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Biomedical subjects

T Matsui

Publications and source records attributed to T Matsui.

At least 955 records · Page 53Linked to original sources
PubMed1985

Effects of calmodulin antagonists and cytochalasins on proliferation and differentiation of human promyelocytic leukemia cell line HL-60.

To identify the possible roles of Ca2+-related proteins, calmodulin and microfilaments in leukemic cells, we tested the effect of calmodulin antagonists and cytochalasins on proliferation and differentiation of human promyelocytic leukemic HL-60 cells. The growth of HL-60 was inhibited by N-(6-aminohexyl)-5-chloro-1-naphthalenesulfonamide, N-(4-aminobutyl)-5-chloro-2-naphthalenesulfonamide, and trifluoperazine dihydrochloride. In contrast, the 1,25-dihydroxyvitamin D3 [1,25-(OH)2D3]-induced differentiation of HL-60, as judged by plasma-membrane antigenic changes detected by monoclonal antibodies (OKM1, OKT9), nitroblue tetrazolium reduction, and induction of phagocytotic capacity, was not inhibited by N-(6-aminohexyl)-5-chloro-1-naphthalenesulfonamide or N-(4-aminobutyl)-5-chloro-2-naphthalenesulfonamide, although phagocytosis was depressed by N-(6-amino-hexyl)-5-chloro-1-naphthalenesulfonamide or N-(4-aminobutyl)-5-chloro-2-naphthalenesulfonamide. Trifluoperazine dihydrochloride also failed to inhibit the antigenic change induced by 1,25-(OH)2D3. Cytochalasins B and D, microfilament-disrupting agents, inhibited the cytoplasmic division and the growth of HL-60 but did not inhibit the 1,25-(OH)2D3-induced differentiation. These findings suggest that the calmodulin- and microfilament-dependent process may be involved in the proliferation of HL-60, but not in the differentiation induced by 1,25-(OH)2D3.

Calcitriol↗
PubMed1985

[Clinical evaluation of cases of remission induction failure in acute myelogenous leukemia].

Among 73 patients who were admitted to our hospital between 1972 and 1983, 9 died before starting chemotherapy, 29 achieved complete remission (CR) with an initial regimen of induction chemotherapy, while the remaining 35 patients failed to achieve CR with this initial regimen. Patients with high initial WBC counts (greater than 100,000/cmm), old age, temperature (greater than 38 degrees C) and antecedent hematological disorders, were more prone to failure of remission induction therapy. Comparing CR patients and non-CR patients, there seemed to be no difference in sex distribution, initial platelet counts, initial LDH, percentage of blasts in the blood and bone marrow, the incidence of DIC and the regimen used for remission induction. According to Preisler's criteria, remission induction failure cases were further subdivided into various types and the numbers of each type were as follows: Type I (absolute drug resistance) 1, Type II (relative drug resistance) 16, Type III (regeneration failure) 0, Type IV (hypoplastic death) 6 and Type V (early death) 11. Among 18 M1 cases, 8 were Type II or Type V. Four out of 7 M2 cases belonged to Type II and all 3 M3 cases were Type V. Six out of the 35 remission induction failure patients entered CR with the 2nd chemotherapy regimen and 19 patients died during induction treatment with the initial induction regimen. Causes of death were infection (5 cases), bleeding (6 cases), infection and bleeding (3 cases) and organ failure (5 cases).

Adolescent↗
PubMed1985

Amplification and enhanced expression of cellular oncogene c-Ki-ras-2 in a human epidermoid carcinoma of the lung.

The level of c-Ki-ras-2-specific mRNA was found to be markedly enhanced (10- to 20-fold) in a human epidermoid lung carcinoma transplanted into nude mice, compared with that in other lung carcinomas. Analysis of DNA revealed that c-Ki-ras-2 gene was amplified approximately 10-fold in this carcinoma, while c-Ha-ras, c-myc and c-sis were not amplified. Chromosome abnormalities were also observed in this carcinoma.

Aged↗
PubMed1985

Cooperative regulation of c-myc expression in differentiation of human promyelocytic leukemia induced by recombinant gamma-interferon and 1,25-dihydroxyvitamin D3.

The biological activity of recombinant human gamma-interferon (IFN-gamma) to induce the phenotypic differentiation of human promyelocytic leukemia cell line HL-60 and to regulate c-myc expression was evaluated. Treatment with IFN-gamma increased monocyte-associated cell surface antigens detected by monocyte-specific monoclonal antibodies in a dose- and time-dependent manner. These antigenic changes were accompanied by a functional differentiation, determined by the increase of phagocytic capability and superoxide generation. IFN-gamma was also found to suppress the growth of HL-60 cells and reduce expression of a c-myc oncogene. These phenotypic and morphological changes to macrophage-like cells induced by IFN-gamma were similar to those by 1,25-dihydroxyvitamin D3, whereas the plasma membrane antigenic changes were different. Moreover, the combination of IFN-gamma and suboptimal doses of 1,25-dihydroxyvitamin D3 have synergistic effects in augmenting mature monocyte specific antigens (Mo2, 63D3, OKM1, and OKM5). In the reduction of c-myc expression by these drugs, a cooperative effect was observed with the inhibition of transferrin receptor expression and cell growth. These results indicate that human recombinant IFN-gamma induces a monocyte phenotype in the HL-60 cells via a mechanism different from the action of 1,25-dihydroxyvitamin D3.

Antigens, Surface↗
PubMed1985

[Malignant change of duodenal adenoma--a case report and review of the literature].

A 69-year-old woman with a large crater-forming carcinoma of the duodenal bulbus which was associated with a prominent tumor of tubulovillous adenoma in immediate proximity is reported. Histologically, an adenoma-carcinoma sequence was strongly suggested. A review of the literature from both Japan and other countries, after reclassification of histologic patterns, suggested that tubulovillous adenoma in the duodenum may be predominant as compared with that of the colon.

Adenoma↗