Combined cytogenetic and molecular genetic analyses of fifty-nine untreated human prostate carcinomas

Abstract

G-banding analyses and molecular genetic investigations (fluorescence in situ hybridization (FISH) and loss of heterozygosity (LOH) studies) were performed in 59 tumor and nontumorous samples of human prostate carcinoma. Clonal chromosome aberrations were detected in 16 tumors of which nine were poorly differentiated (G3) and 11 in an advanced stage (pT3). Six cases showed numerical chromosome aberrations. The most common numerical aberrations were trisomy 7 and loss of the Y chromosome each present in three tumors. Clonal structural aberrations were detected in 12 tumors. Deletions could be observed in two cases affecting chromosome 6q23 and in two cases affecting chromosomal region 16q. A structural variant of the pericentromeric heterochromatin of chromosome 9 became apparent in six cases. The Y chromosome was involved in clonal translocations in two cases, additionally an inversion occurred on chromosome 19 in one case. All clonal chromosomal changes were found exclusively in the tumor sample. For an analysis of the pericentromeric heterochromatin of chromosome 9, FISH using a chromosome 9-specific sat III DNA probe was carried out on metaphase preparations of tumor and nontumorous tissues of two cases showing var(9)(qh). The FISH data suggest a deletion in the pericentromeric heterochromatin. Loss of heterozygosity studies on chromosomal regions 10q and 16q were carried out because both chromosomes were frequently affected by nonclonal structural aberrations. Loss of heterozygosity could be verified in 11 cases.