Yamazaki E, Kanamori H, Taguchi J, Harano H, Mohri H, Okubo T
The First Department of Internal Medicine, Yokohama City University School of Medicine, Yokohama, Japan.
Blood Cells Mol Dis. 1997 Aug;23(2):213-8. doi: 10.1006/bcmd.1997.0138.
We present here the case of a Japanese female patient with aplastic anemia who developed monosomy 7 and clonal evolution following a treatment with recombinant human granulocyte colony-stimulating factor (rhG-CSF). At the onset of aplastic anemia, cytogenetic analysis was 46, XX and X-inactivation/methylation analysis revealed a polyclonal pattern. After 4 months of administration of rhG-CSF, she had 45, XX, -7 and a clonal pattern, although there were no morphological evidence of a myelodysplastic syndrome or leukemia. The ratio of monosomy 7 to normal analyzed by fluorescence in situ hybridization decreased after discontinuation of rhG-CSF and there were still no dysplastic changes and/or increased numbers of blasts. These results indicate that the acquisition of monosomy 7 following rhG-CSF treatment dose not always cause clonal evolution to induce hematological malignancies.
我们在此报告一例日本女性再生障碍性贫血患者，其在接受重组人粒细胞集落刺激因子（rhG-CSF）治疗后发生了7号染色体单体及克隆进化。再生障碍性贫血发病时，细胞遗传学分析显示为46, XX，X失活/甲基化分析显示为多克隆模式。在给予rhG-CSF 4个月后，她出现了45, XX, -7及克隆模式，尽管没有骨髓增生异常综合征或白血病的形态学证据。在停用rhG-CSF后，通过荧光原位杂交分析的7号染色体单体与正常细胞的比例下降，且仍无发育异常改变和/或原始细胞数量增加。这些结果表明，rhG-CSF治疗后获得7号染色体单体并不总是会导致克隆进化从而诱发血液系统恶性肿瘤。
