Chromosomal changes during development and progression of prostate adenocarcinomas

Chromosomal copy number changes were investigated in 16 prostate carcinomas , 12 prostatic intraepithelial neoplasias (PIN; 4 low-grade and 8 high-grad e) adjacent to the invasive tumour areas, and 5 regional lymph node metasta ses, For this purpose, comparative genomic hybridization (CGH) was performe d and a copy number karyotype for each histomorphological entity was create d. CGH on microdissected cells from non-neoplastic glands was carried out o n 3 different cases to demonstrate the reliability of the overall procedure . None of the non-neoplastic tissue samples revealed chromosome copy number changes. In PIN areas, chromosomal imbalances were detected on chromosomes 7, 8q, Xq (gains), and on 4q, 5q, 8q, 13q and 18q (losses). In the primary tumours, recurrent (at least 25% of cases) gains on chromosomes 12q and 15 q, and losses on 2q, 4q, 5q, Xq, 13q and 18q became apparent. Losses on 8p and 6q as well as gains on 8q and of chromosome 7 were also detected at low er frequencies than previously reported. The pooled CGH data from the prima ry carcinomas revealed a novel region of chromosomal loss on 4q which is al so frequently affected in other tumour entities like oesophageal adenocarci nomas and is supposed to harbour a new tumour suppressor gene. Gains on chr omosome 9q and of chromosome 16 and loss on chromosome 13q were observed as common aberrations in metastases and primary tumours. These CGH results in dicate an accumulation of chromosomal imbalances during the PIN-carcinoma-m etastasis sequence and an early origin of tumour-specific aberrations in PI N areas. (C) 2001 Cancer Research Campaign.