Premium
Molecular analysis of chromosome arm 17q gain in neuroblastoma
Author(s) -
JanoueixLerosey Isabelle,
Penther Dominique,
Thioux Martine,
de Crémoux Patricia,
Derré Josette,
Ambros Peter,
Vielh Philippe,
Bénard Jean,
Aurias Alain,
Delattre Olivier
Publication year - 2000
Publication title -
genes, chromosomes and cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.754
H-Index - 119
eISSN - 1098-2264
pISSN - 1045-2257
DOI - 10.1002/1098-2264(200007)28:3<276::aid-gcc5>3.0.co;2-p
Subject(s) - biology , genetics , chromosome , ploidy , allele , neuroblastoma , tetrasomy , comparative genomic hybridization , chromosome 17 (human) , isochromosome , cytogenetics , gene , microbiology and biotechnology , karyotype , cell culture
Complete or partial gain of the long arm of chromosome 17 (17q) has been shown recently by molecular cytogenetic techniques to be the most frequent chromosomal change in neuroblastoma and to be associated with adverse prognosis. Few reports, however, have focused on the precise mapping of the commonly overrepresented region. We have investigated 17q gain by the analysis of allelic imbalances at microsatellite loci dispersed along chromosome 17 in a series of 69 neuroblastomas. Allelic imbalances for at least two consecutive loci were observed in 39/59 informative cases, that is in agreement with previously reported frequencies of 17q gain. In a subset of the cases, comparative genomic hybridization analysis established the relationship between these allelic imbalances and the gain of 17q material. A partial 17q gain was observed in 9 cases, delineating a common region of 17q gain between the marker D 17 S 787 (75 cM, 360 cR) and the telomere. In most cases, molecular results were suggestive of partial tri‐ or tetrasomy, whereas in 4 cases a higher copy number was documented. Our results also confirm that the presence of additional 17q material is closely associated with 1p36 deletion, MYCN amplification, and diploid or tetraploid chromosomal content. Genes Chromosomes Cancer 28:276–284, 2000. © 2000 Wiley‐Liss, Inc.