Abstract
(1) Background: Colorectal cancer (CRC) is the third most common cancer in human and the fourth leading cause of adult man’s death. Murine tumor cell lines have been established as a model system for CRC, but their cytogenetic properties have so far been only poorly understood. (2) Methods: The two murine colon tumor cell lines CMT-93 and CT26 (also called CT26.WT, CT-26 or CT-26 WT) were investigated in this study by molecular cytogenetic methods, i.e. by multicolor-fluorescence in situ hybridization (mFISH), murine multicolor banding (mcb), and array-based comparative genomic hybridization (aCGH). The thereby characterized chromosomal imbalances and chromosomal breakpoints were compared with those of human CRC by in-silico-translation of murine data into the human genome. (3) Results: CMT-93 and CT26 showed a hyperdiploid and hypertriploid karyotype, respectively. While only clonal aberrations of chromosomes 2, 5, 8, and X were observed for CMT-93, there was greater variability of chromosomal imbalances observed in CT26. Both cell lines tended to form dicentric and neocentric chromosomes and showed 17 (CMT-93) and 28 tumor-associated breakpoints (CT26). Interestingly, imbalances found were almost exclusively gains in somatic chromosomes. Also Y-chromosome was lost in CMT-93 as was loss of one of the X-chromosomes in CT26. In-silico-translation of the in both cell lines observed chromosomal imbalances showed a high agreement with the most frequently in human CRC observed metastatic amplifications. (4) Conclusions: This study revealed that murine tumor cell lines CMT-93 and CT26 are models for human CRCs of advanced tumor stages. This information is important to apply CMT-93 and CT26 for the correspondingly suited questions to be studied.
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