Rao S G, Kothari V, Nadkarni K, Ahuja H, Advani S
Cancer Research Institute, Tata Memorial Centre, Parel, Bombay, India.
Nouv Rev Fr Hematol (1978). 1987;29(4):231-6.
In serum from chronic myelogenous leukemia (CML) patients an activity has been demonstrated, which recruits more CFU-GM (cells committed to granulocyte-macrophage lineage) from normal human bone marrow into clonal proliferation as shown by standard agar colony forming assay, in the presence of supramaximal levels of colony stimulating activity. All sera from CML patients at diagnosis (before therapy) were tested and found to be significantly (P less than 0.001) positive for the recruitment activity. This observation led us to believe that younger or more pluripotent CFU-GM which were hitherto non-responsive to colony stimulating activity become responsive in the presence of CML sera. We investigated whether more pluripotent stem cells (CFUs) are stimulated to proliferate in the chronic phase of CML than at diagnosis (before therapy). An activity was detected which recruits more spleen colony forming cells (CFUs) from normal Swiss mouse bone marrow into the cell cycle as shown by a significant increase (P less than 0.001) in the thymidine suicide index. However both these activities were either lowered or undetectable in normal (blood groups AB) serum. These results indicate that CML sera may contain enhanced levels of early growth factors which stimulate proliferation of pluripotent stem cells resulting in an increased CFU-GM pool in CML. It is suggested that this activity may be responsible for the myeloid hyperplasia associated with CML in the chronic phase.
在慢性粒细胞白血病(CML)患者的血清中已证实存在一种活性物质,在集落刺激活性超最大水平的情况下,通过标准琼脂集落形成试验表明,该物质能使更多来自正常人骨髓的CFU - GM(定向于粒细胞 - 巨噬细胞系的细胞)进入克隆增殖。对所有处于诊断阶段(治疗前)的CML患者血清进行检测,发现其募集活性均呈显著阳性(P小于0.001)。这一观察结果使我们相信,那些迄今对集落刺激活性无反应的更年轻或更具多能性的CFU - GM在CML血清存在时会变得有反应。我们研究了在CML慢性期与诊断时(治疗前)相比,是否有更多的多能干细胞(CFU)被刺激增殖。检测到一种活性物质,通过胸苷自杀指数显著增加(P小于0.001)表明,该物质能使更多来自正常瑞士小鼠骨髓的脾集落形成细胞(CFU)进入细胞周期。然而,在正常(AB血型)血清中,这两种活性要么降低,要么无法检测到。这些结果表明,CML血清可能含有增强水平的早期生长因子,这些因子刺激多能干细胞增殖,导致CML中CFU - GM池增加。有人提出,这种活性可能是导致CML慢性期骨髓增生的原因。