ArticleGenome biology2014
Spatial and temporal evolution of distal 10q deletion, a prognostically unfavorable event in diffuse low-grade gliomas.
Article in Genome biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.
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Who cites it
20 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Reconstructing the molecular life history of gliomas.Acta neuropathologica · 2018Pooled it
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- Integrated systems-genetic analyses reveal a network target for delaying glioma progression.Annals of clinical and translational neurology · 2019Article
- GATAD1 gene amplification promotes glioma malignancy by directly regulating CCND1 transcription.Cancer medicine · 2019Article
- IDH mutation and 1p19q codeletion distinguish two radiological patterns of diffuse low-grade gliomas.Journal of neuro-oncology · 2017Article
- Tumour heterogeneity: principles and practical consequences.Virchows Archiv : an international journal of pathology · 2016Review
- Condensin II mutation causes T-cell lymphoma through tissue-specific genome instability.Genes & development · 2016Article
- MGMT-Methylated Alleles Are Distributed Heterogeneously Within Glioma Samples Irrespective of IDH Status and Chromosome 10q Deletion.Journal of neuropathology and experimental neurology · 2016Article
- Integrated genomic characterization of IDH1-mutant glioma malignant progression.Nature genetics · 2016Article
- miR-146b-5p functions as a tumor suppressor by targeting TRAF6 and predicts the prognosis of human gliomas.Oncotarget · 2015Article
- Article
- Molecular Markers in Low-Grade Glioma-Toward Tumor Reclassification.Seminars in radiation oncology · 2015Review
- Oligodendroglioma: pathology, molecular mechanisms and markers.Acta neuropathologica · 2015Review
- IDH mutation status and role of WHO grade and mitotic index in overall survival in grade II-III diffuse gliomas.Acta neuropathologica · 2015Article
- Evolution of DNA repair defects during malignant progression of low-grade gliomas after temozolomide treatment.Acta neuropathologica · 2015Article
- Article
- DNA copy number analysis of fresh and formalin-fixed specimens by shallow whole-genome sequencing with identification and exclusion of problematic regions in the genome assembly.Genome research · 2014Article
- Tumor mutational burden predicts survival in patients with low-grade gliomas expressing mutated IDH1.Neuro-oncology advancesArticle
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23 authors.
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Abstract
backgroundThe disease course of patients with diffuse low-grade glioma is notoriously unpredictable. Temporal and spatially distinct samples may provide insight into the evolution of clinically relevant copy number aberrations (CNAs). The purpose of this study is to identify CNAs that are indicative of aggressive tumor behavior and can thereby complement the prognostically favorable 1p/19q co-deletion.
resultsGenome-wide, 50 base pair single-end sequencing was performed to detect CNAs in a clinically well-characterized cohort of 98 formalin-fixed paraffin-embedded low-grade gliomas. CNAs are correlated with overall survival as an endpoint. Seventy-five additional samples from spatially distinct regions and paired recurrent tumors of the discovery cohort were analyzed to interrogate the intratumoral heterogeneity and spatial evolution. Loss of 10q25.2-qter is a frequent subclonal event and significantly correlates with an unfavorable prognosis. A significant correlation is furthermore observed in a validation set of 126 and confirmation set of 184 patients. Loss of 10q25.2-qter arises in a longitudinal manner in paired recurrent tumor specimens, whereas the prognostically favorable 1p/19q co-deletion is the only CNA that is stable across spatial regions and recurrent tumors.
conclusionsCNAs in low-grade gliomas display extensive intratumoral heterogeneity. Distal loss of 10q is a late onset event and a marker for reduced overall survival in low-grade glioma patients. Intratumoral heterogeneity and higher frequencies of distal 10q loss in recurrences suggest this event is involved in outgrowth to the recurrent tumor.
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