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  • Germany  (3)
  • METHYLATION  (2)
  • 1
    Keywords: CANCER ; radiotherapy ; SURVIVAL ; tumor ; Germany ; TOXICITY ; FOLLOW-UP ; imaging ; GENE ; TISSUE ; PATIENT ; CONTRAST ; TRIAL ; PROMOTER ; AGE ; EFFICACY ; inactivation ; ORGANIZATION ; METHYLATION ; MULTIFORME ; O-6-METHYLGUANINE-DNA METHYLTRANSFERASE ; PHASE-II ; ONCOLOGY ; ADULT ; METHYLTRANSFERASE ; GLIOMA ; overall survival ; SCIENCE ; MGMT ; methods ; PLUS ; temozolomide ; PROMOTER METHYLATION ; GLIOBLASTOMA ; indomethacin ; MGMT GENE ; EORTC ; BENEFIT ; Follow up
    Abstract: Purpose: To evaluate the toxicity and efficacy of chemoradiotherapy with temozolomide (TMZ) administered in an intensified 1-week on/1-week off schedule plus indomethacin in patients with newly diagnosed glioblastoma. Patients and Methods: A total of 41 adult patients (median Karnofsky performance status, 90%; median age, 56 years) were treated with preirradiation TMZ at 150 mg/m(2) (1 week on/1 week off), involved-field radiotherapy combined with concomitant low-dose TMZ (50 mg/m(2)), maintenance TMZ starting at 150 mg/m(2) using a 1-week on/1-week off schedule, plus maintenance indomethacin (25 mg twice daily). Results: The median follow-up interval was 21.7 months. Grade 4 hematologic toxicity was observed in 15 patients (36.6%). Treatment-related nonhematologic Grade 4-5 toxicity was reported for 2 patients (4.9%). The median progression-free survival was 7.6 months (95% confidence interval, 6.2-10.4). The 1-year survival rate was 73.2% (95% confidence interval, 56.8-84.2%). The presence of O-6-methylguanine-DNA methyltransferase (MGMT) gene promoter methylation in the tumor tissue was associated with significantly superior progression-free survival. Conclusion: The dose-dense regimen of TMZ administered in a 1-week on/1-week off schedule resulted in acceptable nonhematologic toxicity. Compared with data from the European Organization for Research and Treatment of Cancer/National Cancer Institute of Canada trial 26981-22981/CE.3, patients with an unmethylated MGMT gene promoter appeared not to benefit from intensifying the TMZ schedule regarding the median progression-free survival and overall survival. In contrast, data are promising for patients with a methylated MGMT promoter. (C) 2010 Elsevier Inc
    Type of Publication: Journal article published
    PubMed ID: 19836157
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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: brain ; CELLS ; EXPRESSION ; tumor ; TUMOR-CELLS ; CELL ; Germany ; SYSTEM ; DISEASE ; PROTEIN ; DIFFERENTIATION ; SURGERY ; MARKER ; antibodies ; antibody ; LESIONS ; MUTATION ; etiology ; MARKERS ; p53 ; MUTATIONS ; vimentin ; CENTRAL-NERVOUS-SYSTEM ; FREQUENT ; sensitivity ; pathology ; GLIOMAS ; GLIOMA ; GFAP ; SPECIMENS ; GLIOBLASTOMA ; IMMUNOREACTIVITY ; IDH1 ; ASTROCYTES ; HUMAN-BRAIN-TUMORS ; GLIOBLASTOMAS ; P53 EXPRESSION ; IDH1 mutation ; PANEL ; mIDH1R132H ; NEUROPATHOLOGY ; NOGO-A EXPRESSION ; reactive gliosis ; WT1
    Abstract: Differentiation of gliomas and reactive gliosis may be challenging both at primary tumor occurrence and at posttherapy biopsy. The most frequent IDH1 mutation found in the majority of WHO grade II and III gliomas can be visualized with an antibody specifically detecting mutant IDH1(R132H) protein. In this study, mIDH1R132H immunoreactivity in 120 reactive gliosis specimens of various etiologies is compared with Wilms Tumor 1 (WT1) and p53 expression, both markers applied for the differentiation of reactive gliosis and glioma. Although WT1 and p53 positive glial cells were found in 17% and 63% of cases respectively, all samples were negative for mIDH1R132H. Furthermore, we investigated 19 posttherapy gliomas ( 6 WHO II, 13 WHO III) with extensive reactive changes and detected mIDH1R132H positive cells in 13 specimens. In 5 of these cases, tumor cells were missed by conventional staining, showing the improved sensitivity of mIDH1R132H. Thus, mIDH1R132H is a tumor-specific marker that is superior to other established markers to differentiate reactive from neoplastic cells in grade II and III gliomas and allows identifying tumor cells in posttherapy specimens with extensive reactive changes. As IDH mutations are not characteristic of grade IV primary glioblastomas, this antibody cannot differentiate primary glioblastoma from reactive gliosis. Thus, caution has to be taken and a combined panel with other markers is needed
    Type of Publication: Journal article published
    PubMed ID: 20661018
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