Your email was sent successfully. Check your inbox.

An error occurred while sending the email. Please try again.

Proceed reservation?

Export
  • 1
    Keywords: RECEPTOR ; EXPRESSION ; GROWTH ; GROWTH-FACTOR ; INVASION ; tumor ; CELL ; Germany ; PATHWAY ; PATHWAYS ; SYSTEM ; incidence ; GENE ; GENES ; meningioma ; SURGERY ; TRANSDUCTION ; ACTIVATION ; MECHANISM ; mechanisms ; DYNAMICS ; cell cycle ; CELL-CYCLE ; CYCLE ; signal transduction ; chromosome ; SIGNAL ; ACID ; TARGET ; hormone ; PROGRESSION ; COMPARATIVE GENOMIC HYBRIDIZATION ; MUTATION ; genetics ; SIGNAL-TRANSDUCTION ; inactivation ; PATHOGENESIS ; DAMAGE ; HEREDITARY ; MUTATIONS ; STRATEGIES ; TARGETS ; FUTURE ; RECEPTORS ; CYCLE CONTROL ; INITIATION ; 1p ; CHROMOSOMES ; molecular ; MOLECULAR-MECHANISM ; review ; TUMOR-SUPPRESSOR ; SUPPRESSOR GENE ; MALIGNANT PROGRESSION ; development ; MOLECULAR-MECHANISMS ; SUPPRESSOR ; MOLECULAR-GENETICS ; EVENTS ; telomere ; TELOMERASE ACTIVITY ; USA ; HORMONES ; LOSSES ; STEROID-HORMONES ; MOLECULAR PATHOGENESIS ; NERVOUS-SYSTEM TUMORS ; HUMAN BRAIN-TUMORS ; GRADING SYSTEM ; genomic ; GENETIC ALTERATION ; molecular genetics ; TUMOR-SUPPRESSOR GENES ; MAINTENANCE ; cell cycle control ; GROWTH-FACTORS ; refractory ; CASCADE ; CLINICAL-APPLICATIONS ; INTEGRITY ; ANAPLASTIC MENINGIOMAS ; meningioma progression ; meningioma therapy ; NF2 ; NF2 GENE ; RADIATION-INDUCED MENINGIOMAS ; SPORADIC MENINGIOMAS
    Abstract: TO REVIEW OUR CURRENT understanding of the molecular pathogenesis of meningiomas, to suggest topics for future investigations, and to present perspectives for clinical application. Significant progress has been made in recent years in delineating the molecular mechanisms involved in meningioma formation, growth, and malignant progression. However, many questions remain unanswered. Mutations in the NF2 gene probably account for the formation of more than half of all meningiomas. On the other hand, the molecular events underlying the initiation of meningiomas without NF2 mutations have yet to be identified. Investigating hereditary conditions associated with an increased meningioma incidence and the mechanisms underlying the development of radiation-induced meningiomas could potentially yield relevant insights. Meningioma growth is sustained by the dysregulated expression of steroid hormones, growth factors, their receptors, and activation of signal transduction cascades. The underlying genetic causes are unknown. Malignant progression of meningiomas probably involves the inactivation of tumor suppressor genes on chromosomes 1p, 9p, 10q, and 14q. However, with the possible exception of INK4A/INK4B, the actual targets of these chromosomal losses have remained largely elusive. Cell cycle dysregulation and telomerase activation have been recognized as important steps in meningioma progression. Telomere dynamics, cell cycle control, and the mechanisms responsible for deoxyribonucleic acid damage control are tightly interwoven. Investigating genes involved in the maintenance of genomic integrity might significantly deepen the understanding of meningioma progression. An area that has received relatively little attention thus far is the genetic background of meningioma spread and invasion. Possible clinical applications of the molecular data available may include a meningioma grading system based on genetic alterations, as well as therapeutic strategies for refractory meningiomas aimed at interfering with signal transduction pathways
    Type of Publication: Journal article published
    PubMed ID: 17460514
    Signatur Availability
    BibTip Others were also interested in ...
  • 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
    Signatur Availability
    BibTip Others were also interested in ...
  • 3
    Keywords: brain ; CELLS ; tumor ; CELL ; Germany ; human ; FOLLOW-UP ; HYBRIDIZATION ; COMPONENTS ; TUMORS ; NO ; IN-SITU ; PROGRESSION ; COMPARATIVE GENOMIC HYBRIDIZATION ; EXPRESSION ANALYSIS ; HEALTH ; DNA microarray ; ABERRATIONS ; FISH ; REGION ; RECURRENCE ; REGIONS ; SERIES ; FLUORESCENCE ; ORGANIZATION ; fluorescence in situ hybridization ; CHROMOSOMAL IMBALANCES ; GLIOMAS ; DMBT1 ; CLUSTER ; SUBPOPULATION ; GLIOMA ; MALIGNANT GLIOMAS ; ARRAY ; GRADE ; GENOMIC ABERRATIONS ; analysis ; PROFILES ; LOSSES ; FOCAL EPILEPSIES ; GANGLIOGLIOMAS ; NERVOUS-SYSTEM TUMORS ; ENGLAND ; ARRAY-CGH ; comparison ; LOW-GRADE ; PROFILE ; array-based CGH ; genomic aberration ; MOLECULAR CYTOGENETIC ANALYSIS ; tumor genetics
    Abstract: Gangliogliomas are generally benign neuroepithelial tumors composed of dysplastic neuronal and neoplastic glial elements. We screened 61 gangliogliomas [World Health Organization (WHO) grade I] for genomic alterations by chromosomal and array-based comparative genomic hybridization (CGH). Aberrations were detected in 66% of gangliogliomas (mean +/- SEM = 2.5 +/- 0.5 alterations/tumor). Frequent gains were on chromosomes 7 (21%), 5 (16%), 8 (13%), 12 (12%); frequent losses on 22q (16%), 9 (10%), 10 (8%). Recurrent partial imbalances comprised the minimal overlapping regions dim(10)(q25) and enh(12)(q13.3-q14.1). Unsupervised cluster analysis of genomic profiles detected two major subgroups (group I: complete gain of 7 and additional gains of 5, 8 or 12; group II: no major recurring imbalances, mainly losses). A comparison with low-grade gliomas (astrocytomas WHO grade II) showed chromosome 5 gain to be significantly more frequent in gangliogliomas. Interphase fluorescence in situ hybridization (FISH) identified the aberrations to be contained in a subpopulation of glial but not in neuronal cells. Two gangliogliomas and their anaplastic recurrences (WHO grade III) were analyzed. Losses of CDKN2A/B and DMBT1 or a gain/amplification of CDK4 found in the anaplastic tumors were already present in the respective gangliogliomas by array CGH and interphase FISH. In summary, genomic profiling in a large series of gangliogliomas could distinguish genetic subgroups even in this low-grade tumor
    Type of Publication: Journal article published
    PubMed ID: 18371186
    Signatur Availability
    BibTip Others were also interested in ...
  • 4
    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
    Signatur Availability
    BibTip Others were also interested in ...
  • 5
    Keywords: CANCER ; radiotherapy ; SURVIVAL ; tumor ; CLASSIFICATION ; ASSOCIATION ; chemotherapy ; GLIOMAS ; EUROPEAN ORGANIZATION ; temozolomide ; GLIOBLASTOMA ; IDH1 ; ADJUVANT PROCARBAZINE ; PHASE-3 TRIAL ; 1p/19q ; BRAIN-TUMOR GROUP
    Abstract: OBJECTIVE: To explore whether the isocitrate dehydrogenase 1 (IDH1) or 1p/19q status determines the prognostic vs predictive role of O(6)-methylguanine-DNA methyltransferase (MGMT) promoter methylation in the Neuro-Oncology Working Group of the German Cancer Society (NOA)-04 trial anaplastic glioma biomarker cohort. METHODS: Patients (n = 183) of the NOA-04 trial with known MGMT and IDH1 status were analyzed for interdependency of the prognostic vs predictive role of MGMT promoter methylation from IDH1 or 1p/19q status and treatment, using progression-free survival (PFS) as an endpoint. An independent validation cohort of the German Glioma Network (n = 75) and the NOA-08 trial (n = 34) served as a confirmation cohort. RESULTS: In tumors with IDH1 mutation, MGMT promoter methylation was associated with prolonged PFS with chemotherapy +/- radiotherapy (RT) or RT-only groups, and is thus prognostic. In tumors without IDH1 mutation, MGMT promoter methylation was associated with increased PFS in patients treated with chemotherapy, but not in those who received RT alone as the first-line treatment, and is thus chemotherapy-predictive. In contrast, 1p/19q codeletions showed no such association with the prognostic vs predictive value of MGMT. CONCLUSIONS: MGMT promoter methylation is a predictive biomarker for benefit from alkylating agent chemotherapy in patients with IDH1-wild-type, but not IDH1-mutant, malignant gliomas of World Health Organization grades III/IV. Combined IDH1/MGMT assessment may help to individualize clinical decision-making in neuro-oncology.
    Type of Publication: Journal article published
    PubMed ID: 24068788
    Signatur Availability
    BibTip Others were also interested in ...
  • 6
    facet.materialart.
    Unknown
    German Medical Science GMS Publishing House; Düsseldorf
    In:  65. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie (DGNC); 20140511-20140514; Dresden; DOCP 030 /20140513/
    Publication Date: 2014-05-14
    Keywords: epilepsy ; tumor ; outcome ; ddc: 610
    Language: English
    Type: conferenceObject
    Signatur Availability
    BibTip Others were also interested in ...
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...