To evaluate the relationship between the expression of c-myc oncoprotein and the development of leukemia, flow cytometric analysis (FACScan?) of c-myc oncoprotein using monoclonal antibody was performed in 23 clinical leukemic samples (4 cases of ANLL ; 15 cases of ALL; 3 cases of ALL in complete remission ; 1 case of chronic myelomonocytic leukemia).20 cases of control groups (non-leukemic bone marrow aspirates). & 4 ATCC leukemic cell lines(ATCC CCL 240 HL-60, acute promyelocytic leukemia ; ATCC CCL 213 Daudi, Burkitt lymphoma ; ATCC CCL 243 K-562. Chronic myelogenous leukemia in blast crises ; ATCC CRL 1582 Molt-4, acute T-cell leukemia).
The results were summarized as follows.
1. The proportion of myelocytes, basophilic normoblasts. and polychromatophilic normoblasts of the bone marrow aspirate in control group showed weak, but significant correlation with the c-myc oncoprotein staining indices (% positivity of cell staining and/or corrected mean fluorescence intensity, CMFI) (r= 0.35, 0.35, 0.30 respectively). But the proportion of the other immature cells such as blasts, promyelocytes, pronormoblasts, and orthochromic nor-moblasts showed no correlation with the c-myc oncoprotein staining indices.
2. The difference of the percent positivity of c-myc staining in the cells among the immunologic classes of ALL was not significant. But the CMFI of B ALL is significantly higher than that of common ALL or T ALL (F ratio=3.85, p=0.05).
3. The extent of CDl3. CD33, CD34 expression in ANLL showed no correlation with the c-myc oncoprotein staining indices. But that of CD14 expression in ANLL showed negative correlation with CMFI (r= -1.0).
4. There is no significant differences in c-myc oncoprotein staining indices among ANLL, ALL. ALL in complete remission, CMMoL, leukemic cell lines, and control group.
5. The CMFI of c-myc protein staining is high in K-562, Molt-4, HL-60, and Daudi in a decreasing order.
From the above findings, it was concluded that ; first, the malignant transformation of the hematopoietic cells require a complex phenomena in addition to the c-myc oncogene expression because the c-myc oncoprotein is present both in the malignant transformation and in the benign proliferation of hematopoietic cells.
Secondly, in the hematopoietic malignancy c-myc oncogene expression is not only present in acute promyelocytic leukemia, but also in the other myeloid leukemia and lymphoblastic leukemia.
Thirdly, c-myc oncogene expression is diminished in the terminal stage of monocytic differentiation.
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