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Prepublished online as a Blood First Edition Paper on October 31, 2002; DOI 10.1182/blood-2002-08-2394.
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Blood, 15 March 2003, Vol. 101, No. 6, pp. 2349-2354
NEOPLASIA
Low-penetrance genetic susceptibility and resistance loci
implicated in the relative risk for radiation-induced acute myeloid
leukemia in mice
Emma Boulton,
Clare Cole,
Abigail Knight,
Helen Cleary,
Roger Snowden, and
Mark Plumb
From the Department of Genetics and the MRC Toxicology
Unit, University of Leicester; and the Medical Research Council
Radiation and Genome Stability Unit, Chilton, Didcot, Oxon,
United Kingdom.
Inbred CBA/H mice are susceptible to radiation-induced
acute myeloid leukemia (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 × C57BL/6)F1 × CBA/H
backcross mice has revealed at least 2 suggestive loci that contribute
to the overall lifetime risk for r-AML. Neither is necessary or
sufficient for r-AML, but relative risk is the net effect of
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 after irradiation in vivo suggests the
locus confers a proliferative advantage during the leukemogenic
process. The stem cell frequency regulator 1 (Scfr1) locus
maps to distal chromosome 1 and determines the frequency of hemopoietic
stem cells (HSCs) 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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