Kobayashi H, Arai Y, Hosoda F, Maseki N, Hayashi Y, Eguchi H, Ohki M, Kaneko Y
Third Clinical Department, Saitama Cancer Center Hospital, Japan.
Genes Chromosomes Cancer. 1997 Jul;19(3):150-5.
We studied four patients with inv(11)(p15q22) associated with malignant myeloid diseases by using fluorescence in situ hybridization (FISH) with phage and cosmid probes mapped and ordered on 11q22-24. Two of the four patients had non-Hodgkin's lymphoma or acute lymphoblastic leukemia as the primary malignancy and had received cytotoxic chemotherapy, including topoisomerase II inhibitors. The other two had de novo acute myeloid leukemia or myelodysplastic syndrome. FISH analysis showed that all 11q breakpoints were located centromeric to the MLL gene and between cosmids CN2900 and CN1323. We identified a yeast artificial chromosome (YAC) clone that spanned the inv(11) breakpoints on 11q. From this YAC, we identified a P1 clone, which included the breakpoints in at least three of the four patients. It is highly likely that the same gene on the P1 clone is rearranged in leukemic cells of each patient. This gene may be one of the targets for topoisomerase II inhibitors.
我们使用与定位并排列在11q22 - 24上的噬菌体和黏粒探针进行荧光原位杂交(FISH),研究了4例与恶性髓系疾病相关的inv(11)(p15q22)患者。4例患者中有2例以非霍奇金淋巴瘤或急性淋巴细胞白血病作为原发性恶性肿瘤,且接受过细胞毒性化疗,包括拓扑异构酶II抑制剂。另外2例患有原发性急性髓系白血病或骨髓增生异常综合征。FISH分析显示,所有11q断点均位于MLL基因的着丝粒侧,且在黏粒CN2900和CN1323之间。我们鉴定出一个酵母人工染色体(YAC)克隆,其跨越了11q上的inv(11)断点。从这个YAC中,我们鉴定出一个P1克隆,其中至少包含4例患者中3例患者的断点。很有可能P1克隆上的同一个基因在每位患者的白血病细胞中发生了重排。该基因可能是拓扑异构酶II抑制剂的作用靶点之一。