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  • 1
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    German Medical Science; Düsseldorf, Köln
    In:  57. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie e.V. (DGNC), Joint Meeting mit der Japanischen Gesellschaft für Neurochirurgie; 20060511-20060514; Essen; DOCSO.03.01 /20060508/
    Publication Date: 2006-07-31
    Keywords: ddc: 610
    Language: English
    Type: conferenceObject
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  • 2
    Keywords: radiotherapy ; SURVIVAL ; tumor ; evaluation ; Germany ; TOXICITY ; COMMON ; DIAGNOSIS ; GENE ; TISSUE ; TUMORS ; TIME ; PATIENT ; DNA ; INFECTION ; treatment ; PROGRESSION ; PROMOTER ; EFFICACY ; chemotherapy ; INFECTIONS ; RECURRENT ; METHYLATION ; GLIOMAS ; DNA methyltransferase ; LACKING ; PHASE-II ; ONCOLOGY ; ADULT ; METHYLTRANSFERASE ; GLIOMA ; MALIGNANT GLIOMA ; GRADE ; GENE PROMOTER ; MGMT ; TUMOR TISSUE ; methods ; EVENTS ; temozolomide ; GLIOBLASTOMA-MULTIFORME ; CRITERIA ; USA ; PROMOTER METHYLATION ; O-6-methylguanine ; survival rate ; GLIOBLASTOMA ; PROGRESSION-FREE SURVIVAL ; REGIMEN ; evidence ; MGMT GENE ; O-6-methylguanine-DNA-methyltransferase
    Abstract: Purpose Evaluation of toxicity and efficacy of an alternating weekly regimen of temozolomide administered 1 week on and 1 week off in patients with recurrent glioma. Patients and Methods Ninety adult patients with recurrent gliomas accrued in one center received chemotherapy with temozolomide at 150 mg/ m(2)/ d ( days 1 through 7 and 15 through 21 every 4 weeks) with individual dose adjustments according to hematologic toxicity. Results A total of 906 treatment weeks were delivered. Grade 4 hematotoxicity according to the Common Terminology Criteria for Adverse Events ( CTCAE; version 3.0) was observed in 24 treatment weeks ( 2.6%). CTCAE grade 4 lymphopenia eventually developed in 11 patients ( 12%). There were neither cumulative lymphopenias nor opportunistic infections. The progression-free survival ( PFS) rate at 6 months for glioblastoma patients was 43.8%. The median PFS in these patients was 24 weeks ( 95% Cl, 17 to 26 weeks), the median survival time from diagnosis of progression was 38 weeks ( 95% Cl, 30 to 46 weeks), and the 1-year survival rate from progression was 23%. O-6-methylguanine DNA methyltransferase ( MGMT) gene promoter methylation in the tumor tissue was not associated with longer PFS ( log-rank P = .37). Conclusion These data imply that the alternating weekly schedule is feasible, safe, and effective and clearly warrants investigation in randomized studies. Compared with more protracted low-dose temozolomide schedules, the 1-week-on/ 1-week-off schedule may be less toxic. We provide preliminary evidence that this dose-dense schedule is also active in patients with tumors lacking MGMT gene promoter methylation
    Type of Publication: Journal article published
    PubMed ID: 17664483
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  • 3
    Keywords: CANCER ; EXPRESSION ; SURVIVAL ; CELL ; Germany ; GENE ; cell line ; LINES ; PATIENT ; MARKER ; prognosis ; DOMAIN ; tumour ; BIOLOGY ; CELL-LINES ; MOLECULAR-BIOLOGY ; TRANSACTIVATOR ; treatment ; DELETION ; NO ; IDENTIFICATION ; MUTATION ; genetics ; CELL-LINE ; chemotherapy ; LINE ; DELETIONS ; MUTATIONS ; ONCOGENE ; sensitivity ; gene expression profiling ; cell lines ; heredity ; GLIOMAS ; HYPERMETHYLATION ; tumour suppressor gene ; 1p ; TRANSCRIPTS ; molecular biology ; molecular ; ONCOLOGY ; INCREASE ; GLIOMA ; overall survival ; MUTATIONAL ANALYSIS ; LEVEL ; analysis ; SUPPRESSOR ; oligodendroglioma ; ANAPLASTIC OLIGODENDROGLIOMAS ; LOSSES ; ENGLAND ; 5-AZA-2'-DEOXYCYTIDINE ; CpG island ; PHASE-III TRIAL ; 19Q LOSS ; 19Q13.3 ; CITED4 ; MGMT GENE
    Abstract: Deletions of chromosomal arms 1p and 19q are frequent in oligodendroglial tumours and have been associated with sensitivity to radio- and chemotherapy as well as favourable prognosis. By using microarray-based expression pro. ling, we found that oligodendroglial tumours with 1p and 19q losses showed signi. cantly lower expression of the CBP/p300-interacting transactivator with glutamic acid/ aspartic acid-rich carboxyl-terminal domain 4 gene (CITED4) at 1p34.2 as compared to tumours without 1p and 19q losses. Mutational analysis showed no CITED4 mutations in gliomas. However, 1p and 19q losses as well as low expression of CITED4 transcripts were significantly associated with hypermethylation of the CITED4-associated CpG island. In line with the latter. nding, treatment of CITED4 hypermethylated glioma cell lines with 5-aza-2'-deoxycytidine and trichostatine A resulted in a marked increase of the CITED4 transcript levels. Furthermore, CITED4 hypermethylation was signi. cantly associated with longer recurrence-free and overall survival of patients with oligodendroglial tumours. Taken together, our results indicate that CITED4 is epigenetically silenced in the vast majority of oligodendroglial tumours with 1p and 19q deletions and suggest CITED4 hypermethylation as a novel prognostic marker in oligodendroglioma patients
    Type of Publication: Journal article published
    PubMed ID: 17311001
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  • 4
    Keywords: brain ; CELLS ; EXPRESSION ; GROWTH ; tumor ; TUMOR-CELLS ; CELL ; Germany ; human ; GENE ; GENES ; HYBRIDIZATION ; TISSUE ; TUMORS ; DNA ; prognosis ; chromosome ; DELETION ; IN-SITU ; AMPLIFICATION ; COMPARATIVE GENOMIC HYBRIDIZATION ; PROMOTER ; MUTATION ; DELETIONS ; PATHOGENESIS ; TUMOR-SUPPRESSOR GENE ; MUTATIONS ; FLUORESCENCE ; IMBALANCES ; METHYLATION ; TUMOR CELLS ; CHROMOSOMES ; in situ hybridization ; CELL CARCINOMA ; CANDIDATE GENES ; WEIGHT ; MUTATIONAL ANALYSIS ; LEVEL ; analysis ; TUMOR-CELL ; ROLES ; DNA-MICROARRAY ; p53 mutation ; LOSSES ; MOLECULAR PATHOGENESIS ; CANDIDATE ; genomic ; RARE ; CHROMOSOME-9 ; molecular genetics ; LOCI ; array-based CGH ; GLIOMA PROGRESSION ; 9Q34 ; pleomorphic xanthoastrocytomas ; SCLEROSIS GENE TSC1
    Abstract: The molecular pathogenesis of pleomorphic xanthoastrocytoma (PXA), a rare astrocytic brain tumor with a relatively favorable prognosis, is still poorly understood. We characterized 50 PXAs by comparative genomic hybridization (CGH) and found the most common imbalance to be loss on chromosome 9 in 50% of tumors. Other recurrent losses affected chromosomes 17 (10%), 8, 18, 22 (4% each). Recurrent gains were identified on chromosomes X (16%), 7, 9q, 20 (8% each), 4, 5, 19 ( 4% each). Two tumors demonstrated amplifications mapping to 2p23-p25, 4p15, 12q13, 12q21, 21q21 and 21q22. Analysis of 10 PXAs with available high molecular weight DNA by high-resolution array-based CGH indicated homozygous 9p21.3 deletions involving the CDKN2A/p14(ARF)/CDKN2B loci in six tumors (60%). Interphase fluorescence in situ hybridization to tissue sections confirmed the presence of tumor cells with homozygous 9p21.3 deletions. Mutational analysis of candidate genes on 9q, PTCH and TSC1, revealed no mutations in PXAs with 9q loss and no evidence of TSC1 promoter methylation. However, PXAs consistently showed low TSC1 transcript levels. Taken together, our study identifies loss of chromosome 9 as the most common chromosomal imbalance in PXAs and suggests important roles for homozygous CDKN2A/p14ARF/CDKN2B deletion as well as low TSC1 mRNA expression in these tumors
    Type of Publication: Journal article published
    PubMed ID: 16909113
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  • 5
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    German Medical Science; Düsseldorf, Köln
    In:  55. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie e.V. (DGNC), 1. Joint Meeting mit der Ungarischen Gesellschaft für Neurochirurgie; 20040425-20040428; Köln; DOCP 06.59 /20040423/
    Publication Date: 2004-04-22
    Keywords: ddc: 610
    Language: English
    Type: conferenceObject
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  • 6
    ISSN: 1365-2133
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Background  Basal cell carcinoma (BCC) of the skin is the most common human cancer. The genetic alterations underlying BCC development are only partly understood.Objectives  To investigate further the molecular genetics of sporadic BCCs, we performed mutation analyses of 10 skin cancer-associated genes in 42 tumours.Methods  Single-strand conformational polymorphism analysis followed by DNA sequencing was used to screen for mutations in the sonic hedgehog pathway genes PTCH, SMOH, SUFUH and GLI1, in the TP53 tumour suppressor gene, and in the proto-oncogenes NRAS, KRAS, HRAS, BRAF and CTNNB1. Microsatellite markers flanking the PTCH, SUFUH and TP53 loci at 9q22, 10q24 and 17p13, respectively, were studied for loss of heterozygosity (LOH).Results  PTCH mutations were found in 28 of 42 tumours (67%). Microsatellite analysis revealed LOH on 9q22 in 20 of 38 tumours investigated (53%), including 14 tumours with and six tumours without PTCH mutations. SMOH mutations were identified in four of the 42 BCCs (10%) while two tumours demonstrated mutations in SUFUH, including one missense mutation and one silent mutation. None of the BCCs showed LOH at markers flanking the SUFUH locus. Seventeen BCCs (40%) carried TP53 mutations, with only three tumours showing evidence of biallelic TP53 inactivation. TP53 mutations were present in BCCs with and without mutations in PTCH, SMOH or SUFUH. Interestingly, 72% of the TP53 alterations were presumably ultraviolet (UV)-induced transition mutations. In contrast, only 40% of the PTCH and SMOH alterations corresponded to UV signature mutations. No mutations were identified in GLI1, NRAS, KRAS, HRAS, BRAF or CTNNB1.Conclusions  Our data confirm the importance of PTCH, SMOH and TP53 mutations in the pathogenesis of sporadic BCCs. SUFUH alterations are restricted to individual cases while the other investigated genes do not appear to be important targets for mutations in BCCs.
    Type of Medium: Electronic Resource
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