VARIANT COMPLEX TRANSLOCATIONS INVOLVING CHROMOSOME-1, CHROMOSOME-9, CHROMOSOME-9, CHROMOSOME-15 AND CHROMOSOME-17 IN ACUTE PROMYELOCYTIC LEUKEMIA WITHOUT RAR-ALPHA PML GENE FUSION REARRANGEMENT/

Acute promyelocytic leukemia (APL;MS) is specifically characterized by a predominance of malignant promyelocytes having atypical reciprocal translocation involving chromosome 15 and 17 [t(15;17)(q22;q11)] resul ting in the fusion of retinoic acid receptor alpha (RAR alpha) on chro mosome 17 and the putative transcription factor gene PML, ie the trans location generates two fusion transcripts, PML/RAR alpha and RAR alpha /PML. We describe a patient with clinical and morphologic characterist ics of atypical APL but with a previously undescribed variant transloc ation. A 35-year-old Hispanic having atypical APL was referred for cyt ogenetic evaluation. The cytogenetic findings with GTG-banding coupled with FISH analysis revealed the following karyotype: 46,XX,der(9)t(1; 9)(q25;q34)der(9)t(9;?)(q34;?), t(15;17)-(q22;q11)ish. ;9)(q25;q34)(WC P1+,WCP9+),t(9;17;15)-(q34;q11;q22) (WCP9+,WCP15+,PML+;WCP17+,RAR alph a+;-WCP15+,WCP17+,PML-)[20]/46,XX[5]. The chromsome 17q was translocat ed to the chromosome 15q. However, chromosome 15q including the PML ge ne normally translocating to 17q and creating the RAR alpha/PML fusion gene, translocated to chromosome 9q. Does this patient have another s ubset of APL? Or is the genetics of APL different in cases with varian t translocations as opposed to those with atypical t(15;17) translocat ion, though in the majority of the cases their clinical presentation r emains the same.