Here, we report the first molecular cytogenetic characterization of the BALB/cAnN mouse derived B-cell non-Hodgkin lymphoma (B-cell NHL) cell lines A-20. Even though previously used as a model for testing of, for example, dexametason, up to present, no data in the genetic properties of A-20 were available. The present study closed this gap and provides evidence that A-20 is a model for B-cell NHL subgroup sporadic Burkitt's lymphoma. C-myc oncogene is involved in a translocation and copy number alterations as gain of murine 14q material could be observed. Interestingly, the cell line showed the karyotype 39,X,-X or -Y,t(2;15)(qE5;qD2),del(6)(qB3qC3),del(9)(qA3qA4),dup(14)(qE1qE4) in ~95% of the cells, being exceptionally stable for cell lines being established 38 years ago. Still, ~5% of the cells showed polyploidization followed by chromothripsis. It remains to be determined if this can be observed also in other cell lines, just has not been reported yet, and/or if it is a unique feature of A-20. Overall, finally here, the necessary genetic data to identify A-20 as a model for human sporadic Burkitt's lymphoma are provided.
Background: Colorectal cancer (CRC) is the third most common cancer in human, and the fourth leading cause of death in adult men. Murine tumor cell lines have been established as model systems for CRC, but their cytogenetic properties have yet to be fully understood. 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 using molecular cytogenetic methods, i.e., multicolor-fluorescence in situ hybridization (mFISH), murine multicolor banding (mcb), and array-based comparative genomic hybridization (aCGH). The chromosomal imbalances and breakpoints characterized by these methods were compared with those of human CRCs using an in-silico-translation of murine data into the human genome. Results: CMT-93 and CT26 expressed 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), respectively. Interestingly, the imbalances found were almost exclusively gains in somatic chromosomes. In addition, the Ychromosome was lost in CMT-93, as was 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 observed metastatic amplifications in human CRCs. Conclusions: The findings of our study revealed that murine tumor cell lines CMT-93 and CT26 are models for human CRCs of advanced-stage tumors. The information gained here is imperative for the application of CMT-93 and CT26 for future research in CRC.
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