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Karyotypic similarity identified by multiplex‐FISH relates four prostate adenocarcinoma cell lines: PC‐3, PPC‐1, ALVA‐31, and ALVA‐41
Author(s) -
VarellaGarcia Marileila,
Boomer Theresa,
Miller Gary J.
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/gcc.1149
Subject(s) - karyotype , metaphase , biology , multiplex , fish <actinopterygii> , adenocarcinoma , computational biology , cell culture , somatic evolution in cancer , genetics , microbiology and biotechnology , cancer , gene , chromosome , fishery
Recently developed molecular cytogenetic techniques for karyotyping are providing new and important insights regarding the chromosomal changes that occur in solid tumors. We used multiplex‐FISH to analyze four adenocarcinoma cell lines, PC‐3, PPC‐1, ALVA‐31, and ALVA‐41, in which the characterization of a large number of rearranged chromosomes was partially or substantially inconclusive by G‐banding. Although the original descriptions of these lines depict them as distinct entities established from different patients, this study demonstrates that these four lines share numerous, highly rearranged chromosomes, strongly supporting the conclusion that they are derived from the same patient material. Our analysis indicates that PPC‐1, ALVA‐31, and ALVA‐41 were derived from PC‐3 through mechanisms involving clonal progression represented by sequential changes and clonal diversion represented by differing patterns of changes. Extensive cellular heterogeneity was detected in all four lines, and most rearrangements included segments derived from multiple chromosomes. Each line also showed a set of unique derivative chromosomes. However, a limited number of metaphase cells (approximately 10) was analyzed for each line, and numerous single‐cell abnormalities were detected in all of them. Therefore, it is plausible that the number of clonal, shared, and/or unique rearrangements has been underestimated. These cell lines have been utilized as models for understanding the biology of prostate cancer and reportedly differ in their cell physiology. Rather than detracting from their value, a complete understanding of the interrelationships of these lines to one another may provide the opportunity to define the molecular changes that have led to their individual malignant phenotypes. © 2001 Wiley‐Liss, Inc.