Abstract
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.
Original language | English |
---|---|
Pages (from-to) | 461-464 |
Number of pages | 4 |
Journal | Radiation Protection Dosimetry |
Volume | 52 |
Issue number | 1-4 |
DOIs | |
Publication status | Published - 1994 |