Generation of the AML1-EVI-1 fusion gene in the t(3;21)(q26;q22) causes blastic crisis in chronic myelocytic leukemia.

摘要: Abstract The t(3;21)(q26;q22) translocation, which is one of the consistent chromosomal abnormalities found in blastic crisis chronic myelocytic leukemia (CML), thought to play an important role leukemic progression CML acute phase. The AML1 gene, located at translocation breakpoint t(8;21)(q22;q22) leukemia, was also rearranged by translocation. Screening a cDNA library t(3;21)-carrying cell line cells (SKH1) resulted isolation two potentially complete AML1-EVI-1 chimeric cDNAs 6 kb. Two species fusion transcripts 8.2 and 7.0 kb were detected SKH1 cells. These expressed 180 kDa protein containing N-terminal half including runt homology domain fused entire zinc finger EVI-1 protein. transcript all three cases examined RNA-based PCR. findings strongly suggest that t(3;21) results formation new class transcription factor could contribute through interference with growth differentiation.