GAIN OF CHROMOSOME-17 IS THE MOST FREQUENT ABNORMALITY DETECTED IN NEUROBLASTOMA BY COMPARATIVE GENOMIC HYBRIDIZATION

Neuroblastoma behavior is variable and outcome partially depends on ge netic factors, However, tumors that lack high-risk factors such as MYC N amplification or 1p deletion may progress, possibly due to other gen etic aberrations. Comparative genomic hybridization summarizes DNA cop y number abnormalities in a tumor by mapping them to their positions o n normal metaphase chromosomes, We analyzed 23 tumors from nearly equa l proportions of children with stage I, II, III, IV, and IV-S disease by comparative genomic hybridization. We found two classes of copy num ber abnormalities: whole chromosome and partial chromosome, Whole chro mosome losses were frequent at 11, 14, and X. The most frequent partia l chromosome losses were on 1p and 11p. Gains were most frequent on ch romosome 17(72% of cases). The two patterns of gain for this chromosom e were whole 17 gain and 17q gain, with 17q21-qter as a minimal common region of gain, Other common gains were oil chromosomes 7, 6, and 18. High level amplifications were detected at 2p23-25 (MYCN region), at 4q33-35 and at 6p11-22. Chromosome 17q gains were associated with 1p a nd/or 11q deletions and advanced stage. The high frequency of chromoso me 17 gain and its association with bad prognostic factors suggest an important role for this chromosome in the development of neuroblastoma .