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Prepublished online as a Blood First Edition Paper on October 31, 2002; DOI 10.1182/blood-2002-08-2394.
Submitted August 8, 2002
Accepted October 21, 2002
Low penetrance genetic susceptibility and resistance loci implicated in the relative risk of radiation-induced acute myeloid leukaemia in mice
Emma Boulton, Clare Cole, Abigail Knight, Helen Cleary, Roger Snowden, and Mark Plumb*
MRC Radiation and Genome Stability Unit, Chilton, Didcot, United Kingdom
Department of Genetics, University of Leicester, Leicester, United Kingdom
MRC Toxicology Unit, University of Leicester, Leicester, United Kingdom
* Corresponding author; email: map12{at}le.ac.uk.
Inbred CBA/H mice are susceptible to radiation-induced acute myeloid leukaemia (r-AML) and C57BL/6 mice are resistant. A genome-wide screen for linkage between genotype and phenotype (r-AML) of 67 affected (CBA/H x C57BL/6)F1 x CBA/H backcross mice has revealed at least two suggestive loci which contribute to the overall lifetime risk of r-AML. Neither is necessary or sufficient for r-AML, but is the net effect of both susceptibility (distal chromosome 1) and resistance (chromosome 6) loci. An excess of chromosome 6 aberrations in mouse r-AML and bone marrow cells up to 6 months post irradiation in vivo suggests the locus confers a proliferative advantage during the leukaemogenic process. The Stem Cell Frequency Regulator 1 (Scfr1) locus maps to distal chromosome 1 and determines the frequency of haemopoietic stem cells (HSC) in inbred mice suggesting that target size may be one factor in determining the relative susceptibility of inbred mice to r-AML.
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