Isochromosome 8q formation is associated with 8p loss of heterozygosity ina prostate cancer cell line

Citation
Jb. Virgin et al., Isochromosome 8q formation is associated with 8p loss of heterozygosity ina prostate cancer cell line, PROSTATE, 41(1), 1999, pp. 49-57
Citations number
37
Categorie Soggetti
Urology & Nephrology","da verificare
Journal title
PROSTATE
ISSN journal
02704137 → ACNP
Volume
41
Issue
1
Year of publication
1999
Pages
49 - 57
Database
ISI
SICI code
0270-4137(19990915)41:1<49:I8FIAW>2.0.ZU;2-T
Abstract
BACKGROUND. In advanced prostate cancer, loss of chromosomal regions on 8p is frequently associated with gain of 8q. We studied the gross chromosomal abnormalities associated with 8p loss of heterozygosity (LOH) in the prosta te tumor cell line 1542 CP3Tx. The cell line was previously established fro m a primary prostatic adenocarcinoma by immortalization with a recombinant retrovirus carrying the E6 andE7 genes of human papilloma virus type 16. Al lelotyping studies demonstrated LOH at multiple markers on 8p. METHODS. To investigate the relationship of 8p LOH to gross chromosomal rea rrangements, and to screen for other genetic abnormalities in 1542 CP3Tx, w e used comparative genomic hybridization (CGH), conventional karyotyping, f luorescence in situ hybridization (FISH), and allelotyping. RESULTS. CGH revealed loss of the entire 8p arm, associated with gain of th e entire 8q arm. Other abnormalities included chromosome 4 loss and chromos ome 11 gain. The karyotype showed an isochromosome (8q), monosomy 4, and tr isomy 11. FISH and allelotyping confirmed and extended these results. CONCLUSIONS. These results demonstrate that i(8q) formation is a mechanism for associated 8p loss and 8q gain in prostate cancer. Furthermore, the sma ll number of chromosomal abnormalities in this cell line indicates that imm ortalization of low-passage cultures with viral oncogenes provides a method for obtaining cell lines for studying genetic abnormalities in prostate ca ncer. Prostate 41:49-57, 1999. (C) 1999 Wiley-Liss, Inc.