 Specific cytogenetic abnormalities can be found in many people with AML ; the types of chromosomal abnormalities often have prognostic significance . The chromosomal translocations encode abnormal fusion proteins , usually transcription factors whose altered properties may cause the " differentiation arrest " . For example , in acute promyelocytic leukemia , the t ( 15 ; 17 ) translocation produces a PML @-@ RARα fusion protein which binds to the retinoic acid receptor element in the promoters of several myeloid @-@ specific genes and inhibits myeloid differentiation . 
 Specific cytogenetic abnormalities can be found in many people with AML ; the types of chromosomal abnormalities often <a href='got' title='1'><mark>have</mark></a> prognostic significance . The chromosomal translocations encode abnormal fusion proteins , usually transcription factors whose altered properties may cause the " differentiation arrest " . For example , in acute promyelocytic leukemia , the t ( 15 ; 17 ) translocation <a href='uninflect' title='2'><mark>produces</mark></a> a PML @-@ RARα fusion protein which <a href='uninflect' title='3'><mark>binds</mark></a> to the retinoic acid receptor element in the promoters of several myeloid @-@ specific genes and <a href='uninflect' title='4'><mark>inhibits</mark></a> myeloid differentiation . 
Specific cytogenetic abnormalities can be found in many people with AML ; da types of chromosomal abnormalities often got prognostic significance . The chromosomal translocations encode abnormal fusion proteins , usually transcription factors whose altered properties may cause the " differentiation arrest " . fa example , in acute promyelocytic leukemia , tdat ( 15 ; 17 ) translocation produce a PML @-@ RARα fusion protein which bind to thdaetinoic acid receptor element in the promoters of several myeloid @-@ specific genes and inhibit myeloid differentiation .