Amenomori T, Tomonaga M, Yoshida Y, Kuriyama K, Matsuo T, Jinnai I, Ichimaru M, Omiya A, Tsuji Y
Br J Haematol. 1986 Nov;64(3):539-46. doi: 10.1111/j.1365-2141.1986.tb02210.x.
We used a micromethod for cytogenetic analysis from single haematopoietic colonies to study two adults with chronic myelomonocytic leukaemia (CMML) and a boy with juvenile chronic myeloid leukaemia (JCML) carrying distinct chromosome abnormalities, 7q-, der(21), and trisomy 21. We wanted to know if both granulocyte-macrophage (GM) and erythroid precursors are involved in the abnormal clone. In all three patients, their chromosome abnormality was seen in almost all metaphases obtained from GM-colonies and erythroid bursts. Peripheral blood leucocytes stimulated with phytohaemagglutinin exhibited only normal karyotypes. Clones of B-cell produced by Epstein-Barr virus had only normal karyotypes in the CMML patients. These findings indicate that CMML and JCML are clonal haemopathies that originate in a partially committed myeloid progenitor cell.
我们采用一种从单个造血集落进行细胞遗传学分析的微量方法,研究了两名患有慢性粒单核细胞白血病(CMML)的成人以及一名患有青少年慢性粒细胞白血病(JCML)且携带不同染色体异常(7号染色体长臂缺失、21号染色体衍生异常和21三体)的男孩。我们想了解粒细胞 - 巨噬细胞(GM)前体和红系前体是否都参与了异常克隆。在所有三名患者中,从GM集落和红系爆式集落获得的几乎所有中期细胞中都可见到其染色体异常。用植物血凝素刺激的外周血白细胞仅表现出正常核型。在CMML患者中,由爱泼斯坦 - 巴尔病毒产生的B细胞克隆仅具有正常核型。这些发现表明,CMML和JCML是起源于部分定向髓系祖细胞的克隆性血液病。