Deletion and/or rearrangement of chromosome 2 is a very early and possibly initiating event for acute myeloid leukaemia in the CBA mouse. Here an outline is given of a series of cytogenetic and molecular studies which imply that the expression of radiation damage to this chromosome is highly non-random, being dependent upon the presence of specific telomere-like DNA repeat sequences at certain interstitial chromosomal locations. The secondary four-stranded DNA structures that may be formed at such telomeric chromosome sites and the potential role of these recombinogenic structures as preferential targets for radiation induced cytogenetic change are discussed.
|Number of pages||4|
|Journal||Radiation Protection Dosimetry|
|Publication status||Published - 1994|