[Subarachnoid dissemination of the brain tumor cells (author's transl)].
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Animals↗
Biomedical subjects
J Kuratsu
Publications and source records attributed to J Kuratsu.
Rat lymphocyte mitogenesis by aggregation factor from rat ascites hepatoma cell surface.
Two-tumour-cell-aggregation factors derived from rat ascites hepatoma cells had different antigenicity; one, with a strong potency, was not absorbed by immunoadsorbent chromatography with anti-rat serum antibody and the other, with a weak potency, was. The unabsorbed factor possessed mitogenic activity on lymphocytes from thymus, spleen and lymph node of rats; its effect was compared with that of lectins (including phytohaemagglutinin, concanavalin A, pokeweed mitogen, lipopolysaccharide and soybean agglutinin) in the form of increased DNA and protein synthesis, blast transformation and mitosis. In the use of anti-thymocyte serum-resistant spleen cells and hydrocortisone-resistant thymocytes, the cells stimulated were assumed to be T-lymphocytes. DNA synthesis by this factor seemed to be characterized by a 2-step increase, suggesting the presence of 2 subpopulations of the cells activated, especially thymocytes. At high concentration this factor induced no depression of DNA synthesis. Favourable cell density for the response to this factor was 2-8 X 10(6) cells. Its effect was not influenced by treatment of the cells with neuraminidase.
Animals↗
Ventriculolumber perfusion of 3-[(4-amino-2-methyl-5-pyrimidinyl)-methyl]-1-(2-chloroethyl-1-nitrosou rea hydrochloride for subarachnoid dissemination of gliomas.
The toxicity and therapeutic effect of the ventriculolumber perfusion of 3-[(4-amino-2-methyl-5-pyrimidinyl)methyl-1-1(2-chloroethyl)-1-nitros our ea hydrochloride (ACNU) against subarachnoid dissemination of gliomas were studied. Twenty-one patients (6 patients with anaplastic glioma, 7 with glioblastoma and 8 with medulloblastoma or PNET) received ventriculolumber perfusion of ACNU when they were diagnosed as having subarachnoid dissemination. The course of perfusion and cumulative dose of ACNU was 10 times and 95 mg on average, respectively. Most of the patients received systemic chemotherapy in combination with perfusion therapy and some patients with radiotherapy. Response rate was 17% and median survival time after the diagnosis of dissemination was 12 months for anaplastic gliomas, 29% and 12 months for glioblastoma, and 88% and over 25 months for medulloblastoma and PNET. The ventriculolumber perfusion of ACNU was performed for prophylactic purpose in 7 patients with high risk at the early postoperative period in combination with conventional adjuvant therapy. The course of perfusion and cumulative dose of ACNU was 2.3 times and 21 mg on average, respectively. One patient developed subarachnoid dissemination and died 22 months after surgery. Other 6 patients survived without dissemination on median over 29 months after surgery. Side effects encountered were headache in 4 patients, nausea and vomiting in 5, a convulsion in 2, right facial weakness in 1, fecal incontinence in 3 and meningitis in 2. They were all temporary except for facial weakness occurred in one patient. These data suggest that the ventriculolumber perfusion of ACNU is a safe and useful in the treatment and prophylaxis against the subarachnoid dissemination of gliomas.
Adolescent↗
Biological role of thymidine phosphorylase in human astrocytic tumors.
Thymidine phosphorylase (TP) has strong angiogenic activity and is overexpressed in a wide variety of malignant tumors. To elucidate the role of TP in human astrocytic tumors, we immunohistochemically investigated the expression of TP in 62 astrocytic tumors (12 astrocytomas, 12 anaplastic astrocytomas and 38 glioblastomas). Fifty-five astrocytic tumors (88.7%) were immunopositive for TP. The level of TP-expression was significantly correlated with the malignancy grade of astrocytic tumors; most of malignant gliomas highly expressed TP, while a small number of cells were positive in low grade astrocytomas (p < 0.001). Using double-immunostaining, we clarified that TP-expression was predominantly detectable in macrophages. There was no significant correlation between MIB-1 labeling index and TP-expression. However, TP-expression and the microvessel density were well correlated. These suggest that TP, mainly produced by the infiltrated macrophages, may play an important role in the progression of astrocytic tumors via neovascularization. Inhibitor of TP may represent a therapeutic modality for treating malignant gliomas.
Antigens, CD↗
Antiproliferative effect of YM881 (SMANCS) on glioma cells in vitro.
Growth inhibitory activity of YM881 (SMANCS) against 3 human cultured cell lines and one rat cultured cell line derived from glioma cells was assessed quantitatively. YM881 showed potent cytotoxicity against all glioma cell lines tested; the IC50 of this drug was 1.9-8.4 micrograms/ml. YM881 may be classified as a concentration-dependent drug but it has also a time-dependent effect. Flow cytometric studies of the DNA histogram showed accumulation in the G2-M phase with YM881. These findings suggest that YM881 may be useful in the treatment of glioma.
Animals↗
Stimulatory effect of suramin on the proliferation of human glioma cells.
Suramin, a non-specific growth factor antagonist, has been reported to have pleiotrophic action on the proliferation of some kinds of tumours and has therefore attracted attention as an agent in the treatment of cancer. We studied its action on human glioma cell lines in vitro by examining the effect of suramin on the proliferation and the cell cycle and mitogen-activated protein (MAP)-kinase activity of glioma cells. We found that at low concentration (50, 100 micrograms/ml) suramin had a stimulatory effect while at higher concentrations (200, 500 micrograms/ml) it had an inhibitory effect on the proliferation of 4 human glioma cell lines. At low concentrations, suramin stimulated the transition of glioma cells from a quiescent state (G0) to the proliferative phase (S phase); MAP kinase activity was also increased. The stimulatory effect of low concentrations of suramin on the proliferation of glioma cells may have important consequences for glioma patients treated with suramin.
Calcium-Calmodulin-Dependent Protein Kinases↗