Mohamed A N, Mahalak S, Goldfarb S B, Palutke M
Cytogenetic Laboratory, Pathology Department Harper Hospital, Wayne State University, Detroit, Michigan 48201, USA.
Hematopathol Mol Hematol. 1996;10(4):193-9.
We describe two elderly male patients with acute myeloid leukemia transformed from myelodysplastic bone marrow. Neither patients had a history of prior exposure to mutagenic agents or other malignancies. Chromosome analysis at the time of initial diagnosis revealed 47,XY,del(5)(q14q33),+21 in patient 1 and 45,XY,add(1)(q23),-5,del(8)(p11.2p23),der(17)t(5;17)(p12;p11.2) in patient 2. In addition, numerous copies of double minute chromosomes were seen in both patients. We used fluorescence in situ hybridization to identify the amplified sequences presumed to represent the dmins in the leukemic cells. In both cases, it appeared that the dmins were derived from specific amplification of c-myc oncogene.
我们描述了两名患有从骨髓增生异常骨髓转化而来的急性髓系白血病的老年男性患者。两名患者均无先前接触诱变剂或其他恶性肿瘤的病史。初次诊断时的染色体分析显示,患者1为47,XY,del(5)(q14q33),+21,患者2为45,XY,add(1)(q23),-5,del(8)(p11.2p23),der(17)t(5;17)(p12;p11.2)。此外,在两名患者中均可见大量双微体染色体拷贝。我们使用荧光原位杂交来鉴定白血病细胞中推测代表双微体的扩增序列。在这两种情况下,双微体似乎都源自c-myc癌基因的特异性扩增。