T. Ando et al., DIFFERENTIAL ACTIVITIES OF ADENOSINE-DEAMINASE ISOZYMES IN ACUTE-LEUKEMIA, Journal of experimental & clinical cancer research, 12(4), 1993, pp. 211-218
ADA isozymes (ADA(1) and ADA(2)) were analyzed using an ADA inhibitor
[erythro-9-(2-hydroxyl-3-nonyl) adenine,EHNA] which inhibited over 99%
of ADA(1) and did not inhibit ADA(2) at all. The ratio of ADA(1) and
ADA(2)(ADA(1)/ADA(2)) on acute promyelocytic leukemic cell lines (HL-6
0) which differentiated to mature blood cells by 12-0-tetradecanoyl-ph
orbol-13-acetate (TPA) was repressed, while in the proliferation stage
of HL-60 cells, the ratio increased. ADA(1) and ADA(2) activities of
leukemic cells obtained from 33 Patients with acute myeloid leukemia (
AML), chronic myeloid leukemia (CML) and CML in blast crisis (CML-BC)
and 7 normal leukocytes were determined using this inhibitor/method. T
he levels ofADA(1) activity in almost all AMLs except two (cases 5 and
7, M(2) and M(3)) were higher than in normal leukocytes, but levels o
f ADA(2) were almost the same as normal leukocytes in all AMLs. In the
two stages of CML between chronic phase and blast crisis the ADA(1) a
ctivity tended to be higher in peripheral blood mononuclear cell blast
transformation than in chronic phase CML. On the other hand, ADA(2) a
ctivity showed no change in these samples. Similarly, ADA(1) activity
of chronic phase CML was lower than in normal leukocytes. These result
s suggested that the ratio of ADA(1)/ADA(2) may represent a biochemica
l marker for AML and CML-BC, together with the extent of the different
iation in leukemia cells.