Tanaka K, Arif M, Eguchi M, Kyo T, Dohy H, Kamada N
Department of Cancer Cytogenetics, Hiroshima University, Japan.
Blood. 1997 Jan 15;89(2):596-600.
Seven secondary leukemia patients were treated for solid tumors or malignant lymphoma with anticancer drugs or radiation. We studied bone marrow samples from these patients by fluorescence in situ hybridization (FISH). Of the seven patients, three had increased signals for the ABL oncogene (9q34) on interphase nuclei and at metaphase. One of the three patients also had four signals for the CD3 (MLL) region (11q23). Whole painting probes revealed that these chromosomal regions were translocated onto structurally abnormal chromosomes, resulting in partial tri-, tetra- or penta-somy of these regions. We called this type of translocation "segmental jumping translocation (SJT)." SJT of the ABL oncogene was not detected in samples from 15 patients with de novo acute myelocytic leukemia (AML), 12 with myelodysplastic syndrome (MDS), or 20 with chronic myelocytic leukemia (CML) at the chronic phase. Furthermore, monosomy 7 was also found in the patients with the gene amplification. These results indicate that SJT of ABL and/or CD3 (MLL) genes is associated with the leukemogenesis of secondary leukemia. The SJT may be one mechanism of gene amplification.
7例继发性白血病患者曾接受抗癌药物或放疗以治疗实体瘤或恶性淋巴瘤。我们通过荧光原位杂交（FISH）研究了这些患者的骨髓样本。7例患者中，3例在间期核和中期时ABL癌基因（9q34）信号增加。这3例患者中的1例在CD3（MLL）区域（11q23）也有4个信号。全染色体涂抹探针显示这些染色体区域易位到结构异常的染色体上，导致这些区域部分三体、四体或五体。我们将这种类型的易位称为“节段跳跃易位（SJT）”。在15例新发急性髓细胞白血病（AML）、12例骨髓增生异常综合征（MDS）或20例慢性期慢性髓细胞白血病（CML）患者的样本中未检测到ABL癌基因的SJT。此外，在基因扩增的患者中还发现了7号染色体单体。这些结果表明ABL和/或CD3（MLL）基因的SJT与继发性白血病的白血病发生有关。SJT可能是基因扩增的一种机制。
