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  • 1
    Keywords: brain ; SURVIVAL ; evaluation ; Germany ; DIAGNOSIS ; NETWORK ; DISEASE ; DISEASES ; LONG-TERM ; RISK ; RISKS ; PATIENT ; primary ; RISK-FACTORS ; tumour ; GROWTH-FACTOR RECEPTOR ; ASSOCIATION ; FORM ; DELETION ; PERFORMANCE ; AMPLIFICATION ; RADIATION-THERAPY ; PROMOTER ; AGE ; MUTATION ; risk factors ; DELETIONS ; LONG-TERM SURVIVAL ; MUTATIONS ; PARAMETERS ; SERIES ; LONG-TERM SURVIVORS ; HYPERMETHYLATION ; TP53 ; 1p ; YOUNG ; molecular ; review ; BRAIN-TUMORS ; GLIOMA ; MALIGNANT GLIOMA ; EGFR ; MGMT ; analysis ; HIGH-GRADE GLIOMA ; ELECTRIC UTILITY WORKERS ; RISK-FACTOR ; ENGLAND ; GLIOBLASTOMA ; OCCUPATIONAL RISK ; comparison ; German ; TP53 MUTATIONS ; CHROMOSOME 1P LOSS ; GIANT-CELL GLIOBLASTOMA ; PHASE-III TRIAL ; SUPRATENTORIAL GLIOBLASTOMA
    Abstract: The median survival of glioblastoma patients is similar to 12 months. However, 3-5% of the patients survives for more than 3 years and are referred to as long-term survivors. The clinical and molecular factors that contribute to long-term survival are still unknown. To identify specific parameters that might be associated with this phenomenon, we performed a detailed clinical and molecular analysis of 55 primary glioblastoma long-term survivors recruited at the six clinical centres of the German Glioma Network and one associated centre. An evaluation form was developed and used to document demographic, clinical and treatment-associated parameters. In addition, environmental risk factors, associated diseases and occupational risks were assessed. These patients were characterized by young age at diagnosis and a good initial Karnofsky performance score (KPS). None of the evaluated socioeconomic, environmental and occupational factors were associated with long-term survival. Molecular analyses revealed MGMT hypermethylation in 28 of 36 tumours (74%) investigated. TP53 mutations were found in 9 of 31 tumours (29%) and EGFR amplification in 10 of 38 tumours (26%). Only 2 of 32 tumours (6%) carried combined 1p and 19q deletions. Comparison of these data with results from an independent series of 141 consecutive unselected glioblastoma patients registered in the German Glioma Network revealed significantly more frequent MGMT hypermethylation in the long-term survivor group. Taken together, our findings underline the association of glioblastoma long-term survival with prognostically favourable clinical factors, in particular young age and good initial performance score, as well as MGMT promoter hypermethylation
    Type of Publication: Journal article published
    PubMed ID: 17785346
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  • 2
    Keywords: CANCER ; radiotherapy ; SURVIVAL ; tumor ; Germany ; neoplasms ; THERAPY ; FOLLOW-UP ; DISEASE ; GENE ; TISSUE ; TUMORS ; PATIENT ; chromosome ; PROGRESSION ; AMPLIFICATION ; DESIGN ; resistance ; STRESS ; chemotherapy ; RESECTION ; PRODUCT ; MULTIVARIATE ; PROGNOSTIC VALUE ; sensitivity ; experimental design ; 1p ; CHROMOSOMES ; GENE-PRODUCT ; ONCOLOGY ; RE ; PRODUCTS ; THERAPIES ; END ; GRADE ; biomarker ; oligodendroglioma ; ANAPLASTIC OLIGODENDROGLIOMAS ; HISTOLOGY ; USA ; LOSSES ; OLIGODENDROGLIAL TUMORS ; cancer research ; EXTENT ; - ; PROGRESSION-FREE SURVIVAL ; outcome ; PHASE-III TRIAL
    Abstract: Purpose: The combined loss of genetic material on chromosomes 1p and 19q is strongly associated with favorable outcome in patients with WHO grade 3 anaplastic oligodendroglial tumors. The prognostic value of 1p/19q loss in WHO grade 2 oligodendroglial tumors is less well defined. Importantly, the possible effect of combined 1p/19q loss has not been studied in patients who were! not treated with radiotherapy or chemotherapy. Experimental Design: Seventy-six patients with oligodendroglioma (n = 33), oligoastrocytoma (n = 30), anaplastic oligodendroglioma (n = 6), or anaplastic oligoastrocytoma (n = 7) were identified who had not received radiotherapy or chemotherapy after their first operation until the end of follow-up or until the first progression and had tissue for 1p/19q status available. 1p/19q status was assessed by multiplex ligation - dependent probe amplification. Results: After a median follow-up of 3.8 years, progressive disease was documented in 34 patients. The estimated median progression-free survival was 4.6 years. Fifty-eight of the 76 patients had a combined loss of 1p and 19q. The absence or presence of combined 1p/19q loss was not prognostic for progression-free survival using multivariate adjustment for histology, extent of resection, and gender. Conclusions: Combined 1p/19q loss is not a sensitive prognostic biomarker in patients with oligodendroglial tumors who do not receive radiotherapy or chemotherapy. The gene products lost as a consequence of this codeletion may include mediators of resistance to genotoxic therapies. Alternatively, 1p/19q loss might be an early oncogenic lesion promoting the formation of glial neoplasms, which retain high sensitivity to genotoxic stress
    Type of Publication: Journal article published
    PubMed ID: 18056167
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  • 3
    Keywords: brain ; tumor ; COMMON ; DISEASE ; POPULATION ; RISK ; GENE-EXPRESSION ; validation ; ASSOCIATION ; SUSCEPTIBILITY ; VARIANTS ; BREAST-CANCER ; DELETION ; genetics ; SNP ; RETINOIC ACID ; brain tumor ; VARIANT ; GLIOMA ; SNPs ; METAANALYSIS ; ALLELES ; USA ; NERVOUS-SYSTEM TUMORS ; GLIOBLASTOMA ; LOCI ; 8Q24 ; BIRTH-WEIGHT ; GENOME-WIDE ASSOCIATION ; Genetic ; Genome-wide association studies ; BRAIN-TUMOR
    Abstract: To identify risk variants for glioma, we conducted a meta-analysis of two genome-wide association studies by genotyping 550K tagging SNPs in a total of 1,878 cases and 3,670 controls, with validation in three additional independent series totaling 2,545 cases and 2,953 controls. We identified five risk loci for glioma at 5p15.33 (rs2736100, TERT; P = 1.50 x 10(-17)), 8q24.21 (rs4295627, CCDC26; P = 2.34 x 10(-18)), 9p21.3 (rs4977756, CDKN2A-CDKN2B; P = 7.24 x 10(-15)), 20q13.33 (rs6010620, RTEL1; P = 2.52 x 10(-12)) and 11q23.3 (rs498872, PHLDB1; P = 1.07 x 10(-8)). These data show that common low-penetrance susceptibility alleles contribute to the risk of developing glioma and provide insight into disease causation of this primary brain tumor
    Type of Publication: Journal article published
    PubMed ID: 19578367
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  • 4
    Keywords: CANCER ; PATHWAYS ; DISEASE ; POPULATION ; GENES ; TUMORS ; SUSCEPTIBILITY ; DESIGN ; GLIOBLASTOMA ; GENOME-WIDE ASSOCIATION ; KORA
    Abstract: While gliomas are the most common primary brain tumors, their etiology is largely unknown. To identify novel risk loci for glioma, we conducted genome-wide association (GWA) analysis of two case-control series from France and Germany (2269 cases and 2500 controls). Pooling these data with previously reported UK and US GWA studies provided data on 4147 glioma cases and 7435 controls genotyped for 424 460 common tagging single-nucleotide polymorphisms. Using these data, we demonstrate two statistically independent associations between glioma and rs11979158 and rs2252586, at 7p11.2 which encompasses the EGFR gene (population-corrected statistics, P(c) = 7.72 x 10(-8) and 2.09 x 10(-8), respectively). Both associations were independent of tumor subtype, and were independent of EGFR amplification, p16INK4a deletion and IDH1 mutation status in tumors; compatible with driver effects of the variants on glioma development. These findings show that variation in 7p11.2 is a determinant of inherited glioma risk
    Type of Publication: Journal article published
    PubMed ID: 21531791
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