Allelic loss on chromosome 6q in primary prostate cancer

Citation
V. Srikantan et al., Allelic loss on chromosome 6q in primary prostate cancer, INT J CANC, 84(3), 1999, pp. 331-335
Citations number
23
Categorie Soggetti
Onconogenesis & Cancer Research
Journal title
INTERNATIONAL JOURNAL OF CANCER
ISSN journal
00207136 → ACNP
Volume
84
Issue
3
Year of publication
1999
Pages
331 - 335
Database
ISI
SICI code
0020-7136(19990621)84:3<331:ALOC6I>2.0.ZU;2-Z
Abstract
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.