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Blood, 1 September 2001, Vol. 98, No. 5, pp. 1549-1554
NEOPLASIA
Allelic loss on chromosome 4 (Lyr2/TLSR5) is
associated with myeloid, B-lympho-myeloid, and lymphoid (B and T)
mouse radiation-induced leukemias
Helen Cleary,
Emma Boulton, and
Mark Plumb
From the MRC Radiation and Genome Stability Unit,
Chilton, Didcot, United Kingdom.
The CBA/H mouse model of radiation-induced acute myeloid leukemia
(AML) was re-examined using molecular approaches. In addition to the
typical promyelocytic AMLs, 34% were reclassified as early pre-B
lympho-myeloid leukemias (L-ML) based on leukemic blood cell
morphology, immunoglobulin heavy-chain gene re-arrangements (IgHR), or expression of both lymphoid
(Vpre-B1 and Rag1) and myeloid (myeloperoxidase
and lysozyme M) genes. Allelic loss on chromosome 4 was frequently
detected in AMLs (53%) and L-MLs (more than 95%), and the
preferential loss of the maternally transmitted allele suggests the
locus may be imprinted. A minimally deleted region (MDR) maps to a
3.4-cM interval, which is frequently deleted in radiation-induced
thymic lymphomas (TLSR5) and contains a recessive, maternally
transmitted genetic locus (Lyr2) that confers
resistance to spontaneous and radiation-induced pre-B and T cell
lymphomas, suggesting they are one and the same. Thus, the
Lyr2/TLSR5 locus is frequently implicated in
myeloid, lymphoid (B and T), and mixed-lineage mouse leukemias and
lymphomas. Epigenetic inactivation of one Lyr2/TLSR5 allele
during normal mouse development suggests that only a single hit is
required for its inactivation during leukemogenesis, and this may be a
significant contributing factor to the efficiency of the leukemogenic
process in the mouse.
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