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Fluorescence in situ hybridization analyses of chromosome band 1p36 in neuroblastoma detect two classes of alterations.
Genes Chromosomes Cancer. 2002 Jul; 34(3):299-305.GC

Abstract

Chromosomal alterations in 1p36 were investigated in 196 neuroblastoma tumors using fluorescence in situ hybridization. Additionally, by using the same technique, it was determined whether MYCN was amplified in 149 of these. The most frequent finding was a deletion in 1p36, leading to monosomy of this region (29 cases, 15%). Furthermore, we found tumors with at least two intact copies of chromosome 1 and additional 1p36-deleted copies. Altogether, 21 tumors (11%) displayed this imbalance of 1p36. Similar to the cases with deletion, imbalances were predominantly found in stage 4 tumors (81%), and they were significantly associated with an increased patient age (P = 0.01). Nearly all 1p-deleted tumors showed amplification of MYCN (24/27 analyzed samples, 89%), whereas only 8 of 21 (38%) with imbalance did. Eight cases with imbalance were investigated for loss of heterozygosity (LOH) using microsatellite markers in 1p35-36. Only 4 displayed 1p36 LOH, whereas the remaining 4 were heterozygous. Both patients with deletion of 1p and with imbalance had a poor outcome [3-year rate of event-free-survival (EFS): 33 +/- 15% and 41 +/- 15%], which was significantly worse compared to the outcome of patients without 1p alterations (3-year EFS: 70 +/- 5%; P = 0.01 and P = 0.0059). We conclude that besides monosomic short arm deletions, imbalance of 1p36 is a strong marker of a poor prognosis in neuroblastoma and not necessarily associated with MYCN amplification and LOH.

Authors+Show Affiliations

University Children's Hospital, Department of Pediatric Oncology, Cologne, Germany. Ruediger.Spitz@medizin.uni-koeln.deNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

12007190

Citation

Spitz, Ruediger, et al. "Fluorescence in Situ Hybridization Analyses of Chromosome Band 1p36 in Neuroblastoma Detect Two Classes of Alterations." Genes, Chromosomes & Cancer, vol. 34, no. 3, 2002, pp. 299-305.
Spitz R, Hero B, Westermann F, et al. Fluorescence in situ hybridization analyses of chromosome band 1p36 in neuroblastoma detect two classes of alterations. Genes Chromosomes Cancer. 2002;34(3):299-305.
Spitz, R., Hero, B., Westermann, F., Ernestus, K., Schwab, M., & Berthold, F. (2002). Fluorescence in situ hybridization analyses of chromosome band 1p36 in neuroblastoma detect two classes of alterations. Genes, Chromosomes & Cancer, 34(3), 299-305.
Spitz R, et al. Fluorescence in Situ Hybridization Analyses of Chromosome Band 1p36 in Neuroblastoma Detect Two Classes of Alterations. Genes Chromosomes Cancer. 2002;34(3):299-305. PubMed PMID: 12007190.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Fluorescence in situ hybridization analyses of chromosome band 1p36 in neuroblastoma detect two classes of alterations. AU - Spitz,Ruediger, AU - Hero,Barbara, AU - Westermann,Frank, AU - Ernestus,Karen, AU - Schwab,Manfred, AU - Berthold,Frank, PY - 2002/5/15/pubmed PY - 2002/6/29/medline PY - 2002/5/15/entrez SP - 299 EP - 305 JF - Genes, chromosomes & cancer JO - Genes Chromosomes Cancer VL - 34 IS - 3 N2 - Chromosomal alterations in 1p36 were investigated in 196 neuroblastoma tumors using fluorescence in situ hybridization. Additionally, by using the same technique, it was determined whether MYCN was amplified in 149 of these. The most frequent finding was a deletion in 1p36, leading to monosomy of this region (29 cases, 15%). Furthermore, we found tumors with at least two intact copies of chromosome 1 and additional 1p36-deleted copies. Altogether, 21 tumors (11%) displayed this imbalance of 1p36. Similar to the cases with deletion, imbalances were predominantly found in stage 4 tumors (81%), and they were significantly associated with an increased patient age (P = 0.01). Nearly all 1p-deleted tumors showed amplification of MYCN (24/27 analyzed samples, 89%), whereas only 8 of 21 (38%) with imbalance did. Eight cases with imbalance were investigated for loss of heterozygosity (LOH) using microsatellite markers in 1p35-36. Only 4 displayed 1p36 LOH, whereas the remaining 4 were heterozygous. Both patients with deletion of 1p and with imbalance had a poor outcome [3-year rate of event-free-survival (EFS): 33 +/- 15% and 41 +/- 15%], which was significantly worse compared to the outcome of patients without 1p alterations (3-year EFS: 70 +/- 5%; P = 0.01 and P = 0.0059). We conclude that besides monosomic short arm deletions, imbalance of 1p36 is a strong marker of a poor prognosis in neuroblastoma and not necessarily associated with MYCN amplification and LOH. SN - 1045-2257 UR - https://www.unboundmedicine.com/medline/citation/12007190/Fluorescence_in_situ_hybridization_analyses_of_chromosome_band_1p36_in_neuroblastoma_detect_two_classes_of_alterations_ L2 - https://onlinelibrary.wiley.com/resolve/openurl?genre=article&sid=nlm:pubmed&issn=1045-2257&date=2002&volume=34&issue=3&spage=299 DB - PRIME DP - Unbound Medicine ER -