High frequency of clonal chromosome abnormalities in prostatic neoplasms sampled by prostatectomy or ultrasound-guided needle biopsy

Cancer of the prostate remains poorly characterized cytogenetically. This is due in part to methodological problems and in part to the paucity of radical prostatectomies, until now the main source of material for cytogenetic analyses. We have improved existing techniques for the culturing of prostat...

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Bibliographic Details
Published in:Genes chromosomes & cancer 2000-06, Vol.28 (2), p.211-219
Main Authors: Teixeira, Manuel R., Wæhre, Håkon, Lothe, Ragnhild A., Stenwig, Anna E., Pandis, Nikos, Giercksky, Karl E., Heim, Sverre
Format: Article
Language:English
Subjects:
Biopsy, Needle
Chromosome Aberrations - diagnostic imaging
Chromosome Aberrations - genetics
Chromosome Aberrations - pathology
Chromosome Disorders
Clone Cells
Humans
In Situ Hybridization, Fluorescence
Karyotyping
Male
Prostatectomy - methods
Prostatic Neoplasms - diagnostic imaging
Prostatic Neoplasms - genetics
Prostatic Neoplasms - pathology
Ultrasonography
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Summary:Cancer of the prostate remains poorly characterized cytogenetically. This is due in part to methodological problems and in part to the paucity of radical prostatectomies, until now the main source of material for cytogenetic analyses. We have improved existing techniques for the culturing of prostatic neoplasms removed by radical prostatectomy or sampled by ultrasound‐guided needle biopsy. Successful short‐term cultures were obtained from all 10 prostatectomy samples and from all 10 ultrasound‐guided needle biopsies, always with a pure epithelial morphology. Of the 19 cases yielding a sufficient number of high‐quality metaphases for chromosome banding analysis, the single 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%) karyotypically abnormal invasive carcinomas presented structural chromosomal rearrangements. A recurrent deletion, del(10)(p13), was seen in three tumors; in one of 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 probably was no inactivation of the second TP53 allele. Our study thus leads to the following main conclusions. First, better culturing methods allow the detection of abnormal karyotypes in a much higher percentage of prostatic neoplasms than has hitherto been possible. Second, ultrasound‐guided needle biopsies of prostatic neoplasms are a sufficient source of material for cytogenetic analysis. Third, a terminal deletion of the short arm of chromosome 10, del(10)(p13), seems to identify a subgroup of prostatic cancer. Genes Chromosomes Cancer 28:211–219, 2000. © 2000 Wiley‐Liss, Inc.
ISSN:1045-2257
1098-2264
DOI:10.1002/(SICI)1098-2264(200006)28:2<211::AID-GCC10>3.0.CO;2-Y