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Genomic copy number variation correlates with survival outcomes in glioblastoma patients

ABSTRACT: Genomic copy number variation correlates with survival outcomes in glioblastoma patients

PROVIDER: PRJNA515731 | ENA |

REPOSITORIES: ENA

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Genomic copy number variation correlates with survival outcomes in glioblastoma patients

Project description:Allele-specific copy number analysis of tumors (ASCAT) assesses copy number variations (CNV) while accounting for aberrant cell fraction (ACF) and tumor ploidy. Here, we evaluate if ASCAT-assessed CNV are associated with survival outcomes in patients with WHO grade IV gliomas. Methods: We identified 56 patients with WHO grade IV gliomas. Tumor data analyzed by Affymetrix OncoScan FFPE Assay yielded the log ratio (R) and B-allele frequency (BAF). Input into ASCAT quantified CNV using the segmentation function to measure copy number inflection points throughout the genome. Actuarial overall survival (OS) and progression-free survival (PFS) assessed with Kaplan-Meier method and subgroups compared by the log-rank test. Results were validated on The Cancer Genome Atlas (TCGA) glioblastoma dataset. Results: Our cohort’s median age was 60.4 years (range: 26.1-86.3). Tumors were hyper-methylated at MGMT in 25 (44.6%) with IDH1 mutations in 6 (10.7%). Median follow-up time was 36.4 months, and median PFS and OS were 8 and 14.7 months, respectively. PFS was longer for higher log R and BAF segment counts with hazard ratios (HR) of 0.32 and 0.49 respectively (p<0.001 and p=0.022). Patients with higher log R segment counts had significantly longer 12-month OS (81% vs 46.3%, p=0.0088). In the TCGA validation cohort, higher BAF segment counts had longer 12-month OS with a trend for log R (62.3% vs. 51.9%, p=0.0129 and 63.6% vs. 55.2%, p=0.0696 respectively). Conclusions: Our analysis demonstrated a longer PFS and OS for patients with increased genomic CNV. This may provide a novel method for assessing glioblastoma outcomes.

2019-01-18 | GSE125255 | GEO

Genomic copy number variation correlates with survival outcomes in WHO grade IV glioma.

Project description: Not available

| S-EPMC7192941 | biostudies-literature

Copy number analysis of human glioblastoma multiforme

2009-01-05 | GSE13021 | GEO

Copy number analysis of human glioblastoma multiforme

Project description:Copy number analysis of human GBM samples were performed, and a high frequency of deletions of the PTPRD gene on chromosome 9p23-24.1 were identified. Keywords: SNP microarray, glioblastoma multiforme, copy number, amplification, deletion Genomic DNA from 58 GBM tumor samples were hybridized to Affymetrix 250K NspI Gene Chip Arrays and analyzed by dChip using the hg17 genome assembly.

2009-01-04 | E-GEOD-13021 | biostudies-arrayexpress

Genomic copy number number characterisation of glioblastoma (GBM) cell lines.

Project description:Genomic copy number number characterisation of glioblastoma (GBM) cell lines.

| PRJNA489666 | ENA

Adverse prognosis of glioblastoma contacting the subventricular zone: biological correlates

Project description:Adverse prognosis of glioblastoma contacting the subventricular zone: biological correlates

| PRJNA556417 | ENA

Identification of immune correlates of fatal outcomes in critically ill COVID-19 patients

Project description:Identification of immune correlates of fatal outcomes in critically ill COVID-19 patients

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Copy Number Variation Detection Using Total Variation.

Project description: Not available

| S-EPMC7278034 | biostudies-literature

Copy Number Variation and Clinical Outcomes in Patients With Germline PTEN Mutations.

Project description: Not available

| S-EPMC7042875 | biostudies-literature

Copy number variation comparison between control and CC214-2 resistant GBM39 xenografts

Project description:Here we present genome-wide copy number variation data on two vehicle treated and two CC214-2 (an mTOR kinase inhibitor) resistant GlioBlastoma Multiforme 39 (GBM39) xenografts, showing the absence of significant differences between the two groups, demonstrating that resistance to CC214-2 is due to adaptation rather than gene mutations.

2013-12-06 | GSE53042 | GEO

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