title: Genetic changes in pT2 and pT3 prostate cancer detected by comparative genomic hybridization.
abstract: Prostate-specific antigen (PSA) screening has led to a remarkable increase in prostate cancer cases undergoing operative therapy. Over half of patients with locally advanced cancer (>or=pT3) develop rising PSA levels (biochemical failure) within 10 years. It is very difficult to predict which patients will progress rapidly to advanced disease following biochemical failure (BF). Therefore, a more useful prognostic factor is needed to suggest the most appropriate therapies for each patient. To determine chromosomal aberrations, we examined 30 patients with stage pT2 or pT3 primary prostate adenocarcinomas and no metastases (pN0M0) by comparative genomic hybridization (CGH). Laser capture microdissection (LCM) was used to gather cancer cells from frozen prostate specimens. Common chromosomal alterations included losses on 2q23-24, 4q26-28, 6q14-22, 8p12-22 and 13q21-31, as well as gains on 1p32-36, 6p21 and 17q21-22. Losses at 8p12-22 and 13q21-31 were observed more frequently in pT3 than pT2 tumors (P<0.05 and P<0.01, respectively). Losses at 8p12-22 were more frequent in tumors with BF (P<0.05), and those at 13q12-21 were more frequent in tumors with Gleason score (GS) 7 or more than lower GS (P<0.05). These findings suggest that losses of 8p12-22 and 13q21-31 are important determinants of prostate cancer progression.
authors.affiliation: Department of Urology, Graduate School of Medicine, Chiba University, Chiba, Japan.
authors.forename: S
authors.initials: S
authors.lastname: Fukasawa
authors.forename: M
authors.initials: M
authors.lastname: Kino
authors.forename: M
authors.initials: M
authors.lastname: Kobayashi
authors.forename: H
authors.initials: H
authors.lastname: Suzuki
authors.forename: A
authors.initials: A
authors.lastname: Komiya
authors.forename: T
authors.initials: T
authors.lastname: Imamoto
authors.forename: Y
authors.initials: Y
authors.lastname: Hirokawa
authors.forename: T
authors.initials: T
authors.lastname: Shiraishi
authors.forename: M
authors.initials: M
authors.lastname: Takiguchi
authors.forename: H
authors.initials: H
authors.lastname: Ishida
authors.forename: T
authors.initials: T
authors.lastname: Shindo
authors.forename: N
authors.initials: N
authors.lastname: Seki
authors.forename: T
authors.initials: T
authors.lastname: Ichikawa
mesh_terms: D000230:Adenocarcinoma / Q000235:genetics* / Q000473:pathology*; D000368:Aged; D002869:Chromosome Aberrations; D002882:Chromosomes, Human, Pair 13; D002898:Chromosomes, Human, Pair 8; D020732:Cytogenetic Analysis / Q000379:methods*; D017353:Gene Deletion; D006801:Humans; D008297:Male; D008875:Middle Aged; D009367:Neoplasm Staging; D009693:Nucleic Acid Hybridization / Q000379:methods; D011471:Prostatic Neoplasms / Q000235:genetics* / Q000473:pathology*