ArticlePloS one2011
Absence of common somatic alterations in genes on 1p and 19q in oligodendrogliomas.
Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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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.
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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.
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Who cites it
6 citing papers in PubMed, 14 citations in OpenAlex.
- Double inhibition and activation mechanisms of Ephexin family RhoGEFs.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Three-Dimensional Nuclear Telomere Profiling as a Biomarker for Recurrence in Oligodendrogliomas: A Pilot Study.International journal of molecular sciences · 2020Article
- Review
- Serum microRNAs as potential noninvasive biomarkers for glioma.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016Review
- Mutations in CIC and IDH1 cooperatively regulate 2-hydroxyglutarate levels and cell clonogenicity.Oncotarget · 2014Article
- Concurrent CIC mutations, IDH mutations, and 1p/19q loss distinguish oligodendrogliomas from other cancers.The Journal of pathology · 2012Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A common and histologically well defined subtype of glioma are the oligodendroglial brain tumors. Approximately 70% of all oligodendrogliomas have a combined loss of the entire 1p and 19q chromosomal arms. This remarkably high frequency suggests that the remaining arms harbor yet to be identified tumor suppressor genes. Identification of these causal genetic changes in oligodendrogliomas is important because they form direct targets for treatment. In this study we therefore performed targeted resequencing of all exons, microRNAs, splice sites and promoter regions residing on 1p and 19q on 7 oligodendrogliomas and 4 matched controls. Only one missense mutation was identified in a single sample in the ARHGEF16 gene. This mutation lies within- and disrupts the conserved PDZ binding domain. No similar ARHGEF16 mutations or deletions were found in a larger set of oligodendrogliomas. The absence of common somatic changes within genes located on 1p and 19q in three out of four samples indicates that no additional "second hit" is required to drive oncogenic transformation on either chromosomal arm.
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Registered trials
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