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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↗
PubMedDate not supplied

[Differential diagnosis of multiple gliomas, multicentric gliomas and the other main endocranial multifocal lesions. Presentation of a case].

Multifocal gliomas represent an uncommon lesion, particularly if the supra-tentorial and infra-tentorial spaces are involved. The Authors describe a particular case and they outline the main differences between multiple gliomas and multicentric gliomas. Then, they consider the various possibilities of diagnosis and differential diagnosis of multiple endocranial lesions.

Brain Neoplasms↗
PubMed1980

[Immunofluorescence microscopy of a malignant glioma with regard to the occurrence and significance of glioma specific antibodies].

The paper deals with the question of the occurrence and possible importance of the glioma-specific humoral antibodies to the growth of malignant gliomas. The use of the immunofluorescence technique by means of fluorescein isothiocyanate labelled antihuman immunoglobulin sera permits to make the presence of antibodies of various types in the tumor cell membranes of autopsy material probable. Such non-cytotoxic antibodies might promote the growth of malignant gliomas by an inhibition of the cell-mediated immunoreaction (efferent enhancement).

Adult↗
PubMed1996

Effects of hepatocyte growth factor (HGF) on human glioma cells in vitro: HGF acts as a motility factor in glioma cells.

Expression of c-Met, the receptor for hepatocyte growth factor (HGF), and the biological roles of HGF were examined in cultured human glioma cells. All of the 5 glioma cell lines examined expressed c-Met protein as well as the c-met gene. Expression of the c-met gene was also confirmed in a glioblastoma tissue. Three cell lines (MGM-3, U251, KG-1-C) demonstrated chemotactic response to HGF in a dose-dependent manner. The response was not only chemotactic but also chemokinetic as judged by a checkerboard analysis. The amounts of c-Met mRNA and protein were abundant in the cell lines which showed a migratory response to HGF. Moreover, c-Met protein expression was highest in U251 with the highest migratory response to HGF. Among the cell lines, KG-1-C produced notable amounts of HGF protein as well as of c-Met, suggesting that HGF may act in an autocrine fashion in this case. HGF did not act as an apparent growth factor in the glioma cell lines examined. Furthermore, HGF stimulated the production of metalloproteinase, probably gelatinase A, in U251 cells.

Cell Division↗
PubMed2004

Invasive phenotype observed in 1,3-bis(2-chloroethyl)-1-nitrosourea-resistant sublines of 9L rat glioma cells: a tumor model mimicking a recurrent malignant glioma.

OBJECT: Chemotherapy is suspected of having an effect on the generation of phenotypical heterogeneity and the development of drug resistance in tumors. Recurrent gliomas feature drug resistance as well as greater invasive growth than original tumors. The authors investigated phenotypical changes in invasion observed in 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU)-resistant sublines of the 9L rat gliosarcoma. METHODS: Two established BCNU-resistant sublines, derived from 9L gliosarcoma cells by treating these cells with BCNU in vivo or in vitro, were used in the study. An in vitro examination confirmed the resistance of the cells to BCNU treatment. The cells were implanted into the striatum of Fisher 344 rats, and histological examinations were performed to compare the growth patterns of the resultant tumors. A new brain tumor model was established by implanting 9L-2 cells in Fisher 344 rats. The 9L-2 and BTRC-19 cells displayed a distinct increase in BCNU resistance compared with the 9L cells. Both BCNU-resistant sublines developed a tumor mass with invasive margins, which is not the case with 9L tumor models. The newly developed 9L-2 tumor model demonstrated 100% tumor uptake with consistent growth patterns. CONCLUSIONS: Cells that acquire drug resistance also demonstrated invasive growth. Because the 9L-2 and BTRC-19 cells were derived from 9L cells that had been treated with BCNU in vivo and in vitro, this change in phenotype was likely caused by the drug treatment, which may have implications for chemotherapy of gliomas. The tumor model that developed from the 9L-2 cells can be used as a model of a recurrent glioma, which features drug resistance and invasive growth.

Animals↗
PubMedDate not supplied

Comparative amplification analysis of human glioma tissue and glioma derived fragment spheroids using reverse chromosome painting (RCP).

Tumor fragment spheroids (TFS) represent an organotypic in vitro model with preserved cytoarchitecture and matrix components of the native tumor in situ. In order to determine whether DNA amplifications within gliomas remain stable in spheroid culture, tumor fragment spheroids were established from 15 human gliomas including 14 glioblastoma and one anaplastic astrocytoma. Native tumor tissue, monolayers as well as TFS were evaluated for DNA amplification using reverse chromosome painting (RCP). A modified protocol for DNA isolation from TFS was established. Amplifications in the original tumor tissue were found on chromosomes 12q13-15, tel, 4q12-13 and 11p12-13, an amplification on 11p12-13 is reported for the first time. By RCP we could demonstrate that amplified domains on 12q13-15 and 4q12-13 in three tumors were maintained in TFS whereas the amplification on 11p12-13 could not be confirmed in TFS. In monolayer cultures, all amplifications which were detected in primary culture were lost until passage 5. The results of this first comparative study of DNA amplification in glioma by analyzing native tumor tissue and tumor fragment spheroids enables us to conclude that TFS seems to be a promising in vitro model for the study of DNA amplification under cell culture conditions.

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↗
PubMed1994

Transfection of glioma cells with the neural-cell adhesion molecule NCAM: effect on glioma-cell invasion and growth in vivo.

The tumor growth and the invasive capacity of a rat glioma cell line (BT4Cn) were studied after transfection with the human transmembrane 140-kDa isoform of the neural-cell adhesion molecule, NCAM. After s.c. injection, the NCAM-transfected cells showed a slower growth rate than the parent cell line (BT4Cn). Upon intracerebral implantation with BT4Cn cells and different clones of NCAM-transfected cells, all animals developed neurological symptoms within 13-16 days. However, the tumors showed different growth characteristics. The NCAM-transfected BT4Cn cells were localized in the region of the injection site, with a sharply demarcated border between the tumor and brain tissue. In contrast, the parental cell line showed single-cell infiltration and more pronounced destruction of normal brain tissue. Using a 51Cr-release assay, spleen cells from rats transplanted with BT4Cn tumor cells generally showed a lower cytotoxic response than the spleen cells from rats transplanted with the transfected variants of BT4Cn cells, indicating that the transfection procedure in itself mediated an activation of the immune system. The present data suggest that NCAM may influence the malignant behavior of rat glioma cells in vivo.

Animals↗
PubMed1996

A strategy for selective anti-cancer drug concentration increase in rat glioma tissue with Ca(2+)-channel blocker co-administration: calcium kinetics in intra-glioma arteriolar smooth muscle cells.

A rat glioma model was employed to estimate the Ca2+ kinetics in the tumor arteriolar smooth muscle cells. Electron microcytochemistry revealed that the density of intracellular Ca2+ deposits in the intra-tumor arteriolar smooth muscle cells was significantly greater, with slightly higher membrane Ca(2+)-adenosine triphosphatase (ATPase) activity, compared to the contralateral cerebral arterioles. Furthermore, the administration of tyrphostin, a tyrosine kinase inhibitor, specifically increased only the intra-tumor blood flow. These findings suggest that the condition of the intra-tumor arteriole alters the susceptibility to contraction by the accelerated Ca2+ influx into the cytoplasm mediated through the tyrosine kinase pathway. After the administration of diltiazem, which also has a blocking effect on the Ca(2+)-channel mediated through this pathway, the local intra-tumor blood flow showed an increase of 39% with a marked decrease of intracellular Ca2+ concentration of the arteriolar smooth muscle cells in the tumor, while the blood flow in the basal ganglia increased by only 8%. The intra-tumor concentration of Nimustine-HCl (ACNU) with co-administration of diltiazem was significantly increased compared to that without the co-administration. Co-administration of diltiazem may be a valuable strategy in chemotherapy for glioma in affording the selective increase of intra-tumor concentration of the anti-cancer drug.

Animals↗
PubMed1994

A rat glioma model, CNS-1, with invasive characteristics similar to those of human gliomas: a comparison to 9L gliosarcoma.

A glioma cell line, CNS-1, was developed in the inbred Lewis rat to obtain a histocompatible astrocytoma cell line with infiltrative and growth patterns that more closely simulate those observed in human gliomas. Rats were given weekly intravenous injections for a six month period with N-nitroso-N-methylurea to produce neoplasm in the central nervous system. Intracranial tumor was isolated, enzymatically and mechanically digested, and placed into culture. The tumor cell line injected subcutaneously on the flanks of Lewis rats grew extensively in situ as cohesive tumor masses but did not metastasize. Intracranially, CNS-1 demonstrated single cell infiltration of paranchyma and leptomeningeal, perivascular, and periventricular spread with expansion of the tumor within choroid plexus stroma. CNS-1 cells titrated in right frontal brain of Lewis rats at 10(5), 5 x 10(5), 10(5), 5 x 10(4) cells per group had mean survival times ranging from 20.5 to 30.2 days. CNS-1 was immunoreactive for glial fibrillary acidic protein, S100 protein, vimentin, neural cell adhesion molecule, retinoic acid receptor alpha, intercellular adhesion molecule, and neuron specific enolase. The CNS-1 cells commonly had one or more trisomies of chromosomes 11, 13 or 18; losses, possibly random, of chromosomes (3, 5, 19, 30, X or Y) were noticed, and a marker chromosome made up of approximately 3 chromosomes was usual. Comparisons of CNS-1 to 9L gliosarcoma tumor were made. The glial CNS-1 tumor model provides an excellent system in which to investigate a variety of immunological therapeutic modalities. It spreads within brain in a less cohesive mass than 9L and is accepted without rejection in non-central nervous system sites by Lewis rats.

Animals↗
PubMed1997

The role of protein kinase C (PKC) in the evolution and proliferation of malignant gliomas, and the application of PKC inhibition as a novel approach to anti-glioma therapy.

The present article reviews the role of the second messenger enzyme protein kinase C (PKC) in the growth regulation of high-grade gliomas, and evaluates the efficacy of therapeutic strategies directed against PKC for blocking the proliferation of these malignancies in in vitro and in vivo models. The translation of such strategies to the treatment of patients with malignant gliomas may provide a novel approach for improving the otherwise grim outlook associated with these neoplasms.

Animals↗
PubMed1994

Tectal plate gliomas. Part I: Microsurgery of the tectal plate gliomas.

A series of 12 patients with tectal plate gliomas, is presented treated by direct surgery. Mean age was 19 years. All patients presented with signs of raised intracranial pressure and supratentorial hydrocephalus on CT scan. Diplopia was the most common local sign. CT scan and MR imaging showed 4 intrinsic, 6 exophytic, and 2 ventrally infiltrating tectal tumours. The histological diagnosis was low-grade astrocytoma in 7, high-grade astrocytoma in 2, oligodendroglioma in one, oligo-astrocytoma in one, and ependymoma in one case. The suboccipital supra- and transtentorial approach was used in every cases. Tumour resection was generous at the level of the superior colliculi, but on the contrary, resection was limited at the level of inferior colliculi due to the auditory risk. Tumour removal was total (macroscopically) in 9 cases and partial in 3 cases. There were 4 surgical complications and one death related to surgery. Parinaud's syndrome was the most-common postoperative sequelae. Auditory hallucinations and the acoustic neglect syndrome were seen once. In three cases additional radiotherapy and chemotherapy were given once with severe sequelae. The treatment of tectal plate gliomas is controversial. The role of different therapeutic options remains open. We consider the tectal plate as a relatively safer territory for surgery than the ventral part of the midbrain. The brain stem auditory evoked potentials (BAEPs) and middle latency potentials (MLPs) monitoring can help to determine the appropriate limit of surgery.

Adolescent↗
PubMed1994

Tectal plate gliomas. Part II: CT scans and MR imaging of tectal gliomas.

CT scans and MR images were analyzed in 12 patients with histologically proved tectal plate gliomas. In an attempt to identify the nature of these lesions, their radiological characteristics were correlated with the histological results. In four of our patients CT scan failed to show the tumour. MR imaging demonstrated the tectal distortion in all cases. Contrast enhancement, calcification, cystic portions, exophytic nature were observed in both high and low-grade gliomas. We conclude that in the case of intrinsic tectal tumours, the most probable diagnosis is that of low-grade astrocytoma while in the case of exophytic tectal tumours, the differential diagnosis from pineal region tumour is required and a histological verification is necessary.

Adolescent↗
PubMed2003

Familial gliomas. Analysis of six families with cerebral gliomas and without other inheritable syndromes.

Although a familial tendency to develop brain tumors in the absence of well-recognized hereditary disorders is an important issue, it has been rarely reported. Studies of the familial occurrence of gliomas have yielded conflicting results. This phenomenon may be imputable to chance or environmental or hereditary factors. Furthermore, epidemiological and genetic investigations are fundamental to evidence of whether hereditary factors are active in the development of these tumors. We describe a group of six families, in each of which more than one member had glioma, and discuss the probable mechanisms of oncogenesis in familial tumors in light of the pertinent literature.

Adolescent↗
PubMed1986

The GTP-binding regulatory proteins of neuroblastoma x glioma, NG108-15, and glioma, C6, cells. Immunochemical evidence of a pertussis toxin substrate that is neither Ni nor No.

Amounts of the guanine nucleotide binding regulatory proteins which are also pertussis toxin substrates (such as Ni and No) were measured in rat glioma, C6BU-1, cells and in neuroblastoma X glioma, NG108-15, hybrid cells. Measurements were performed both by quantitating pertussis toxin catalyzed ADP-ribosylation and by quantitative immunoblotting with affinity purified antibodies specific for Ni or No. The amounts of pertussis toxin substrate in C6 and NG108-15 cells are 7.5 and 0.6 pmol/mg membrane protein, respectively. These levels are minimum values and higher estimates of the total amounts of N proteins in the two cells are obtained by quantitative immunoblot analysis of the beta-subunit common to all N proteins. Immunoblots with specific antibodies show that NG108-15 cells contain 3.8 pmol/mg of No and detectable but small (less than 0.1 pmol/mg) amounts of Ni. In contrast, C6 cell membranes contain no detectable No and only 0.14 pmol/mg Ni. Thus, C6 cells contain large amounts of a pertussis toxin substrate which is neither Ni nor No.

Animals↗
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↗
PubMed2006

Expression of CXC chemokine receptors 1-5 and their ligands in human glioma tissues: role of CXCR4 and SDF1 in glioma cell proliferation and migration.

Chemokines have been involved in cellular processes associated to malignant transformation such as proliferation, migration and angiogenesis. The expression of five CXC chemokine receptors and their main ligands was analysed by RT-PCR in 31 human astrocytic neoplasms. The mRNAs for all the receptors analysed were identified in a high percentage of tumours, while their ligands showed lower expression. CXCR4 and SDF1 were the most frequently mRNA identified (29/31 and 13/31 of the gliomas studied, respectively). Thus, we further analysed the cell localization of CXCR4 and SDF1 in immunohistochemistry experiments. We show a marked co-localization of CXCR4 and SDF1 in tumour cells, mainly evident in psudolpalisade and microcystic degeneration areas and in the vascular endothelium. In addition, hSDF1alpha induced a significant increase of DNA synthesis in primary human glioblastoma cell cultures and chemotaxis in a glioblastoma cell line. These results provide evidence of the expression of multiple CXC chemokines and their receptors in brain tumours and that in particular CXCR4 and SDF1 sustain proliferation and migration of glioma cells to promote malignant progression.

Base Sequence↗
PubMed1997

Growth factor profiles of human gliomas. Do non-tumour cells contribute to tumour growth in glioma?

BACKGROUND: Growth factors play a role in proliferation and motility of malignant glial cells, through autocrine and paracrine mechanisms. Also, proliferation of non-tumour cells, e.g., endothelial cells, is likely to be controlled by growth factors. Several growth factors with their appropriate receptors can be involved, but studies on tissue specimens evaluating this in glioma are rare. MATERIALS AND METHODS: We evaluated the potential role of Transforming growth factor-alpha (TGF-alpha) and Epidermal growth factor receptor (EGF-R), the Platelet-derived growth factor A- and B-chain (PDGF-A and PDGF-B) and its receptors (PDGFR alpha and PDGFR beta, and basic fibroblast growth factor (bFGF) in gliomas by analysing 86 of these tumours on the single cell level for the presence of immunoreactive growth factors and receptors. In a few cases double-staining experiments were done to directly visualize co-expression of factor and receptor. RESULTS: Multiple growth factors and their receptors are present in astrocytic tumours; the higher the grade, the more growth factors and the more positive cells are found. Oligodendroglial tumours and pilocytic astrocytomas showed little expression. Autocrine and paracrine mechanisms were frequently possible in the astrocytic tumours, often more than one loop could be involved. Interestingly, it was also frequently possible that non-tumour cells produced a growth factor for which the tumour cells expressed the receptor. CONCLUSIONS: Multiple growth factors appear to be involved in astrocytic tumours, with frequent autocrine and paracrine loops. Expression of these molecules seems to increase with increasing grade. The results argue for a contribution of non-tumour cells to the growth of a tumour.

Astrocytoma↗