| Research Abstract |
By the g-6-PD isozyme study, many myeloproliferative disorders are demonstrated to be a pluripotent stem cell disease. However, this method is not applicable for Japanese patients because there are rare heterozygote patients for G-6-PD isozyme in Japan. Now, We have developed a new method, simultaneous analysis of morphology and karyotype on single colonies, by which we can clarify not only the cell lineage involvement of many hematologic malignancies in much more patients than in cases using G-6-PD isozyme method, but also we can follow up the change of normal or abnormal clones in various clinical stage. We have already demonstrated that idoipathic myelofibrosis, erythroleukemia, chronic myelogenous leukemia(CML), chronic myelomonocytic leukemia(CMML), and juvenile type chronic myelogenous leukemiz(J-CML) are a pluripotent stem cell disorder. Since 1987 to 1988, we have provided new evidence as follows: 1) Newly arising clones in blastic phase of CML are not restricted to committed cells, but can differentiate into erythroblasts, basophils, eosinophils, macrophages as the clones in chronic phase do in vitro culture condition. 2) Differentiation between de novo Ph-positive ALL and lymphoid crisis of CML can be done by this method; in de novo Ph-positive ALL, Ph chromosome is found only in lymphoid blast colonies but not in erythroid, myeloid and/or megakaryocyte colonies, whereas in lymphoid crisis of CML, Ph chromosome can be found in erythroid, myeloid and/or megakaryocyte colonies. 3) Increasing cells in transient abnormal myelopoiesis(TAM) is not responsively, but "clonally" proliferating. 4) Newly developed clones in clonal evolution in J-CML may arise in the other place than the bone marrow, and appear earlier in the peripheral blood than in the bone marrow.
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