kaplan-Meier estimates for progression-free survival showed that the tumors with mutant IDH, -1p/19q, or +7q (in the absence of +7p) survived longer than tumors with wild-type IDH, +7, or -10q. As tumors with +7 (IDH wild-type) showed a more aggressive clinical nature, they are probably not a subtype that developed from the slowly progressive tumors with +7q (IDH mutant). Thus, tumors with a gain on chromosome 7 (mostly astrocytic) comprise multiple lineages, and such differences in their biological nature should be taken into consideration during their clinical management.

Indexed as

Genes, NeoplasmWorld Health OrganizationAstrocytomaCell LineageComparative Genomic HybridizationDisease ProgressionGliomaHumansIsocitrate DehydrogenaseKaplan-Meier EstimateMaleMutationNeoplasm GradingIDH1 protein, humanIsocitrate DehydrogenaseAstrocytomaschromosome 7DNA copy numbergenetic subgroupingIDH

Identifiers

PMID27196377
PMCPMC4982592
OpenAlexW2483064167

What OpenQuestion holds

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LicenceCC BY-NC-ND
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Registered trials

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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.