Genetic changes in familial prostate cancer by comparative genomic hybridization.
BACKGROUND
Germline mutations in recessive cancer predisposition genes are uncovered by somatic genetic deletions during tumor development. Analysis of genetic changes in tumor tissues from patients with an inherited predisposition may therefore highlight regions of the genome containing susceptibility or modifier genes. Our aim was to characterize genetic changes in familial prostate cancer


METHODS
Twenty-one primary prostate cancers from 19 Finnish prostate cancer families were analyzed for somatic genetic changes by comparative genomic hybridization (CGH).


RESULTS
The average number of genetic alterations per tumor was 4.0 +/- 1.9, distributed equally among losses and gains. The most common losses were found at chromosomal regions 13q14-q22 (29%), 8p12-pter (24%), and 6q13-q16 (14%), and the most common gains at 19p (25%), 19q (14%) and 7q (14%).


CONCLUSIONS
These results suggest that prostate cancers in genetically predisposed individuals arise for the most part through similar somatic genetic progression pathways as sporadic prostate cancers. This also implies that the biological properties of tumors from the two groups may not be different from one another.
Rökman
A
A
Laboratory of Cancer Genetics, Institute of Medical Technology, University of Tampere and Tampere University Hospital, Lenkkeilijänkatu 8, P.O. Box 607, FIN-33101 Tampere, Finland. loanro@uta.fi
Koivisto
P A
PA
Matikainen
M P
MP
Kuukasjärvi
T
T
Poutiainen
M
M
Helin
H J
HJ
Karhu
R
R
Kallioniemi
O P
OP
Schleutker
J
J
D000368:Aged; D000369:Aged, 80 and over; D002277:Carcinoma / Q000235:genetics*; D002869:Chromosome Aberrations; D020022:Genetic Predisposition to Disease / Q000235:genetics; D006801:Humans; D007621:Karyotyping; D008297:Male; D008875:Middle Aged; D009693:Nucleic Acid Hybridization; D011471:Prostatic Neoplasms / Q000235:genetics*