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Titolo:
Genetic imbalances revealed by comparative genomic hybridization in ewing tumors
Autore:
Ozaki, T; Paulussen, M; Poremba, C; Brinkschmidt, C; Rerin, J; Ahrens, S; Hoffmann, C; Hillmann, A; Wai, D; Schaefer, KL; Boecker, W; Juergens, H; Winkelmann, W; Dockhorn-Dworniczak, B;
Indirizzi:
Univ Munster, Gerhard Domagk Inst Pathol, Dept Orthopaed, D-48149 Munster,Germany Univ Munster Munster Germany D-48149 Orthopaed, D-48149 Munster,Germany Univ Munster, Dept Pediat Hematol & Oncol, D-48149 Munster, Germany Univ Munster Munster Germany D-48149 l & Oncol, D-48149 Munster, Germany Univ Munster, Dept Orthopaed, D-48149 Munster, Germany Univ Munster Munster Germany D-48149 Orthopaed, D-48149 Munster, Germany
Titolo Testata:
GENES CHROMOSOMES & CANCER
fascicolo: 2, volume: 32, anno: 2001,
pagine: 164 - 171
SICI:
1045-2257(200110)32:2<164:GIRBCG>2.0.ZU;2-5
Fonte:
ISI
Lingua:
ENG
Soggetto:
HEPATOCELLULAR-CARCINOMA; COPY NUMBER; CHROMOSOME-TRANSLOCATION; CHIMERIC TRANSCRIPTS; PROSTATE-CANCER; FUSION PROTEINS; DNA-SEQUENCES; SARCOMA; FAMILY; EWS;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
48
Recensione:
Indirizzi per estratti:
Indirizzo: Dockhorn-Dworniczak, B Univ Munster, Gerhard Domagk Inst Pathol, Dept Orthopaed, Domagkstr 17, D-48149 Munster, Germany Univ Munster Domagkstr 17 Munster Germany D-48149
Citazione:
T. Ozaki et al., "Genetic imbalances revealed by comparative genomic hybridization in ewing tumors", GENE CHROM, 32(2), 2001, pp. 164-171

Abstract

Ewing tumors are characterized by reciprocal translocations involving the EWS gene on 22q12 fused to ETS transcription-factor family members. Little is known about further aberrations contributing to tumor development and progression. Sixty-two frozen tumors with known EWS rearrangements (52 primary tumors, 10 relapses) of ET patients registered in the EICESS protocol. were analyzed by comparative genomic hybridization (CGH). The median number of changes in 52 primary and 10 relapsed cases was 2.5 and 5.0 per tumor (P = 0.153). Frequent abnormalities included gains of chromosomes 8, 12, 20,, and 1q and losses of 16q and 19q. Neither number nor type of aberration wasassociated with histology, tumor size, disease stage, tumor localization, or histologic tumor response to chemotherapy. Among the 52 primary tumors, 26 with Type I fusion (EWS exon 7 to FL11 exon 6) and 26 with other fusion types had a median of 2.0 and 3.0 aberrations per tumor, respectively (P = 0.031). Combinations of gains of chromosomes 8 and 12, gains of chromosome 20, and either gains of 8q or 18q and losses of 16q and 17p frequently occurred. The cumulative overall survival (OAS) was different between 35 patients with <5 aberrations and 13 patients with <greater than or equal to>5 aberrations (P = 0.009). Univariate analysis showed that patients with gains of 1q, 2q, 12, and 20 or losses of 16q and 17p had significantly lower OAS than those without aberrations. By multivariate analysis, loss of 16q (relative risk [RR] = 5.3; P = 0.0006) was an independent prognostic factor. (C) 2001 Wiley-Liss, Inc.

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Documento generato il 05/04/20 alle ore 12:05:14