A NEW COMPLEX TRANSLOCATION (15-20-17)(Q22-P13-Q21) IN ACUTE PROMYELOCYTIC LEUKEMIA

We describe here a 39-year-old male with acute promyelocytic leukemia (APL) carrying a new complex translocation (15;20;17). A chromosomal a nalysis of the bone marrow cells showed 46,XI: t(15;20;17)(q22;p13;q21 ). Fluorescence in situ hybridization (FISH) analysis using plasmid DN A libraries of chromosomes 15, 17, and 20 revealed three derivative ch romosomes, der(15)t(15;17), der(17)t(17;20), and der(20)t(15;20). Fluo rescence in situ hybridization with cosmid DNA probes flanking the bre akpoints of t(15;17) did not show the retinoic acid receptor alpha (RA R alpha)/PML fusion signal usually generated on the der(17)t(15;17). H owever, rearrangement of the RAR alpha gene and expression of the PML/ RAR alpha chimeric transcript were identified by Southern blot and rev erse-transcriptase polymerase chain reaction (RT-PCR) analyses, respec tively. Our results confirmed that the PML/RAR alpha gene on the der(1 5)t(15;17), not the RAR alpha/PML gene, must be essential to leukemoge nesis In APL. Furthermore, considering another reported case with a 20 p13 aberration, it is possible that 20p13 is a nonrandom breakpoint in APL with a complex translocation. (C) Elsevier Science Inc., 1998.