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Chromosome 16 inversion in acute myelogenous leukemias with bone marrow eosinophilia.

hematological malignancies. There are two principal mechanisms of oncogene activation by translocations and inversions; proto-oncogene activation by juxtaposing genes having potent enhancer effects, like immunoglobulin genes, and formation of fusion genes encoding for oncogenic chimeric proteins (1). Representatives of the former include c-myc of t(8: 14), and cabl oft(9;22) is a good example of the latter. Interestingly, such chromosomal aberrations have been found to be specific to particular subtypes of leukemias, implying cytogenetic-clinicopathological correlations, which might allow understanding of the pathogenesis of these important malignancies. One of the most frequent chromosomal rearrangements detected in the de novo acute myelogenous leukemia (AML)is the chromosome 16 inversion [inv(16)(pl3;q22)], which has been reported to account for up to 12% of the karyotypic abnormalities found with this neoplasm (2). This abnormality is highly correlated with, but not uniformly restricted to, acute myelomonocyticleukemias with bone marroweosinophilia (5% or more of the nonerythroid cells), the French-AmericanBritish (FAB) type M4Eo (3). Of this subgroup, almost all have inv(16), del(16)(q22), ort(16; 16)(pl3;q22), and in the majority