A CUTE MYELOGENOUS leukemia (AML) is one of the most frequent hematopoietic malignancies and accounts for 46% of all major leukemias in the United States. This disease is characterized by the proliferation of a malignant clone, resulting in the production of blasts and other immature granulocytes, monocytes, erythrocytes, and/or megakaryocytes. The diagnosis of AML and its subclassifications, AML-MO through AML-M7, is based on morphologic features and on cytochemical and immunologic studies of the neoplastic

Recurring chromosomal translocations are relatively common in neoplasms, particularly leukemias, lymphomas, and some sarc0m, 3'~ and several recurring chromosomal translocations have been identified that are closely linked to distinct morphologic and clinical features in W. Cloning of the translocation breakpoints has identified the genes involved in the breakpoint junction, and this in turn has led to a determination of the manner in which the genes are altered. The genes can be altered in the level of their expression or in the properties of the encoded proteins. These alterations appear to play an integral role in the development and possibly in the progression of leukemia and other types of cancer? In myeloid leukemias, chromosomal translocations virtually always disrupt normal genes by altering the normal properties of proteins through gene fusion. A classic example is the BCRIABL fusion in the 9; 22 translocation, seen in almost all patients with chronic myelogenous leukemia (CML), and in at least 30% of adult patients with acute lymphoblastic leukemia (ALL). 6 In many acute myeloid leukemias, one of the genes involved in the fusion is most often a transcription factor that appears to have a direct role in hematopoiesis and that following the translocation is frequently fused to a second gene not normally active in hematopoietic cells. In some instances the same gene is involved in fusion with more than one chromosomal partner. 5, 7.'0 The (8; 21)(q22; q22) translocation, reported in about 40% of karyotypically abnormal cases of AML-M2,* is one of the most common examples of association between a nonrandom reciprocal translocation and a specific subtype of AML. The peripheral blood (PB) and bone marrow (BM) specimens of AML-M2 patients with at (8; 21)(Fig 1A) exhibit immunophenotypic markers that may include CD19 and, less often, CD. 56. In addition, the cells show typical morphologic features that include prominent Auer rods, strongly myeloperoxidase-positive blasts, marrow eosinophilia, homogeneous