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Human bone marrow-derived fibroblastoid colonies have been quantitatively developed in a liquid culture. A linear relationship between cell number plated and colony number formed supports their clonal origin and hydroxyurea killing indicates that the fibroblastoid colony forming cell (CFU-F) is not in cell cycle in normal bone marrow. Adipose cells were induced in the fibroblastoid colonies by the addition of hydrocortisone (optimal concentration: 10(-6) M). Furthermore, adherent layers with adipocytes provided a more favourable condition for maintaining haemopoiesis in Dexter-system cultures. These results indicate that CFU-F belongs to stromal precursor cells intimately involved in the formation of the haemopoietic microenvironment. Colony incidence of CFU-F was almost normal in most patients with aplastic anaemia, haemopoietic dysplasia and chronic myelogenous leukaemia. However, in acute myelogenous leukaemia, it varied with the stage of the disease. It is concluded that the colony assay is useful for investigating stroma/haemopoietic cell interactions.

Bone marrow-derived fibroblastoid colony-forming cells (CFU-F) and granulocyte/macrophage precursor cells (CFU-GM) were studied in patients with acute leukemia. The numbers of CFU-F and CFU-GM were significantly lower in patients with acute myelogenous leukemia (AML) and acute lymphocytic leukemia (ALL) at diagnosis than in normal subjects, although patients with AML had a very wide range of CFU-F colony-forming efficiency. However, a suppressive effect of leukemic cells on normal CFU-F colony formation was not observed. CFU-F and CFU-GM in patients with acute leukemia recovered to normal levels when complete remission (CR) was achieved and decreased again at relapse. Serial studies showed that the increase in CFU-F preceded the recovery of CFU-GM. In AML, furthermore, patients who achieved CR had a higher number of CFU-F than patients without CR, suggesting that the CFU-F level at diagnosis may contribute to the prediction of the likelihood of remission induction in patients with AML.

The number of bone marrow-derived fibroblastoid colony-forming cells (CFU-F) and the production of colony-stimulating activity (CSA) by bone marrow stromal cells were studied in 71 patients with myeloproliferative disorders (MPD). The numbers of CFU-F in chronic-phase chronic myelogenous leukemia (CML), polycythemia vera (PV) and essential thrombocythemia (ET) were not different from those in normal subjects. However, the number of CFU-F in acute-phase CML was markedly decreased. Bone marrow adipocyte colony-forming capacity (adipo-CFC), which was previously shown to reflect both the number of pre-adipocytes and the stromal cell function in vivo, was increased in patients with chronic-phase CML, PV and ET, but was absent in acute-phase CML patients. The production of CSA by marrow stromal cells of MPD patients, however, was not different from that of normal subjects. These results suggest that the characteristics of marrow stromal and its precursor cells of chronic-phase MPD patients were not different from those of normal subjects, however, they became changed in acute-phase CML patients.