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At least 19 recordsLinked to original sources
PubMed1992

Bradykinin and muscarine induce Ca(2+)-dependent oscillations of membrane potential in rat glioma cells indicating a rhythmic Ca2+ release from internal stores: thapsigargin and 2,5-di(tert-butyl)-1, 4-benzohydroquinone deplete InsP3-sensitive Ca2+ stores in glioma and in neuroblastoma-glioma hybrid cells.

Continuous superfusion of rat glioma cells with medium containing bradykinin (from 0.2 nM) induced a transient hyperpolarization followed by regular hyperpolarizing oscillations of the membrane potential. Similar repetitive hyperpolarizing oscillations were caused by extracellularly applied bradykinin or muscarine or by intracellularly injected GTP-gamma-S. The frequency of the oscillations was 1 per minute at bradykinin concentrations ranging from 0.2 nM to 2 microM, but the amplitude and duration increased with rising peptide concentration. The muscarine-induced oscillations were blocked by atropine. In the presence of extracellular Ca2+, the substances thapsigargin, 2,5-di(tert-butyl)-1,4-benzohydroquinone (tBuBHQ), and ionomycin reversibly suppressed the bradykinin-induced oscillations. Thapsigargin and tBuBHA, which are known to block the Ca2+ ATPase of endoplasmic reticulum, caused a transient rise in cytosolic Ca2+ activity, monitored with Fura-2, in suspensions of rat glioma cells or of mouse neuroblastoma-rat glioma hybrid cells. After a transient Ca2+ rise caused by thapsigargin, tBuBHQ, or ionomycin, the Ca2+ response to bradykinin which is known to be due to release of Ca2+ from internal stores was suppressed. This indicates that thapsigargin and tBuBHQ deplete internal Ca2+ stores as already seen previously for ionomycin. Thus, the inhibition of the membrane potential oscillations by thapsigargin, tBuBHQ, and ionomycin indicates that the oscillations are associated with activation of InsP3-sensitive Ca2+ stores. In some cells composite oscillation patterns which consisted of two independent oscillations with different amplitudes that overlapped additively were seen. We discuss that this pattern and the concentration dependency of the oscillations could be due to "quantal" Ca2+ release from stores with different inositol 1,4,5-triphosphate sensitivities. Subsidence of the oscillations after omission of extracellular Ca2+ seems to be due to a lack of replenishment of the intracellular stores with Ca2+, which comes from the extracellular compartment.

Animals↗
PubMed1992

Protein kinase C activity correlates with the growth rate of malignant gliomas: Part II. Effects of glioma mitogens and modulators of protein kinase C.

The proliferation rates of gliomas may be modulated by the protein kinase C (PKC) signal transduction system. The present study was undertaken to further examine the role of PKC system in growth regulation of gliomas in vitro by measurement of PKC activity over various phases of tumor growth and by assessing its potential role as a signal transduction system induced by serum mitogens and the known glioma mitogens epidermal growth factor and fibroblast growth factor. All human glioma lines examined, and the rat glioma C6, displayed high PKC activity relative to nonmalignant glial cells, which correlated with their proliferation rates over their respective growth phase. Frozen surgical human malignant glioma specimens also displayed high PKC activity. The relatively selective PKC inhibitor staurosporine (SP) reduced PKC activity and corresponding growth rates in a dose-related manner. Stimulation of PKC with phorbol esters under different concentrations of serum in the growth medium indicated that the high PKC activity, which correlated with their rapid growth rates, is highly susceptible to down-regulation by these agents. Epidermal growth factor and fibroblast growth factor increased both PKC activity and the growth rate of glioma line A172; addition of SP reduced the growth rate to levels observed in SP-treated control tumors, indicating that PKC may be a common signal transduction system induced by these mitogens. These results implicate PKC as an important signal transduction system regulating glioma growth, and offers a potential target for tumor inhibition.

Animals↗
PubMed1978

Scanning electron microscopy of malignant gliomas. A comparative study of glioma cells in smear preparations and in tissue culture.

Smear preparations from 15 malignant gliomas, 2 metastatic carcinomas and from normal brain were examined by scanning electron microscopy. Tissue culture preparations from malignant gliomas were also studied. In the better differentiated areas of gliomas, the cells in smears were stellate with multiple long interweaving processes 0.25--1.3 micrometer in diameter which could be distinguished from myelinated nerve fibers (1.3--5 micrometer) and from fibrin (0.08--0.3 micrometer) by their thickness and arrangement in the tissue. The relationship of glial processes to blood vessels within the tumour was well demonstrated in smears. Metastatic carcinoma cells lacked the processes seen in glioma cell smears and did not show the same relationship to blood vessels. The more anaplastic glioma cells had fewer processes and ovoid cell bodies covered with surface ruffles and microvilli similar to the cell membrane projections in the nuclear regions of glioma cells in culture. The relationship of the surface morphology of glioma cells in smears to the known invasive nature of these tumours is discussed.

Brain Neoplasms↗
PubMed1979

Lactic dehydrogenase in ethylnitrosourea-induced rat gliomas. Total lactic dehydrogenase activity and isozymes in autochthonous gliomas and cloned transplantable astrocytomas.

Total lactic dehydrogenase (LDH) levels and LDH isozyme patterns were measured in homogenates of 12 autochthonous ethylnitrosourea-induced rat gliomas and 5 cloned rat astrocytoma cell lines maintained in culture and transplanted to brain or flank sites in syngeneic hosts. The total LDH values in the autochthonous gliomas did not differ appreciably from normal brain controls, but the proportions of the cathodal isozymes, LDH4 and LDH5, were increased to a degree similar to that reported by others in spontaneous human malignant astrocytic gliomas. The cloned astrocytoma lines, both in vitro and in transplants at intracerebral or subcutaneous sites, commonly demonstrated elevated total LDH values and, without exception, showed a preponderance of isozymes, LDH4 and LDH5, that was distinctly more marked than in autochthonous tumors. Especially in cultured and transplanted rat gliomas, these findings suggest that astrocytic tumor cells maintain energy supplies by utilizing anaerobic glycolysis in relatively hypoxic environments. These data further underscore the need to develop laboratory brain tumor models for use in therapy trials that not only retain the convenience and predictability of transplantable gliomas but also approximate closely the metabolic properties of human spontaneous gliomas.

Animals↗
PubMed1990

Induction of cytotoxicity in human T cells coated with anti-glioma x anti-CD3 bispecific antibody against human glioma cells.

A bifunctional hetero-F(ab')2 antibody fragment was developed that contained the Fab portions from anti-CD3 and anti-glioma monoclonal antibodies. The antibody simultaneously recognized two different molecules, the CD3 complex on effector T cells and a human glioma-associated antigen; thus, it could cross-link effector and target cells. This bispecific F(ab')2 fragment induced peripheral blood mononuclear cells (PBMC's) from healthy donors to lyse cells of the human glioma cell line, U251MG, which are resistant to natural killer cell-mediated cytolysis. The effect of the bispecific antibody on lymphokine-activated killer (LAK) cell activity was tested in patients suffering from malignant glioma. For this study, PBMC's from these patients were preactivated with recombinant interleukin-2 and their killer activity against U251MG cells was investigated in vitro with and without the bispecific antibody. The LAK cell activity of the PBMC's from patients with malignant gliomas was found to be suppressed compared with those of healthy donors. However, after preincubation with bispecific antibody, the patients' LAK cells exhibited marked cytolytic activity against U251MG cells. These findings suggest that this bispecific antibody may be a useful addition to anti-glioma immunotherapy.

Antibodies, Monoclonal↗
PubMed1991

[Total removal of hypothalamic glioma 15 years after irradiation of right optic glioma].

Hypothalamic glioma was found in a 17 year old male patient 15 years after irradiation of right optic glioma. It was totally removed by surgery. He was first admitted to Ryukyu University Hospital at the age of 1 year and 11 months, with right exophthalmos and visual disturbance. Diagnosis was anterior type of right optic glioma. This was treated by irradiation (47 Gy). Follow-up CT scans revealed no regrowth in intraorbital and intracranial regions. At the age of 17 years, CT scan and MRI showed an enhanced mass in the hypothalamus above the suprasellar cistern. Total removal was performed by bifrontal interhemispheric trans-lamina terminalis approach. Histological diagnosis was pilocytic astrocytoma. Postoperatively, consciousness remained disturbed for 3 weeks because of infarction in the bilateral medial nucleus of the thalamus. Radical excision of hypothalamic glioma was reviewed in the literature. We concluded that such excision has a potentially good outcome, and should be attempted when circumstances indicate its feasibility.

Adolescent↗
PubMed1992

[Experimental studies on the antitumor activity of glioma-infiltrating lymphocytes against autologous glioma].

In the present study, antitumor activity of glioma-infiltrating lymphocytes (GILs) was compared to that of lymphokine-activated killer (LAK) cells. Results suggested that killing activity of GILs against autologous glioma cells was significantly higher than that of LAK cells (P less than 0.05), but their activity against allogeneic glioma cells was not different from that of LAK cells (P greater than 0.05). Analysis of cell surface phenotypes showed that CD4+ cells were a main portion of LAK cells, and CD8+ were predominant in the GILs. In the beginning, growth of GILs was slower than that of LAK cells. As time went on, generation of GILs was faster than that of LAK cells. The results suggested that GILs were superior to LAK cells for adoptive immunotherapy in patients with brain glioma.

Brain Neoplasms↗
PubMed1977

Alanine inhibition of pyruvate kinase in gliomas and meningiomas. A diagnostic tool in surgery for gliomas?

In gliomas a shift was found in the composition of enzymes, manifested by abnormal inhibition of pyruvate kinase by alanine. This study demonstrates the appearance of the MII-type isoenzyme in various gliomas. This MII type is also found in meningiomas but not in normal brain tissue. The method of enzyme examination described may be valuable as a diagnostic aid in the surgery of gliomas.

Alanine↗
PubMed1990

[DAPI-DNA cytofluorometric study of glioma cells--application of DAPI-DNA cytofluorometry to paraffin embedded archival glioma tissue for nuclear DNA content analysis].

Using DAPI-DNA cytofluorometry, the author analyzed nuclear DNA content of formalin fixed, paraffin embedded, glioma material obtained from 14 glioma cases at surgery. Sections of 10 microns were deparaffinized. Following simultaneous DAPI (4,6-diamidino-2-phenylindole dihydroporphyrin chloride)/HP (hematoporphyrin) staining, DAPI binds DNA and DNA-DAPI complexes emit blue fluorescence when exited by ultraviolet (UV) light. Through Zeiss fluorescence microscope, the author measured nuclear fluorescence intensity with histological verification of glioma cells. A DNA histogram was obtained with fluorescence intensity recorded on the abscissa and number of cells plotted on the ordinate. Samples of 20 normal non-neoplastic astrocytes taken from apparently normal brain tissue included in the histological slide were used as diploid (2 C) control. Based on DNA content, tumor cells were classified into 4 groups: N-group composed of cells with 2 C DNA content (normoploid), S-group with less than 2 C (hypoploid), L-group more than 4 C (hypertetraploid), I-group between 2 C and 4 C (intermediate ploidy). Intermediate ploidy was significantly higher and normoploid was significantly lower in glioblastoma compared with those of benign astrocytoma. Thus, DNA content and histological malignancy were well correlated. Due to limitation of measuring diaphragm of turret in the microscope, some extra large cell could not be included in it and was excluded from the measurement.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1979

Reactive glioma in intracranial sarcoma: a form of mixed sarcoma and glioma ("sarcoglioma"): report of eight cases.

The clinicopathologic features of eight new cases of combined intracranial sarcoma and glioma are described. This type of mixed cerebral tumor is histologically characterized by a peripheral distribution of the gliomatous elements in relation to a more centrally situated meningeal or intracerebral sarcoma, and by the frequent presence of gradual transitions from reactive to frankly neoplastic astrocytes. In six of the eight cases, the additional development of either infiltrating astrocytoma or frank glioblastoma in the adjacent brain was demonstrated; this was interpreted as a further expression of malignant glial reaction. It is suggested that these tumors be termed "sarcogliomas" to distinguish them from the type of mixed glioma and sarcoma that has recently been redesignated "gliosarcoma."

Adolescent↗
PubMed1976

Two separate membrane-bound antigens on human glioma cells in tissue culture detected with sera from glioma patients by immunofluorescence.

Sera from patients with malignant and benign gliomas, as well as sera from healthy donors, were tested by indirect immunofluorescence to detect antibodies against antigens on the membrane of glioblastoma, astrocytoma, reactive perimetastatic glia, normal glia and fibroblasts in tissue culture. Sera from glioblastoma patients reacted with glioblastoma, astrocytoma and reactive glial cells; they were negative on normal glia and on fibroblasts, whereas sera from astrocytoma patients were unreactive. Sera from control patients were positive in 7 out of 15 cases, although some differences were noted in the pattern of reaction. Absorption with astrocytoma powder, with glioblastoma and reactive glial cells indicated that all the positive cell lines expressed an astrocytoma-associated antigen "A", while only glioblastoma lines and reactive glial line shared a supplementary antigen "G". Neither of these 2 antigens seemed to be present in significant amount in normal brain, since the positive reactions could not be abolished by absorption with normal brain powder. The relationship between these 2 antigens and the process of increasing malignancy in gliomas is briefly discussed.

Antibodies, Neoplasm↗
PubMed1979

Synergism between BCNU and irradiation in the treatment of anaplastic gliomas. An in vivo study using the avian sarcoma virus-induced glioma model.

The therapeutic effects of irradiation, BCNU, or combined irradiation and BCNU were studied in the avian sarrcoma virus (ASV)-induced glioma model in rats. Whole-head orthovoltage radiation therapy was given in six equal fractions over 2 weeks, and BCNU was administered intraperitoneally as a single dose of 10 mg/kg. Two series of experiments were performed in order to duplicate the results. In Series I, the median survival times of the experimental groups, in days after randomization were as follows: control group (no treatment), 69; group receiving 200 rads, 84 (p less than 0.05); group receiving BCNU, 80.5 (p less than 0.1); and group receiving 2000 rads + BCNU, 112 (p less than 0.001). In Series 2, the median survival times were: control group, 73.5; group receiving 2300 rads, 85 (p less than 0.01); group receiving BCNU, 92.5 (p less than 0.025); and group receiving 2300 rads + BCNU, 123.5 (p less than 0.001). In both series, combined therapy was significantly better than either radiation or BCNU alone. This is the first time that a synergistic effect of BCNU and irradiation has been reported in an in vivo brain-tumor model and supports the clinical use of this combination in the treatment of malignant gliomas.

Animals↗
PubMed1975

Boron neutron capture therapy of cerebral gliomas. II. Utilization of the blood-brain barrier and tumor-specific antigens for the selective concentration of boron in gliomas.

The use of the blood-brain barrier and of tumor-specific antibodies to concentrate boron selectivity in gliomas for neutron capture therapy is considered experimentally and theoretically. The time-dependent concentration of two anionic boranes, B12 H11 SH2- and B12 H11 SOSB12 H114-, in the blood, brain, and tumor of rats bearing a tumor of gliomatous origin is reported. The rate of clearance of each anionic borane from the blood is correlated with the fraction of non-protein bound anion in the plasma. The use of antibodies to carry therapeutical useful amounts of boron to tumor-specific or tumor-associated antigens on the tumor cell surface will require different numbers of boron atoms bound per antibody depending on several immunological and physical parameters. Calculations using published values of antibody-antigen association constants and of cell surface antigen densities predict that in order to obtain 10mug 10B/g tumor from 10 to over 10,000 boron-10 atoms will have to be bound per tumor antigenic site.

Animals↗
PubMed1991

[Isolation and expansion of glioma-infiltrating lymphocytes in vitro: an analysis of their surface phenotypes and antitumor activities].

The present study was conducted in order to examine the feasibility of isolating and growing glioma-infiltrating lymphocytes in vitro as possible effector cells for use in an adoptive immunotherapy. Thirty surgical specimens obtained from patients with malignant astrocytomas were studied. The glioma-infiltrating lymphocytes were separated from tumor tissue, expanded in the presence of interleukin-2, and evaluated their anti-tumor activities in vitro. Eighteen of 30 cultures of glioma-derived lymphocytes expanded with a substantial increase in cell numbers, of at least 5 x 10(8) cells up to 5 x 10(9), 4 to 8 weeks after the initiation of culture. The expanding glioma-derived lymphocytes consisted of 88 +/- 10% CD3+ T cells including both CD4+ and CD8+ subpopulations. CD16 was expressed on 4 +/- 5% of the cells and three cultures studied exhibited 14% +/- 1 of CD56+ cells. After 4 to 8 weeks of the proliferation period, the lymphocytes ceased to grow in all cultures. The glioma-derived effector lymphocytes could lyse almost all the autologous tumor targets as well as allogeneic glioma cells. The cytotoxic activity of the glioma-derived lymphocytes appeared to be similar or inferior to that of interleukin-2-activated peripheral blood lymphocytes obtained from the same patients in killing autologous glioma cells. The glioma-derived effector cells could also lyse three-dimensional glioma targets (spheroids), but this lytis activity was clearly lower than that of the activated peripheral blood lymphocytes. Ability of these effector cells to infiltrate glioma tissue was doubtful, since after 24-hours coculture of effector cells with target spheroids, the effector cells scarcely infiltrated the spheroids. In summary, glioma-derived lymphocytes expanded in bulk culture with interleukin-2 consisted predominantly of T-lymphoblasts with the ability to kill autologous glioma cells and also to lyse glioma spheroids. However a benefit of use of the glioma-derived lymphocyte as a novel effector cells in clinical trail replacing the IL-2-activated peripheral blood lymphocytes could not be found.

Adult↗