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The incidence of acute myeloid leukemia (AML) in CBA/H mice following exposure to single acute doses of ionizing radiation has previously been determined. A high proportion of these AMLs are characterized by rearrangement of murine chromosome 2 in the C2 and/or E5-F regions, and there is evidence that these events are a direct consequence of radiation damage to multipotential hemopoietic cells. Using a combination of in situ chromosome hybridization and mRNA analyses, we show that the cytokine gene interleukin-1 beta (IL-1 beta) is encoded in the chromosome 2 F region and is translocated in a chromosome 2---2 rearrangement in an x-ray-induced AML (N36). Also, IL-1 beta is specifically deregulated in N36 and in two other chromosome 2-rearranged AMLs but not in a fourth, which has two cytogenetically normal chromosome 2 copies. We suggest that radiation-induced specific chromosome 2 rearrangement associated with IL-1 beta deregulation may initiate murine leukemogenesis through the uncoupling of normal proliferative control mechanisms in multipotential hemopoietic cells.

Type

Journal article

Journal

Mol Carcinog

Publication Date

1989

Volume

2

Pages

226 - 232

Keywords

Animals, Bone Marrow, Chromosome Mapping, Gene Expression Regulation, Gene Rearrangement, Interleukin-1, Karyotyping, Leukemia, Myeloid, Acute, Leukemia, Radiation-Induced, Mice, Mice, Inbred CBA, Polymorphism, Restriction Fragment Length