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5q11, 8p11, and 10q22 are recurrent chromosomal breakpoints in prostate cancer cell lines
Author(s) -
Pan Yi,
Lui WengOnn,
Nupponen Nina,
Larsson Catharina,
Visakorpi Tapio,
Bergerheim Ulf S.R.,
Kytölä Soili
Publication year - 2001
Publication title -
genes, chromosomes and cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.754
H-Index - 119
eISSN - 1098-2264
pISSN - 1045-2257
DOI - 10.1002/1098-2264(2000)9999:9999<::aid-gcc1075>3.0.co;2-h
Subject(s) - comparative genomic hybridization , du145 , biology , breakpoint , lncap , karyotype , genetics , medulloblastoma , prostate cancer , cancer research , cancer , prostate , gene , chromosomal translocation , microbiology and biotechnology , chromosome
Prostate cancer cell lines have been widely used as model systems characterizing pathogenetic, functional, and therapeutic aspects of prostate cancer development. However, their chromosomal compositions are poorly characterized. In this study, five prostate cancer cell lines—TSU‐Pr1, JCA‐1, NCI‐H660, ALVA‐31, and PPC‐1—were investigated by G‐banding, comparative genomic hybridization (CGH), and spectral karyotyping. The results were combined with our previous findings in the prostate cancer cell lines PC‐3, DU145, and LNCaP. By comparative genomic hybridization (CGH), the most frequent losses were observed at 13q, 8p, 9p, and 4q, whereas gains were most commonly seen at 8q, 10q, and 18p. The composite karyotypes were characterized by multiple numerical and structural chromosomal aberrations. Recurrent breakpoints at 5q11, 8p11, and 10q22 were observed to participate in deletion and translocation events in five of the cell lines, suggesting the importance of tumor suppressor and/or oncogenes in these regions. ALVA‐31 and PPC‐1 shared nine identical derivative chromosomes, two of which have also been detected in PC‐3. In addition, the identification of the same homozygous deletion at D10S541 and of an identical TP53 gene mutation in all three cell lines suggests a common origin of these cell lines. © 2000 Wiley‐Liss, Inc.