PMID- 10379872
OWN - NLM
STAT- MEDLINE
DCOM- 19990716
LR  - 20191024
IS  - 1045-2257 (Print)
IS  - 1045-2257 (Linking)
VI  - 25
IP  - 3
DP  - 1999 Jul
TI  - 1q23 gain is associated with progressive neuroblastoma resistant to aggressive 
      treatment.
PG  - 261-9
AB  - Neuroblastoma is one of the most common malignant tumors of childhood and is 
      characterized by regressive and progressive disease. Genetic factors that define 
      progression of neuroblastomas are still unknown. We performed comparative genomic 
      hybridization (CGH) on 27 neuroblastomas and dual-color fluorescence in situ 
      hybridization (FISH) to identify genetic aberrations associated with progressive 
      neuroblastoma showing resistance to aggressive treatment. 17q21-q25 gains and 
      MYCN amplification were associated with stage 4 neuroblastomas; however, these 
      genetic aberrations had no significant relation to the progression of stage 4 
      neuroblastomas. A novel chromosomal gain at 1q21-q25 was found in 8 of 16 cases 
      (50%) of stage 4 neuroblastoma. Gain of 1q21-q25 was observed in all of the 
      progressive cases (8/8), which showed resistance to chemotherapy, including 5 
      fatal neuroblastomas in stage 4, whereas 1q21-q25 gain was not found in any of 
      the 8 remission cases in stage 4. Survival analysis also showed that 1q21-q25 
      gain was associated with a poor outcome. High xenotransplantability in nude mice 
      was observed for the tumors with 1q21-q25 gain (4/5; 80%). These data show that 
      1q21-q25 gain is strongly associated with progression of stage 4 neuroblastoma. 
      Furthermore, by dual-color FISH analysis using cosmid clones, the 1q21-q25 gain 
      was narrowed to increase in DNA copy number on 1q23 in the fatal type of stage 4 
      neuroblastoma showing this gain. These results suggest that DNA amplification at 
      1q23 may play a role in the development of progressive neuroblastoma in an 
      advanced stage.
FAU - Hirai, M
AU  - Hirai M
AD  - Department of Biochemistry and Molecular Oncology, Institute of Basic Medical 
      Sciences, University of Tsukuba, Ibaraki, Japan.
FAU - Yoshida, S
AU  - Yoshida S
FAU - Kashiwagi, H
AU  - Kashiwagi H
FAU - Kawamura, T
AU  - Kawamura T
FAU - Ishikawa, T
AU  - Ishikawa T
FAU - Kaneko, M
AU  - Kaneko M
FAU - Ohkawa, H
AU  - Ohkawa H
FAU - Nakagawara, A
AU  - Nakagawara A
FAU - Miwa, M
AU  - Miwa M
FAU - Uchida, K
AU  - Uchida K
LA  - eng
PT  - Comparative Study
PT  - Journal Article
PL  - United States
TA  - Genes Chromosomes Cancer
JT  - Genes, chromosomes & cancer
JID - 9007329
SB  - IM
MH  - Animals
MH  - Child
MH  - Child, Preschool
MH  - Chromosome Aberrations/*genetics
MH  - Chromosomes, Human, Pair 1/*genetics
MH  - Disease Progression
MH  - Drug Resistance, Neoplasm
MH  - Female
MH  - Gene Amplification/genetics
MH  - Gene Dosage
MH  - Humans
MH  - Infant
MH  - Male
MH  - Mice
MH  - Mice, Inbred BALB C
MH  - Mice, Nude
MH  - Neoplasm Staging
MH  - Neuroblastoma/drug therapy/*genetics/pathology
EDAT- 1999/06/24 10:00
MHDA- 2000/06/20 09:00
CRDT- 1999/06/24 10:00
PHST- 1999/06/24 10:00 [pubmed]
PHST- 2000/06/20 09:00 [medline]
PHST- 1999/06/24 10:00 [entrez]
AID - 10.1002/(SICI)1098-2264(199907)25:3<261::AID-GCC8>3.0.CO;2-# [pii]
AID - 10.1002/(sici)1098-2264(199907)25:3<261::aid-gcc8>3.0.co;2-# [doi]
PST - ppublish
SO  - Genes Chromosomes Cancer. 1999 Jul;25(3):261-9. doi: 
      10.1002/(sici)1098-2264(199907)25:3<261::aid-gcc8>3.0.co;2-#.