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 genetic factors. However, tumors that lack high-risk factors such as MYCN amplification or 1p deletion may progress, possibly due to other genetic aberrations. Comparative genomic hybridization summarizes DNA copy number abnormalities in a tumor by mapping them to their positions on normal metaphase chromosomes. We analyzed 29 tumors from nearly equal proportions of children with stage I, II, III, IV, and IV-S disease by comparative genomic hybridization. We found two classes of copy number abnormalities: whole chromosome and partial chromosome. Whole chromosome losses were frequent at 11, 14, and X. The most frequent partial chromosome losses were on 1p and 11q. Gains were most frequent on chromosome 17 (72% of cases). The two patterns of gain for this chromosome were whole 17 gain and 17q gain, with 17q21-qter as a minimal common region of gain. Other common gains were on 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 and/or 11q deletions and advanced stage. The high frequency of chromosome 17 gain and its association with bad prognostic factors suggest an important role for this chromosome in the development of neuroblastoma.
Plantaz
D
D
Department of Laboratory Medicine, Division of Molecular Cytometry, University of California, San Francisco 94143-0808, USA.
Mohapatra
G
G
Matthay
K K
KK
Pellarin
M
M
Seeger
R C
RC
Feuerstein
B G
BG
D002675:Child, Preschool; D002869:Chromosome Aberrations / Q000235:genetics* / Q000473:pathology*; D025063:Chromosome Disorders; D002886:Chromosomes, Human, Pair 17; D002889:Chromosomes, Human, Pair 2; D017353:Gene Deletion; D016259:Genes, myc; D006801:Humans; D017404:In Situ Hybridization, Fluorescence / Q000379:methods; D007223:Infant; D008297:Male; D009447:Neuroblastoma / Q000235:genetics* / Q000473:pathology*