A previous study indicated that a highly inbred CBNH 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 CBNH colony and rescreening of the original colony, we show that, whereas germline telomere sequence polymorphism is frequent in CBNH 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 IS0 kb revealed that the germline telomere mutation frequency was highest for restriction fragments >SO kb. The hypervariability of these high-molecular-weight fragments resulted in each CBNH 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 AML. 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 Genes