Role of telomeric sequences in murine radiation-induced myeloid leukaemia

E. I.M. Meijne, A. R.J. Silver*, Simon Bouffler, D. J. Morris, E. Winter Van Kampen, S. Spanjer, R. Huiskamp, R. Cox

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

10 Citations (Scopus)


A previous study indicated that a highly inbred CBA/H mouse colony contained four genotypic variants for telomere-like repeat (TLR) sequence arrays and that one variant subpopulation that constituted 20% of the colony contributed the vast majority (>90%) of radiation-induced acute myeloid leukaemias (AMLs). Through screening of a satellite CBA/H colony and rescreening of the original colony, we show that, whereas germline telomere sequence polymorphism is frequent in CBA/H mice, there is no genetic link between a specific TLR locus variant and susceptibility to AML. Studies on telomere-hybridising fragments between 200 bp and 150 kb revealed that the germline telomere mutation frequency was highest for restriction fragments >50 kb. The hypervariability of these high-molecular-weight fragments resulted in each CBA/H mouse from the highly inbred colony having a different genotype. Although it was not possible to ascribe a specific somatic telomere mutation to AML development, telomere rearrangements were common in induced AMLs. Some terminal telomere-hybridising restriction fragments were shortened in AML samples in comparison with normal tissue, but, insofar as the reduction in size was relatively small, it seems unlikely that telomere erosion is a major contributor to the molecular pathology of murine radiation-induced AML.

Original languageEnglish
Pages (from-to)230-237
Number of pages8
JournalGenes Chromosomes and Cancer
Issue number4
Publication statusPublished - Aug 1996


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