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  • SURVIVAL  (5)
  • 1
    Keywords: EXPRESSION ; SURVIVAL ; BLOOD ; CELL ; Germany ; GENE ; GENES ; PATIENT ; recombination ; ANTIGEN ; ASSOCIATION ; LYMPHOMA ; DIFFERENCE ; MUTATION ; ABERRATIONS ; DELETIONS ; B-CELLS ; AGGRESSIVE VARIANTS ; ATM GENE ; CD38 EXPRESSION ; CENTROCYTIC LYMPHOMA ; CHROMOSOMAL IMBALANCES ; CHRONIC LYMPHOCYTIC-LEUKEMIA ; COMPLETE REMISSION ; IMMUNOGLOBULIN GENES ; MAJOR TRANSLOCATION CLUSTER ; SOMATIC HYPERMUTATION
    Abstract: Immunoglobulin variable heavy chain gene (V-H) mutation status and VDJ rearrangement structure were analyzed in 141 patients with mantle cell lymphoma (MCL) and correlated with biologic and clinical characteristics; 29% of the MCLs displayed mutated V-H using a 98% germline homology cutoff. Striking differences occurred in the VH mutation subgroups with respect to the use of specific V genes. Rearrangements involving V4-34 and V3-21 were almost exclusively unmutated, whereas rearrangements using V4-59 and V3-23 were typically mutated. Significant association occurred between mutated V-H with shorter CDR3 lengths and the use of J(H)4b. V3-21 and V4-59 were involved in highly characteristic rearrangements, implying that antigen specificity might have been involved in MCL development. There was no evidence for isotype switch recombination or Bcl-6 expression in any MCL. ZAP70 expression was not different in V-H-mutated or unmutated MCL. Although the deletions 11q- and 17p- showed a balanced distribution, an overrepresentation was observed for trisomies +3q, +8q, and tetraploidy in the V-H-unmutated subgroup and +12q in the V-H-mutated subgroup. Clinically, mutated V-H was associated with a higher rate of complete remission, but there was no correlation between VH mutation status and other clinical characteristics or overall survival. (Blood. 2003; 102:3003-3009) (C) 2003 by The American Society of Hematology
    Type of Publication: Journal article published
    PubMed ID: 12842981
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  • 2
    Keywords: EXPRESSION ; SURVIVAL ; CELL ; CLINICAL-TRIAL ; Germany ; THERAPY ; TOOL ; DISTINCT ; GENOME ; HYBRIDIZATION ; microarray ; validation ; DNA ; treatment ; chromosome ; DISCOVERY ; CLINICAL-TRIALS ; chemotherapy ; leukemia ; ABERRATIONS ; MARKERS ; FRAGMENTS ; IMBALANCES ; CD38 EXPRESSION ; MANTLE CELL LYMPHOMA ; NON-HODGKINS-LYMPHOMA ; AMPLIFICATIONS ; DNA COPY NUMBER ; GENE MUTATION STATUS
    Abstract: B cell chronic lymphocytic leukemia (B-CLL) is characterized by a highly variable clinical course. Recurrent chromosomal imbalances provide significant prognostic markers. Risk-adapted therapy based on genomic alterations-has become an option that is currently being tested in clinical trials. To supply a robust tool for such large scale studies, we developed a comprehensive DNA microarray dedicated to the automated analysis of recurrent genomic imbalances in B-CLL by array-based comparative genomic hybridization (matrix-CGH). Validation of this chip in a series of 106 B-CLL cases revealed a high specificity and sensitivity that fulfils the criteria for application in clinical oncology. This chip is immediately applicable within clinical B-CLL treatment trials that evaluate whether B-CLL cases with distinct chromosomal abnormalities should be treated with chemotherapy of different intensities and/or stem cell transplantation. Through the control set of DNA fragments equally distributed over the genome, recurrent genomic imbalances were discovered: trisomy of chromosome 19 and gain of the MYCN oncogene correlating With an elevation of MYCN mRNA expression
    Type of Publication: Journal article published
    PubMed ID: 14730057
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  • 3
    Keywords: EXPRESSION ; SURVIVAL ; tumor ; Germany ; neoplasms ; GENE ; GENES ; GENOME ; HYBRIDIZATION ; microarray ; SAMPLE ; SAMPLES ; transcription ; ACTIVATION ; DNA ; mechanisms ; TARGET ; STAGE ; IN-SITU ; AMPLIFICATION ; COMPARATIVE GENOMIC HYBRIDIZATION ; LYMPHOMA ; DNA microarray ; microarrays ; ABERRATIONS ; DELETIONS ; POLYMERASE-CHAIN-REACTION ; DNA AMPLIFICATION ; FLUORESCENCE ; gene amplification ; IMBALANCES ; GAINS ; B-CELL LYMPHOMA ; CGH ; matrix-CGH ; DNA COPY-NUMBER
    Abstract: DNA amplifications are important mechanisms for protooncogene activation. Comparative genomic hybridization (CGH) to metaphase chromosome preparations has revealed amplifications in 10-20% of B-cell lymphomas (B-NHL). We analysed a series of 16 aggressive non-Hodgkin lymphomas by the new approach termed Matrix-CGH (M-CGH) using genomic DNA microarrays as hybridization target. For M-CGH, a dedicated B-cell lymphoma chip was constructed containing 496 genomic targets covering oncogenes, tumor suppressor genes as well as chromosome regions frequently altered in B-NHL. In 10 of 16 samples a total of 15 DNA amplifications were identified. The amplicons included BCL2, REL, CCND1, CCND2, JAK2, FGF4 and MDM2. Four of the 15 amplifications remained undetected by chromosomal CGH. The respective amplicons mapped to bands 2p13, 9p13-p21 and 12q24 and, were confirmed by fluorescence in situ hybridization. Furthermore, for four genomically amplified genes real-time quantitative reverse transcription polymerase chain reaction revealed elevated mRNA expression levels. These data show the superior diagnostic sensitivity of the newly developed diagnostic tool. As only a small portion of the genome (approximately 1.5%) has been analysed by the present DNA array, it is likely that gene amplifications are much more common in aggressive lymphomas than previously assumed
    Type of Publication: Journal article published
    PubMed ID: 12618769
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  • 4
    Keywords: SPECTRA ; CANCER ; SURVIVAL ; tumor ; carcinoma ; Germany ; human ; NEW-YORK ; HYBRIDIZATION ; SAMPLE ; SAMPLES ; TUMORS ; PATIENT ; DNA ; LYMPH-NODES ; chromosome ; BREAST ; breast cancer ; BREAST-CANCER ; COMPARATIVE GENOMIC HYBRIDIZATION ; COPY NUMBER ; COPY-NUMBER ; DIFFERENCE ; AGE ; LINKAGE ANALYSIS ; OVARIAN-CANCER ; WOMEN ; METASTASIS ; ABERRATIONS ; TUMOR-SUPPRESSOR GENE ; REGION ; PROGNOSTIC-FACTORS ; REGIONS ; BREAST-CARCINOMA ; CARCINOMAS ; DNA AMPLIFICATION ; GAINS ; SUSCEPTIBILITY GENE ; ALLELIC LOSS ; CGH ; COPY NUMBER CHANGES ; CARCINOMA IN-SITU ; YOUNG-WOMEN ; early onset breast cancer,comparative genomic hybridization,loss of 8p,gain of 8q ; HETEROZYGOSITY REGION ; HISTOLOGICAL GRADE
    Abstract: Sporadic breast cancer in young women is different from the one in older patients regarding pathological features and aggressiveness of the tumors, but the spectrum of genetic alterations are largely unknown. We used comparative genomic hybridization (CGH) to analyze DNA copy number changes in 88 tumor samples from women less than or equal to35 years of age. Findings were compared to histopathological data including tumor type, grading, lymph nodes and metastasis. Genomic gains clustered to chromosome arms 1q (64.8%), 8q (61.4%), 17q (50.0%), 20q (33.0%), 3q (20.5%), 1p (17.0%), 5p (17.0%) and 15q (17%). Losses were commonly located on 8p (19.3 %), 11q (11.4%), 16q (11.4%), 17p (1 1.4%) and 18q (10.2%). A comparison with published CGH data from breast carcinomas of similar type and grade showed the following differences: (1) gains were much more frequent than losses, and (2) losses on 8p22-p23 were more prevalent in patients with positive lymph node metastasis (p = 0.02), and Grade III tumors were associated with gains on the long arm of chromosome 8 (p = 0.01). Therefore, alterations in these genomic regions may be responsible for the reduced survival of patients with early onset breast cancer. (C) 2003 Wiley-Liss, Inc
    Type of Publication: Journal article published
    PubMed ID: 14520696
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  • 5
    Keywords: CANCER ; SURVIVAL ; tumor ; CELL ; Germany ; human ; GENE ; GENES ; HYBRIDIZATION ; SAMPLE ; SAMPLES ; MOLECULAR CHARACTERIZATION ; PATIENT ; DNA ; PAIRS ; chromosome ; FREQUENCY ; DELETION ; IDENTIFICATION ; IN-SITU ; COMPARATIVE GENOMIC HYBRIDIZATION ; LYMPHOMA ; NUMBER ; leukemia ; ABERRATIONS ; DELETIONS ; TUMOR-SUPPRESSOR GENE ; REGION ; PROGNOSTIC-FACTORS ; REGIONS ; ONCOGENE ; FLUORESCENCE ; ATM GENE ; CHRONIC LYMPHOCYTIC-LEUKEMIA ; MANTLE CELL LYMPHOMA ; HIGH-FREQUENCY ; NON-HODGKINS-LYMPHOMA ; F ; ONCOLOGY ; CHROMOSOME-TRANSLOCATION ; H MUTATION STATUS
    Abstract: Tumor samples of 53 patients with t(11;14)-positive mantle cell lymphomas (MCLs) were analyzed by matrix-based comparative genomic hybridization (matrix-CGH) using a dedicated DNA array. In 49 cases, genomic aberrations were identified. In comparison to chromosomal CGH, a 50%. higher number of aberrations was found and the high specificity of,matrix-CGH was demonstrated by fluorescence in situ hybridization (FISH) analyses. The 11q gains and 13q34 deletions, which have not been described as frequent genomic aberrations in MCL, were identified by matrix-CGH in 15 and 26 cases, respectively. For several genomic aberrations, novel consensus regions were defined: 8p21 (size of the consensus region, 2.4 megabase pairs [Mbp]; candidate genes: TNFRSF10B, TNFRSF10C, TNFRSF10D); 10p13 (2.7 Mbp; BM/1); 11q13 (1.4 Mbp; RELA); 11q13 (5.2 Mbp; CCND1); 13q14 (0.4 Mbp; RFP2, BCMSUN) and 13q34 (6.9 Mbp). In univariate analyses correlating genomic aberrations and clinical course, 8p- and 13q14- deletions were associated with an inferior overall survival. These data provide a basis for further studies focusing on the identification of pathogenetically or clinically relevant genes, in MCL
    Type of Publication: Journal article published
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