Rithidech K N, Bond V P, Cronkite E P, Thompson M H
Medical Department, Brookhaven National Laboratory, Upton, NY 11973.
Exp Hematol. 1993 Mar;21(3):427-31.
G-banded metaphase chromosomes prepared from 14 male CBA/Ca mice with histologically confirmed myeloid leukemia (ML) were studied in an effort to identify specific chromosomal changes associated with radiation leukemogenesis. The chromosome studies were undertaken as part of a larger investigation of radiation carcinogenesis, in which mice were exposed to radiation of several different qualities, i.e., x-rays, gamma-rays and "monoenergetic" fast neutrons of 5 mean energies ranging from 0.2 to 14 MeV. The 14 ML cases showed no histologically phenotypic differences and they were transplantable in syngeneic mice. We detected a specific chromosomal deletion in 1 copy of mouse chromosome 2 at regions D-E in all radiation-induced ML cells, regardless of radiation quality. Our results strongly implicate the involvement of genes within or close to regions D-E of chromosome 2 in radiation leukemogenesis. In addition to the specific deletion in chromosome 2, loss or gain of the Y chromosome was also detected in some cells from 6 ML cases. Because this hypo- or hyperploidy occurred in only a small fraction of leukemic cells, a causative role in radiation leukemogenesis appears unlikely.
为了确定与辐射诱发白血病相关的特定染色体变化，我们对14只经组织学确诊患有髓系白血病（ML）的雄性CBA/Ca小鼠制备的G带中期染色体进行了研究。染色体研究是作为一项更大规模的辐射致癌研究的一部分进行的，在该研究中，小鼠暴露于几种不同性质的辐射下，即X射线、γ射线和5种平均能量范围从0.2到14 MeV的“单能”快中子。这14例髓系白血病病例在组织学上没有表型差异，并且它们可在同基因小鼠中移植。我们在所有辐射诱导的髓系白血病细胞中，在小鼠2号染色体D - E区域的1个拷贝中检测到了特定的染色体缺失，无论辐射性质如何。我们的结果强烈表明2号染色体D - E区域内或附近的基因参与了辐射诱发白血病过程。除了2号染色体的特定缺失外，在6例髓系白血病病例的一些细胞中还检测到了Y染色体的丢失或增加。由于这种亚倍体或超倍体仅发生在一小部分白血病细胞中，因此其在辐射诱发白血病过程中似乎不太可能起致病作用。
