Molecular analysis of chromosome arm 17q gain neuroblastoma

Complete or partial gain of the long arm of chromosome 17 (17q) has been sh own recently by molecular cytogenetic techniques to be the most frequent ch romosomal change in neuroblastoma and to be associated with adverse prognos is. Few reports, however, have focused on the precise mapping of the common ly 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 consecu tive loci were observed in 39/59 informative cases, that is in agreement wi th previously reported frequencies of 17q gain. in a subset of the cases, c omparative genomic hybridization analysis established the relationship betw een these allelic imbalances and the gain of 17q material. A partial 17q ga in was observed in 9 cases, delineating a common region of 17q gain between the marker D17S787 (75 cM, 360 cR) and the telomere. In most cases, molecu lar results were suggestive of partial tri- or tetrasomy, whereas in 4 case s a higher copy number was documented. Our results also confirm that the pr esence of additional 17q material is closely associated with 1 p36 deletion , MYCN amplification, and diploid or tetraploid chromosomal content. (C) 20 00 Wiley-Liss, Inc.