Molecular genetic analyses of human prostate cancer (CaP) has revealed freq
uent loss of specific chromosome regions suggesting the presence of putativ
e tumor suppressor gene(s) (TSG) on these chromosome loci whose inactivatio
n may play a role in prostate tumorigenesis. To understand the role of 6q a
lterations in CaP, we have undertaken a comprehensive analysis of proximal
6q. Genomic DNA from tumor and normal prostate tissues from radical prostat
ectomy specimens of 38 patients were analyzed by polymerase chain reaction
(PCR) for 13 polymorphic microsatellite loci on 6q. Allelic losses of 1 or
more polymorphic loci were detected in 11 of 38 patients (29%). Six of 11 t
umors showing any 6q deletion were found to have allelic losses at D6S1056
and D6S300 loci. Our results revealed a 1.5 megabase interval between D6S10
56 and D6S300 at 6q16.3-21 as the minimal region of deletion, which may con
tain the putative TSG involved in prostate tumorigenesis. One of the tumor
samples demonstrated homozygous deletion at a distal location D6S314 (6q23-
24), suggesting another locus potentially associated with Cap. Although the
relationship of 6q loss of heterozygosity (LOH) with various clinico-patho
logic variables, i.e., cancer recurrence or pathologic stage, did not revea
l a statistically significant association, the risk for 6q LOH to non-organ
confined (pT3) disease was 5-fold higher than for organ confined disease.
Int. J. Cancer (Pred. Oncol) 84:331-335, 1999. (C) 1999 Wiley-Liss, Inc.