ArticlePloS one2012
Amplified and homozygously deleted genes in glioblastoma: impact on gene expression levels.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 44 citations in OpenAlex.
- Unravelling the link between circadian clock genes and brain tumors: From pathological disruptions to potential therapeutic interventions.Frontiers in pharmacology · 2025Review
- Chromosome 7 Gain Compensates for Chromosome 10 Loss in Glioma.Cancer research · 2024Article
- Variances in the Expression Profile of Circadian Clock-Related Genes in Astrocytic Brain Tumors.Cancers · 2024Article
- ELAVL2 loss promotes aggressive mesenchymal transition in glioblastoma.NPJ precision oncology · 2024Article
- Intramedullary Spinal Cord Tumors: Whole-Genome Sequencing to Assist Management and Prognosis.Cancers · 2024Article
- Discovery of Potent and Oral Bioavailable MAT2A Inhibitors for the Treatment of MTAP-Deleted Tumors.ACS medicinal chemistry letters · 2023Article
- Adjusting the Molecular Clock: The Importance of Circadian Rhythms in the Development of Glioblastomas and Its Intervention as a Therapeutic Strategy.International journal of molecular sciences · 2021Review
- Hypoxia, metabolism, and the circadian clock: new links to overcome radiation resistance in high-grade gliomas.Journal of experimental & clinical cancer research : CR · 2020Review
- Article
- HeterogeneousCancers · 2020Article
- Insights About Circadian Clock and Molecular Pathogenesis in Gliomas.Frontiers in oncology · 2020Review
- Ranking genomic features using an information-theoretic measure of epigenetic discordance.BMC bioinformatics · 2019Article
- Comparable Genomic Copy Number Aberrations Differ across Astrocytoma Malignancy Grades.International journal of molecular sciences · 2019Article
- Identification of Dysregulated Competitive Endogenous RNA Networks Driven by Copy Number Variations in Malignant Gliomas.Frontiers in genetics · 2019Article
- Specific Targeting ofCancer research · 2018Article
- Genetic and Epigenetic Features of Rapidly Progressing IDH-Mutant Astrocytomas.Journal of neuropathology and experimental neurology · 2018Article
- Prognostic stratification of adult primary glioblastoma multiforme patients based on their tumor gene amplification profiles.Oncotarget · 2018Article
- Hi-C as a tool for precise detection and characterisation of chromosomal rearrangements and copy number variation in human tumours.Genome biology · 2017Article
- Elucidation of the genetic and epigenetic landscape alterations in RNA binding proteins in glioblastoma.Oncotarget · 2017Article
- Deletion and downregulation of MTAP contribute to the motility of esophageal squamous carcinoma cells.OncoTargets and therapy · 2017Article
Corrections and comments
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Authors and funding
12 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundGlioblastoma multiforme (GBM) displays multiple amplicons and homozygous deletions that involve relevant pathogenic genes and other genes whose role remains unknown. METHODOLOGY: Single-nucleotide polymorphism (SNP)-arrays were used to determine the frequency of recurrent amplicons and homozygous deletions in GBM (n = 46), and to evaluate the impact of copy number alterations (CNA) on mRNA levels of the genes involved. PRINCIPAL
findingsRecurrent amplicons were detected for chromosomes 7 (50%), 12 (22%), 1 (11%), 4 (9%), 11 (4%), and 17 (4%), whereas homozygous deletions involved chromosomes 9p21 (52%) and 10q (22%). Most genes that displayed a high correlation between DNA CNA and mRNA levels were coded in the amplified chromosomes. For some amplicons the impact of DNA CNA on mRNA expression was restricted to a single gene (e.g., EGFR at 7p11.2), while for others it involved multiple genes (e.g., 11 and 5 genes at 12q14.1-q15 and 4q12, respectively). Despite homozygous del(9p21) and del(10q23.31) included multiple genes, association between these DNA CNA and RNA expression was restricted to the MTAP gene.
conclusionsOverall, our results showed a high frequency of amplicons and homozygous deletions in GBM with variable impact on the expression of the genes involved, and they contributed to the identification of other potentially relevant genes.
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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.