Abstract

Cells of acute myeloid leukemia (AML) from C3H/He mice express an increased amount of RNA for an endogenous retrovirus-like retrotransposon, intracisternal A-particle element. We analyzed the transcription of other mouse retrotransposons in C3H-derived tumor cells and found that all the AML lines from different mice overexpress early-transposon (ETn) RNA. In contrast, only faint levels of ETn were detected in the cells from other tumors, including hepatoma and lymphoma. The polyadenylation sites of the ETn RNA in the AML cells varied. We also determined the binding site for the nuclear extract of the AML cells in the long terminal repeat sequence of ETn. The overexpression of ETn as a common phenotype of AML cells suggests that myeloid cells with this phenotype are the origin of all the AML cells or that the phenotype is acquired during leukemogenesis.

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