Different mechanisms of mitotic instability in cancer cell lines

  • Authors:
    • Alexandra Klein
    • Klaus D. Zang
    • Wolf-Ingo Steudel
    • Steffi Urbschat
  • View Affiliations

  • Published online on: December 1, 2006     https://doi.org/10.3892/ijo.29.6.1389
  • Pages: 1389-1396
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Abstract

Chromosomes of human malignant tumours display not only structural recombinations but also a wide variety of mostly non-random numerical aberrations. However, only little is known about the mechanisms leading to recurrent aneuploidies. We therefore investigated whether the malsegregation of specific chromosomes is due to a defect of the mitotic spindle apparatus. We analyzed mitoses of cell lines of six gliomas and of one breast carcinoma by combined immunohistochemistry and fluorescence in situ hybridization for non-disjunction of chromosomes 7, 8, 10, 12, 17, and 18 and observed three different phenomena. i) Five of six glioma cell lines showed a bipolar spindle but displayed a chromosome-specific malsegregation of all chromosomes studied with high but significantly different frequencies. Chromosomes 7 and 8 showed non-disjunction in about 75 and 50%, respectively. Although chromosomes 10, 12, 17, and 18 displayed equal separation during mitosis in 72, 86, 73, and 78%, respectively, a relevant percentage of an average of 24% of dividing cells showed even malsegregation of these chromosomes. ii) Only one of the glioma cell lines displayed multipolar spindles in one-third of the investigated cells resulting in non-specific aneuploidy. iii) The breast cancer cell line MCF7 displayed a bipolar spindle, but high frequencies of non-disjunction of all six investigated chromosomes but without preferential loss or gain of specific chromosomes indicating a different mechanism of chromosome malsegregation. In a small percentage of mitoses the chromatids of both homologous chromosomes were not separated mimicking the mechanism in the first meiotic division. This mechanism of double non-disjunction, not detectable by conventional cytogenetic analysis, procreates cell clones with genomic separation for particular chromosomes resulting in homozygosity for mutations which had been present heterozygously in the initial tumour cells.

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December 2006
Volume 29 Issue 6

Print ISSN: 1019-6439
Online ISSN:1791-2423

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Spandidos Publications style
Klein A, Zang KD, Steudel W and Urbschat S: Different mechanisms of mitotic instability in cancer cell lines. Int J Oncol 29: 1389-1396, 2006.
APA
Klein, A., Zang, K.D., Steudel, W., & Urbschat, S. (2006). Different mechanisms of mitotic instability in cancer cell lines. International Journal of Oncology, 29, 1389-1396. https://doi.org/10.3892/ijo.29.6.1389
MLA
Klein, A., Zang, K. D., Steudel, W., Urbschat, S."Different mechanisms of mitotic instability in cancer cell lines". International Journal of Oncology 29.6 (2006): 1389-1396.
Chicago
Klein, A., Zang, K. D., Steudel, W., Urbschat, S."Different mechanisms of mitotic instability in cancer cell lines". International Journal of Oncology 29, no. 6 (2006): 1389-1396. https://doi.org/10.3892/ijo.29.6.1389