骨髄増殖性疾患並びに骨髄異形成症候群におけるEndogenous CFU-Cの検討

抄録

An endogenous colony formation assay was performed on 24 patients with chronic myelogenous leukemia in the chronic phase (CML-CP), 11 patients with CML-accerelated phase (CML-AP), nine patients with CML-blastic crisis (CML-BC), nine patients with polycythemia vera, two patients with essential thrombocythemia, two patients with primary myelofibrosis, two patients with juvenile CML (JCML), one patient with chronic neutrophilic leukemia, two patients with unclassified myeloproliferative disorder (UMPD), five patients with refractory anemia with excess of blasts (RAEB), 10 patients with RAEB in transformation (RAEBt) or overt leukemia, and 10 patients with chronic myelomonocytic leukemia (CMML). Endogenous colony formation was observed in two patients with CML-AP, one patient with CML-BC, two patients with JCML, one patient with UMPD, one patient with RAEBt, and seven patients with CMML.
All of these endogenous colonies were identified as CFU-C by chemical staining. In some patients with CML or RAEBt, endogenous colonies were observed when progression of disease occurred. Endogenous colony formation was partially inhibited by the depletion of phagocytes in five patients with CMML or RAEBt. Four of these patients revealed increased releases of granulocyte-macrophage colony stimulating factor (GM-CSF) to the culture medium, and the addition of anti-GM-CSF antibody totally inhibited the formation of endogenous colony in one case. Patients who formed endogenous colonies often had chromosomal abnormalities and short survival.
These findings suggest that paracrine or autocrine GM-CSF plays an important role in endogenous colony formation and that such endogenous colony formation is one of the risk factors in hematological malignancies.