Molecular studies of chromosomal translocation (15;17) in acute promyelocytic leukemia (APL) have shown that retinoic acid receptor A (RARA) gene on chromosome 17 is juxtaposed to the PML gene on chromosome 15. This results in a PML-RARA chimeric gene. Our work has demonstrated that the PML breakpoints in APL patients are clustered in two limited regions, PML-bcr1 and PML-bcr2, separated from each other by about 10 kb. DNA sequence of PML-bcr1 and primary structure of the junctional region of reciprocal chromosomal translocation in a patient have been determined in this paper. Compared to those of two previously reported cases abroad, we found that the breakpoint may be situated in the topoisomerase II cleavage site. A working model has been proposed for the mechanism of DNA illegitimate recombination in t (15;17).