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H Umadome

Publications and source records attributed to H Umadome.

22 records · Page 2Linked to original sources

Interleukin-2 receptor (Tac antigen) expressed on adult T cell leukemia cells.

We studied the expression of the interleukin-2 (IL-2) receptor and the proliferative response to exogenous IL-2 of peripheral blood leukemic cells from patients with adult T cell leukemia (ATL) in order to see whether IL-2 receptor expressed on ATL cells is different from normal IL-2 receptor and whether it plays a role in the neoplastic growth in ATL. Peripheral blood leukemic cells from 42 patients with ATL examined expressed IL-2 receptors that were detected by anti-Tac monoclonal antibody when examined immediately after the separation of cells or after the culture for 24 or 48 h. The number of anti-Tac binding sites ranged from 3,100 to 11,400 in fresh cells and from 3,600 to 96,000/cell in short-term cultured leukemic cells, whereas phytohemagglutinin-P (PHA-P)-stimulated normal T cells exhibited 6,900-35,000 anti-Tac binding sites per cell. ATL-derived and human T cell leukemia/lymphoma virus, type I (HTLV-I)-infected cell lines such as MT-1 and Hut102 expressed a much higher number of anti-Tac binding sites. Leukemic cells from 15 patients with ATL examined showed no or very poor proliferative response to various concentrations of immunoaffinity-purified IL-2, although they expressed Tac antigen (Ag). Radiolabeled IL-2 binding experiments demonstrated that ATL leukemic cells could bind IL-2, and they expressed both high and low affinity IL-2 receptors, although the number of high affinity IL-2 receptor was much less than that of low affinity IL-2 receptor and that of anti-Tac binding sites. In contrast, leukemic T cells from a patient with T cell chronic lymphocytic leukemia (CLL), in whom HTLV-I infection was not demonstrated, responded as well as PHA-P-stimulated normal T cells, and their IL-2 receptors, unlike ATL cells, were modulated (down regulated) by anti-Tac antibody. No differences were noted between ATL cells and normal activated T cells in one-dimensional sodium dodecyl sulfate polyacrylamide gel electrophoresis analysis of the IL-2 receptor. Thus, leukemic cells in ATL spontaneously and continuously express IL-2 receptor, which appears to be abnormally regulated and unresponsive to IL-2. These results, taken together with those on normal IL-2 receptors on HTLV-I-negative T-CLL cells, suggest that abnormal expression of the IL-2 receptor in ATL is closely associated with HTLV-I infection and may play a role in the neoplastic growth of ATL cells.

Adult↗

Abnormal expression of interleukin-2 receptor (Tac antigen) in adult T-cell leukemia.

Human T-cell leukemia/lymphoma virus type I(HTLV-I) infection appears to be closely associated with the leukemogenesis of adult T-cell leukemia (ATL), although its mechanism remains unclear. Since our previous report that leukemic cells from patients with ATL expressed Tac antigen (Ag) (interleukin-2 (IL-2) receptor) on their cell surface, we have been studying IL-2 receptors on ATL leukemic cells to see whether they are different from normal IL-2 receptors and whether they play a role in the neoplastic growth of ATL cells. Peripheral blood leukemic cells from 35 patients with ATL expressed IL-2 receptors which were detected by anti-Tac monoclonal antibody when examined immediately after the separation of cells or after culture for 24 or 48 hr. The number of anti-Tac binding sites ranged from 4,300 to 11,400 in fresh cells and from 6,100 to 96,000/cell in short term cultured leukemic cells, whereas phytohemagglutinin-P(PHA-P)-stimulated normal T cells exhibited 7,000 to 35,000 anti-Tac binding sites/cell. HTLV-I-infected cell lines such as MT-1 and HUT-102 expressed a markedly enhanced number of Tac Ag molecules. Leukemic cells from 15 ATL patients showed no or very poor proliferative response to various concentrations of IL-2, although they expressed Tac Ag. Radiolabeled IL-2 binding experiments revealed that ATL leukemic cells could bind IL-2 although the number of IL-2 binding sites was much less than that of anti-Tac binding sites. IL-2 receptors on ATL cells, unlike normal activated T cells, were not modulated (down-regulated) by anti-Tac antibody.(ABSTRACT TRUNCATED AT 250 WORDS)

Antigens, Surface↗

Echocardiographic features of the false tendons in the left ventricle.

M mode and two dimensional echocardiographic features consistent with previously reported autopsy findings of false tendons were seen in 5 of approximately 1,000 consecutive echocardiographic examinations. Later, the presence of false tendon was proved at autopsy in one of the five cases. Examination in three cases revealed heart disease: aortic regurgitation, third degree atrioventricular (A-V) block with aortic regurgitation and invasive thymoma with pericardial effusion; examination in two cases revealed no heart disease. In three cases, M mode echocardiograms revealed in the outflow tract of the left ventricle abnormal linear echoes that strongly mimicked those in other disorders such as discrete subaortic stenosis or flail aortic valve. In two cases, there were abnormal linear echoes in the left ventricle toward the apex. In three cases, two dimensional echocardiograms revealed long-string-like echoes stretching from the upper part of the interventricular septum across the ventricular cavity to the lateral wall of the left ventricle in long and short axis views or in four chamber views. In two cases, long slender echoes between the lower parts of the interventricular septum and the left ventricle were seen in apical long axis views. These string-like echoes seem to represent the false tendons previously reported at autopsy, although actual pathologic confirmation was available in only one of the five cases. It is concluded that (1) M mode and two dimensional echocardiograms can demonstrate the presence of false tendons, (2) two dimensional echocardiograms are useful in differentiating false tendons from other conditions causing abnormal linear echoes in the outflow tract of the left ventricle on M mode echography.

Adult↗