ArticleBrain pathology (Zurich, Switzerland)2011
Alterations in the RB1 pathway in low-grade diffuse gliomas lacking common genetic alterations.
Article in Brain pathology (Zurich, Switzerland), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 35 citations in OpenAlex.
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- Impact of the methylation classifier and ancillary methods on CNS tumor diagnostics.Neuro-oncology · 2022Article
- A case series of extraneural metastatic glioblastoma at Memorial Sloan Kettering Cancer Center.Neuro-oncology practice · 2021Article
- Genetic and expression variations of cell cycle pathway genes in brain tumor patients.Bioscience reports · 2020Article
- Secondary INI1-deficient rhabdoid tumors of the central nervous system: analysis of four cases and literature review.Virchows Archiv : an international journal of pathology · 2020Review
- RADIO-IBAG: RADIOMICS-BASED INTEGRATIVE BAYESIAN ANALYSIS OF MULTIPLATFORM GENOMIC DATA.The annals of applied statistics · 2019Article
- Molecular Analysis of Pediatric Oligodendrogliomas Highlights Genetic Differences with Adult Counterparts and Other Pediatric Gliomas.Brain pathology (Zurich, Switzerland) · 2016Article
- Activation of the NRF2 pathway and its impact on the prognosis of anaplastic glioma patients.Neuro-oncology · 2015Article
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- Multidimensional analysis of gene expression reveals TGFB1I1-induced EMT contributes to malignant progression of astrocytomas.Oncotarget · 2014Article
- Oncolytic adenoviruses: A thorny path to glioma cure.Genes & diseases · 2014Article
- Outcomes of pediatric low-grade gliomas treated with radiation therapy: a single-institution study.Journal of pediatric hematology/oncology · 2014Article
- Intratumoral heterogeneity of genomic imbalance in a case of epithelioid glioblastoma with BRAF V600E mutation.Brain pathology (Zurich, Switzerland) · 2014Article
- Common chromosome fragile sites in human and murine epithelial cells and FHIT/FRA3B loss-induced global genome instability.Genes, chromosomes & cancer · 2013Article
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- Recent innovations in the management of low-grade gliomas.Current treatment options in neurology · 2012Article
- Frequent ATRX, CIC, FUBP1 and IDH1 mutations refine the classification of malignant gliomas.Oncotarget · 2012Article
- Clinical stratification of glioblastoma based on alterations in retinoblastoma tumor suppressor protein (RB1) and association with the proneural subtype.Journal of neuropathology and experimental neurology · 2012Article
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Authors and funding
14 authors at 6 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We recently reported that the vast majority (>90%) of low-grade diffuse gliomas (diffuse astrocytoma, oligoastrocytoma and oligodendroglioma) carry at least one of the following genetic alterations: IDH1/2 mutation, TP53 mutation or 1p/19q loss. Only 7% of cases were triple-negative (ie, lacking any of these alterations). In the present study, array comparative genomic hybridization (CGH) in 15 triple-negative WHO grade II gliomas (eight diffuse astrocytomas and seven oligodendrogliomas) showed loss at 9p21 (p14(ARF) , p15(INK4b) , p16(INK4a) loci) and 13q14-13q32 (containing the RB1 locus) in three and two cases, respectively. Further analyses in 31 triple-negative cases as well as a total of 160 non-triple-negative cases revealed that alterations in the RB1 pathway (homozygous deletion and promoter methylation of the p15(INK4b) , p16(INK4a) and RB1 genes) were significantly more frequent in triple-negative (26%) than in non-triple-negative cases (11%; P = 0.0371). Multivariate analysis after adjustment for age, histology and treatment showed that RB1 pathway alterations were significantly associated with unfavorable outcome for patients with low-grade diffuse glioma [hazard ratio, 3.024 (1.279-6.631); P = 0.0057]. These results suggest that a fraction of low-grade diffuse gliomas lacking common genetic alterations may develop through a distinct genetic pathway, which may include loss of cell-cycle control regulated by the RB1 pathway.
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