The t(9;22)(q34;q11) translocation is found in about 90% of chronic myeloid leukemia (CML) patients. About 5–10% of CML patients have complex variant translocations involving a third chromosome in addition to chromosomes 9 and 22. Herein, we describe a CML-chronic phase male with a complex translocation involving chromosome 16, t(9;22;16)(q34;q11;q24). First, he was treated with interferon-alpha and intermittent hydroxyurea, but only a partial cytogenetic response was attained. Subsequently, the patient was treated with imatinib mesylate because of an additional chromosome abnormality, trisomy 8. A major molecular response was obtained after one year's imatinib therapy, and the follow-up chromosomal analysis performed 4 years and 3 months after the initiation of imatinib therapy displayed a normal karyotype of 46,XY. 1. Introduction Chronic myeloid leukemia (CML) is characterized by the t(9;22)(q34;q11) translocation, in which the BCR gene at 22q11 is fused to the ABL gene at 9q34. The BCR/ABL fusion gene is thought to play a role in the leukemogenesis of CML and is a target of tyrosine kinase inhibitors, such as imatinib mesylate. About 5–10% of CML patients have complex variant translocations involving a third chromosome in addition to chromosomes 9 and 22. All chromosomes have been reported to act as the third chromosome, but breakpoint clustering at 1p36, 3p21, 5q13, 6p21, 9q22, 11q13, 12p13, 17p13, 17q21, 17q25, 19q13, 21q22, 22q12, and 22q13 has been reported [1, 2]. On the other hand, only a few cases involving chromosome 16 have been reported. Herein, we describe a CML-chronic phase male with a complex translocation involving chromosome 16, t(9;22;16)(q34;q11;q24), for which imatinib mesylate was effective, even after a new subclone, +8, appeared. 2. Case Report A 55-year-old man was referred to us in November 2000 because of leukocytosis. No lymphadenopathy or hepatosplenomegaly was detected. Peripheral blood analysis showed a white blood cell count of /L with 1% blasts, 0.5% promyelocytes, 5.5% myelocytes, 1% metamyelocytes, 64% neutrophils, 8% lymphocytes, 2% monocytes, 3.5% eosinophils, and 14.5% basophils. His hemoglobin level was 14.6？g/dL, and his platelet count was /L. His serum level of lactate dehydrogenase was 423？U/L (reference range, 106–211？U/L). Bone marrow aspiration revealed less than 5% blasts, and karyotype analysis of his bone marrow cells showed the following karyotype: 46,XY,t(9;22;16)(q34;q11;q24) [20] (Figure 1(a)). In addition, fluorescent in situ hybridization showed BCR/ABL fusion signals in 92.2% cells, as shown in
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