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approximately 95% of acute promyelocytic leukemias ( apls , fab aml - m3 ) carry the t(15;17)(q22;q21 ) , which fuses the retinoic acid alpha - receptor ( rar ) sequence to the pml gene sequence .
the remaining apl gene fusions are composed of rare variant fusions of rar with stat5 , numa , plzf , and npm .
the resulting fusion gene products play a pivotal role in the pathogenesis of apl and apl sensitivity to all - trans retinoic acid and arsenic trioxide [ 1 , 3 ] .
these deletions are apparently very rare compared to similar deletions in other leukemias associated with disease - specific cytogenetic changes [ 4 , 5 , 6 , 7 , 8 ] . additionally , t(15;17)(q22;q21 ) is rare in non - apl acute myeloid leukemias ( amls ) , with only rare examples of this translocation identified in aml without maturation and aml with maturation ( fab m1 and m2 subtypes , respectively ) . to our knowledge ,
what we describe here is the first case of a rar deletion in a case of aml without maturation ( fab aml - m1 ) .
a 51-year - old male with a history of hepatitis c and a forty pack - year smoking history presented with neutropenia over the course of several months .
a peripheral blood smear confirmed neutropenia with conspicuous atypical lymphocytes and large granular lymphocytes ( fig .
bone marrow biopsy revealed an erythroid predominant hypocellular marrow with a fat - to - cell ratio of 65:35 .
the marrow blasts were negative for myeloperoxidase on immunoperoxidase staining , were small with scant cytoplasm , and had no significant granularity .
minimal maturation was evident on the myeloperoxidase staining , reiterating the morphologic features of the marrow cells .
blast percentages were determined on a 500-cell differential in bone marrow and/or a 200-peripheral blood smear differential .
erythroid maturation was evident with cd71 staining and appeared macronormoblastic and megaloblastoid . based on these findings , a diagnosis of aml - m1 ( aml without maturation ) was rendered .
no clonal t - cell gene rearrangements , flt3 internal duplications or d835 mutations , or npm1 exon 12 mutations were detected .
however , the aml panel revealed loss of the rar/17q locus as detected by the rara(f ) probe .
t(15;17)(q22;q21 ) characterizes apl and plays an important role in the pathogenesis of this disease and its sensitivity to all - trans retinoic acid and arsenic trioxide [ 1 , 3 ] .
additionally , a small number of apl with complex chromosomal rearrangements involving deletions at the rar/17q locus have been described [ 4 , 5 , 6 , 7 , 8 ] . to our knowledge , rar/17q locus deletions have not previously been detected in aml without differentiation ( aml - m1 ) .
the significance of the rar/17q locus deletion in this aml type is currently unknown , although loss of the retinoic acid alpha - receptor is associated with increased cellular growth potential .
further analysis of the function of this deletion in the aml - m1 subtype would be difficult due to the rarity of this molecular event .
acute promyelocytic leukemia ( apl ) is characterized by a t(15;17 ) which fuses the 17q retinoic acid alpha - receptor sequence to the 15q pml gene sequence . 
 the resulting fusion product plays a role in the development and maintenance of apl , and is very rarely found in other acute myeloid leukemia ( aml ) subtypes . 
 rare complex apl genomic rearrangements have retinoic acid alpha - receptor sequence deletions . here 
 we report a retinoic acid alpha - receptor sequence deletion in a case of aml without differentiation . to our knowledge 
 , this is the first example of a retinoic acid alpha - receptor sequence deletion in this aml subtype .