PMID- 9485032
OWN - NLM
STAT- MEDLINE
DCOM- 19980319
LR  - 20071114
IS  - 0008-5472 (Print)
IS  - 0008-5472 (Linking)
VI  - 58
IP  - 4
DP  - 1998 Feb 15
TI  - A molecular cytogenetic analysis of 7q31 in prostate cancer.
PG  - 759-66
AB  - Gains of chromosome 7 and alterations of the 7q-arm have been frequently observed 
      in multiple cancers using various cytogenetic and molecular genetic techniques. 
      Using PCR analysis of microsatellite markers, we have previously reported that 
      allelic imbalance of 7q31 is common in prostate cancer and is associated with 
      higher tumor grade and advanced pathological stage. In an effort to better 
      understand the chromosome 7 alterations in prostate cancer, we undertook a 
      molecular cytogenetic study of 25 prostate specimens using fluorescence in situ 
      hybridization (FISH) with DNA probes for the chromosome 7 centromere and for 5 
      loci mapped to 7q31 (D7S523, D7S486, D7S522, D7S480, and D7S490) and 1 locus at 
      7q11.23 (ELN). Six tumors had no apparent anomaly for any chromosome 7 probe. 
      Nine tumors showed apparent simple gain of a whole chromosome 7, whereas one 
      tumor had apparent simple loss of a whole chromosome 7. Four tumors had gain of 
      the chromosome 7 centromere and additional overrepresentation of the 7q-arm. One 
      tumor had overrepresentation of 7q31 without any apparent anomaly of the 
      chromosome 7 centromere, and one tumor had apparent loss of the chromosome 7 
      centromere with no apparent anomaly of the 7q-arm. Three tumors had gain of the 
      chromosome 7 centromere and loss of the 7q31 region. Gain of 7q31 was strongly 
      correlated with tumor Gleason score. Multiplex PCR studies of these specimens 
      supported these FISH observations. Mutation screening and DNA sequencing of the 
      MET gene, which is mapped to 7q31, revealed only the presence of simple sequence 
      polymorphisms but no apparent acquired disease-associated mutations. FISH 
      analysis of metaphases from an aphidicolin-induced, chromosome 7 only, somatic 
      cell hybrid demonstrated that the DNA probe for D7S522 spans the common fragile 
      site FRA7G at 7q31. Our data indicate that the 7q-arm, particularly the 7q31 
      region, is genetically unstable in prostate cancer, and some of the gene dosage 
      differences observed may be due to fragility at FRA7G.
FAU - Jenkins, R B
AU  - Jenkins RB
AD  - Department of Laboratory Medicine, Mayo Clinic, Rochester, Minnesota 55905, USA.
FAU - Qian, J
AU  - Qian J
FAU - Lee, H K
AU  - Lee HK
FAU - Huang, H
AU  - Huang H
FAU - Hirasawa, K
AU  - Hirasawa K
FAU - Bostwick, D G
AU  - Bostwick DG
FAU - Proffitt, J
AU  - Proffitt J
FAU - Wilber, K
AU  - Wilber K
FAU - Lieber, M M
AU  - Lieber MM
FAU - Liu, W
AU  - Liu W
FAU - Smith, D I
AU  - Smith DI
LA  - eng
GR  - P20 CA 58225/CA/NCI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Cancer Res
JT  - Cancer research
JID - 2984705R
RN  - 0 (Proto-Oncogene Proteins)
SB  - IM
MH  - *Chromosome Aberrations
MH  - Chromosome Breakage
MH  - Chromosome Deletion
MH  - Chromosome Fragile Sites
MH  - *Chromosome Fragility
MH  - *Chromosomes, Human, Pair 7
MH  - DNA Mutational Analysis
MH  - Gene Dosage
MH  - Humans
MH  - In Situ Hybridization, Fluorescence
MH  - Male
MH  - Monosomy
MH  - Polymerase Chain Reaction
MH  - Prostatic Neoplasms/*genetics
MH  - Proto-Oncogene Proteins/genetics
MH  - Trisomy
EDAT- 1998/03/04 00:00
MHDA- 1998/03/04 00:01
CRDT- 1998/03/04 00:00
PHST- 1998/03/04 00:00 [pubmed]
PHST- 1998/03/04 00:01 [medline]
PHST- 1998/03/04 00:00 [entrez]
PST - ppublish
SO  - Cancer Res. 1998 Feb 15;58(4):759-66.