Mr. Teixeira et al., High frequency of clonal chromosome abnormalities in prostatic neoplasms sampled by prostatectomy or ultrasound-guided needle biopsy, GENE CHROM, 28(2), 2000, pp. 211-219
Cancer of the prostate remains poorly characterized cytogenetically. This i
s due in part to methodological problems and in part to the paucity of radi
cal prostatectomies, until now the main source of material for cytogenetic
analyses. We have improved existing techniques for the culturing of prostat
ic neoplasms removed by radical prostatectomy or sampled by ultrasound-guid
ed needle biopsy, Successful short-term cultures were obtained from all 10
prostatectomy samples and from all 10 ultrasound-guided needle biopsies, al
ways with a pure epithelial morphology. Of the 19 cases yielding a sufficie
nt number of high-quality metaphases for chromosome banding analysis, the s
ingle atypical epithelial hyperplasia had a normal karyotype, whereas both
prostatic intraepithelial neoplasias and 12 of 16 (75%) invasive carcinomas
were shown to have clonal abnormalities. Ten of the 12 (83%) karyotypicall
y abnormal invasive carcinomas presented structural chromosomal rearrangeme
nts. A recurrent deletion, del(10)(p13), was seen in three tumors; in one o
f them the terminal nature of the deletion was confirmed by two-color FISH.
A del(17)(p11) was seen in one PIN lesion, but since the analysis of exons
4-8 of the TP53 tumor suppressor gene revealed no mutations, there probabl
y was no inactivation of the second TP53 allele. Our study thus leads to th
e following main conclusions. First, better culturing methods allow the det
ection of abnormal karyotypes in a much higher percentage of prostatic neop
lasms than has hitherto been possible. Second, ultrasound-guided needle bio
psies of prostatic neoplasms are a sufficient source of material for cytoge
netic analysis. Third, a terminal deletion of the short arm of chromosome 1
0, del(10)(p13), seems to identify a subgroup of prostatic cancer. Genes Ch
romosomes Cancer 28:211-219, 2000. (C) 2000 Wiley-Liss, Inc.