Upregulating mutations in the TERT promoter commonly occur in adult malignant gliomas and are strongly associated with total 1p19q loss
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Title
Upregulating mutations in the TERT promoter commonly occur in adult malignant gliomas and are strongly associated with total 1p19q loss
Authors
Keywords
Glioblastoma, Oligodendroglioma, TERT, Telomerase, Total 1p19q loss, IDH1
Journal
ACTA NEUROPATHOLOGICA
Volume 126, Issue 2, Pages 267-276
Publisher
Springer Nature
Online
2013-06-13
DOI
10.1007/s00401-013-1141-6
References
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Note: Only part of the references are listed.- Frequent ATRX, CIC, FUBP1 and IDH1 mutations refine the classification of malignant gliomas
- (2015) Yuchen Jiao et al. Oncotarget
- Whole-exome sequencing identifies ATRX mutation as a key molecular determinant in lower-grade glioma
- (2015) Kasthuri Kannan et al. Oncotarget
- Prognostic significance of telomerase-associated parameters in glioblastoma: effect of patient age
- (2013) Daniela Lötsch et al. NEURO-ONCOLOGY
- TERT promoter mutations occur frequently in gliomas and a subset of tumors derived from cells with low rates of self-renewal
- (2013) P. J. Killela et al. PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
- TERT Promoter Mutations in Familial and Sporadic Melanoma
- (2013) S. Horn et al. SCIENCE
- Highly Recurrent TERT Promoter Mutations in Human Melanoma
- (2013) F. W. Huang et al. SCIENCE
- Alternative lengthening of telomeres: remodeling the telomere architecture
- (2013) Dimitri Conomos et al. Frontiers in Oncology
- CIC and FUBP1 mutations in oligodendrogliomas, oligoastrocytomas and astrocytomas
- (2012) Felix Sahm et al. ACTA NEUROPATHOLOGICA
- Frequent ATRX mutations and loss of expression in adult diffuse astrocytic tumors carrying IDH1/IDH2 and TP53 mutations
- (2012) Xiao-Yang Liu et al. ACTA NEUROPATHOLOGICA
- Molecular and Morphologic Correlates of the Alternative Lengthening of Telomeres Phenotype in High-Grade Astrocytomas
- (2012) Doreen N. Nguyen et al. BRAIN PATHOLOGY
- Molecular pathogenesis of IDH mutations in gliomas
- (2012) Koichi Ichimura Brain Tumor Pathology
- Novel anticancer therapeutics targeting telomerase
- (2012) Maria Ruden et al. CANCER TREATMENT REVIEWS
- Driver mutations in histone H3.3 and chromatin remodelling genes in paediatric glioblastoma
- (2012) Jeremy Schwartzentruber et al. NATURE
- Prevalence of the Alternative Lengthening of Telomeres Telomere Maintenance Mechanism in Human Cancer Subtypes
- (2011) Christopher M. Heaphy et al. AMERICAN JOURNAL OF PATHOLOGY
- MGMT CpG island is invariably methylated in adult astrocytic and oligodendroglial tumors with IDH1 or IDH2 mutations
- (2011) Shani Mulholland et al. INTERNATIONAL JOURNAL OF CANCER
- Concurrent CIC mutations, IDH mutations, and 1p/19q loss distinguish oligodendrogliomas from other cancers
- (2011) Stephen Yip et al. JOURNAL OF PATHOLOGY
- Mutations in CIC and FUBP1 Contribute to Human Oligodendroglioma
- (2011) C. Bettegowda et al. SCIENCE
- An RNA-dependent RNA polymerase formed by TERT and the RMRP RNA
- (2009) Yoshiko Maida et al. NATURE
- IDH1 mutations are present in the majority of common adult gliomas but rare in primary glioblastomas
- (2009) Koichi Ichimura et al. NEURO-ONCOLOGY
- Comprehensive genomic characterization defines human glioblastoma genes and core pathways
- (2008) Roger McLendon et al. NATURE
- Real-time quantitative polymerase chain reaction (qPCR) analysis with fluorescence resonance energy transfer (FRET) probes reveals differential expression of the fourERBB4juxtamembrane region variants between medulloblastoma and pilocytic astrocytoma
- (2008) N. Zeng et al. NEUROPATHOLOGY AND APPLIED NEUROBIOLOGY
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