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PubMed1987

Heterogeneity of regional cerebral glucose metabolism demonstrated in situ in rat brain by 19F NMR rotating frame zeugmatography: one dimensional chemical shift imaging of normal and gliosarcoma implanted brain.

Using 19-fluorine (19F) as nuclear magnetic resonance (NMR) signal probe and 2-fluoro-2-deoxy-D-glucose (2-FDG) as metabolic probe, one dimensional "imaging" (metabolite mapping) of pathway specific glucose metabolism in the pentose monophosphate shunt (PMS) and aldose reductase sorbitol (ARS) pathways were performed in situ in rat brain utilizing one dimensional rotating frame zeugmatography. Normal brain showed highest PMS activities in the brainstem consonant with known spatially heterogeneous concentration of glucose-6-phosphate dehydrogenase, the rate limiting enzyme for the PMS. The brain harboring sufficiently large gliosarcoma in the cerebrum showed a higher PMS/ARS area ratio indicating higher PMS activities in tumor which was localized by zeugmatography. The present study demonstrated the feasibility of studying regional glucose metabolism in the PMS and ARS utilizing 2-FDG.

Aldehyde Reductase↗
PubMed2002

Evaluation and optimization of DNA delivery into gliosarcoma 9L cells by a cholesterol-based cationic liposome.

This paper reports results concerning the transfection of gliosarcoma cells 9L using an original cholesterol-based cationic liposome as carrier. This cationic liposome was prepared from triethyl aminopropane carbamoyl cholesterol (TEAPC-Chol) and a helper lipid, dioleoyl phosphatidyl ethanolamine (DOPE). The used concentration of liposome was not cytotoxic as revealed by the MTT test. TEAPC-Chol/DOPE liposomes allowed the plasmids encoding reporter genes to enter the nucleus as observed both by electron microscopy and functionality tests using fluorescence detection of green fluorescent protein (GFP) and luminometric measurements of luciferase activity. By changing the cationic lipid/DNA molar charge ratio, optimal conditions were determined. Further, improvement of the transfection level has been obtained by either precondensing plasmid DNA with poly-L-lysine or by adding polyethylene glycol (PEG) in the transfection medium. The optimal conditions determined are different depending on whether the transfection is made with cells in culture or with tumors induced by subcutaneous (s.c.) injection of cells in Nude mice. For in vivo assays, a simple method to overcome the interference of haemoglobin with the chemiluminescence intensity of luciferase has been used. These results would be useful for gaining knowledge about the potential for the cationic liposome TEAPC-Chol/DOPE to transfect brain tumors efficiently.

Animals↗
PubMed1990

Analysis of interleukin 2 and various effector cell populations in adoptive immunotherapy of 9L rat gliosarcoma: allogeneic cytotoxic T lymphocytes prevent tumor take.

Recombinant interleukin 2 (rIL-2) and various effector cell populations were used for adoptive immunotherapy in the Fischer strain 9L rat gliosarcoma model. The in vivo cytotoxicities of nonspecifically activated lymphocytes and specifically activated cytotoxic T lymphocytes (CTLs) were assessed in a modified in vivo neutralization (Winn) assay. Effector cells (10(6)) and 9L tumor cells (10(5] were combined with 10(4) units of rIL-2 and stereotactically implanted into the right frontal centrum semiovale of the Fischer (F344) rat. At 7 and 14 days, additional effector cells (10(6] and rIL-2 (10(4) units) were administered through the same burr hole. Nonspecifically activated splenocytes were lymphokine-activated killer (LAK) cells, both plastic-adherent and nonadherent, whereas specifically activated CTLs were either syngeneic (genetically identical) or allogeneic (genetically dissimilar). Syngeneic CTLs were T lymphocytes from Fischer rats primed in vivo with 9L cells and restimulated in vitro. Allogeneic CTLs were generated by exposing DA rat lymphocytes either to irradiated Fischer lymph node cells or to 9L Fisher tumor cells in vitro. Control groups included rats bearing 9L tumor who were untreated, those who received peripheral (i.p. or s.c.) administration of rIL-2, or those who received syngeneic unstimulated T lymphocytes and rIL-2. For a set of animals given the same inoculum of 9L tumor, significantly improved survival was shown for groups treated with nonadherent or adherent LAK cells (P less than or equal to 0.0003), syngeneic CTLs (P = 0.0327), or allogeneic CTLs (P = 0.0025) over untreated control animals by using Mantel-Haenzel nonparametric logrank equations. Only treatment with allogeneic CTLs prevented tumor take.

Animals↗
PubMed1992

Differential inhibition of proliferation of human squamous cell carcinoma, gliosarcoma and embryonic fibroblast-like lung cells in culture by plant flavonoids.

We investigated the antiproliferative effect of two polyhydroxylated (quercetin and taxifolin) and two polymethoxylated (nobiletin and tangeretin) flavonoids against three cell lines in tissue culture. Tangeretin and nobiletin markedly inhibited the proliferation of a squamous cell carcinoma (HTB 43) and a gliosarcoma (9L) cell line at 2-8 micrograms/ml concentrations. Quercetin displayed no effect on 9L cell growth at these concentrations, while at 8 micrograms/ml it inhibited HTB 43 cell growth. Taxifolin slightly inhibited HTB 43 cell growth at 8 micrograms/ml, while moderately inhibiting HTB 43 cell growth at 2-8 micrograms/ml. The proliferation of a human lung fibroblast-like cell line (CCL 135) was relatively insensitive to low concentrations of the above flavonoids.

Carcinoma, Squamous Cell↗
PubMed1980

Primary intracerebral tumor with mixed chondrosarcoma and glioblastoma--gliosarcoma or sarcoglioma?

An unusual primary intracerebral tumor with combined features of chondrosarcoma and glioblastoma multiforme is presented. Glial elements showing a spectrum of hyperplastic and neoplastic changes were intermingled with sarcomatous areas, similar to that recently described by Lalitha and Rubinstein as "sarcoglioma." Many vessels in the gliomatous regions contained proliferating endothelial cells with marked cytologic abnormalities. Although no direct extension out of the vessel wall was conclusively identified, the possibility of sarcomatous change could not be completely excluded. We conclude that, in this case, we could not establish whether the sarcoma was primary and the glioma secondary ("sarcoglioma") or vice versa ("gliosarcoma"), nor could we rule out that the two components originated from the same ancestral pluripotential cells.

Brain↗
PubMed1988

Patterns of epithelial metaplasia in malignant gliomas. II. Squamous differentiation of epithelial-like formations in gliosarcomas and glioblastomas.

Six cases are reported (four gliosarcomas and two glioblastomas) in which the epithelial-like areas of glial anaplasia showed focal squamous cell differentiation, characterized by the development of epithelial whorls, keratin pearls and immunopositivity for cytokeratin. The expression of glial fibrillary acidic protein and the development of squamous metaplasia usually were mutually exclusive. Autopsy findings in two patients and clinical work-up in five failed to disclose a primary extraneural malignancy. It is suggested that squamous differentiation may represent an extreme form of epithelial metaplasia in a malignant glioma. This possibility should be kept in mind in the diagnostic evaluation of such cases, especially in view of the current emphasis on the immunomorphologic demonstration of intermediate filament tumor markers.

Adult↗
PubMed1990

Anticopper treatment inhibits pseudopodial protrusion and the invasive spread of 9L gliosarcoma cells in the rat brain.

The copper ion, a cofactor of angiogenesis, is sequestered in human brain tumors and the adjacent brain. The invasive spread of neoplastic cells has been linked to angiogenesis and involves similar mechanisms of migration and tumor-matrix interaction. In this report, copper depletion inhibited the infiltrative spread of the normally invasive 9L gliosarcoma. Twenty made Fischer 344 rats were each injected with 1 X 10(5) 9L cells; 10 rats were treated with a low-copper diet and penicillamine. In the normocupremic control rats, a "diffuse" invasive pattern was observed in all 10 animals. In the hypocupremic group, a "nodular" pattern, with a discrete border between tumor and brain, was found in 7 of 10 rats (P less than 0.01). In a second experiment, the brains of 16 tumor-bearing rats were studied by electron microscopy. In the 8 normocupremic control rats, cytoplasmic extensions and pseudopodial protrusions, cytological markers of invasive cells, were prominent at the tumor-brain interface. In striking contrast, pseudopodia were absent along the border of the tumors in the 8 hypocupremic rats. These findings suggest a biological role of copper in the neoplastic spread of brain tumor cells. Pharmacological and metabolic alteration of the cellular microenvironment to inhibit invasiveness represents a novel therapeutic approach, especially for tumors of the brain in which malignancy is a function of regional invasiveness.

Animals↗
PubMed1987

Cytotoxic effect and induction of sister chromatid exchange in exponentially growing rat 9L gliosarcoma cells after brief exposure to BrdU.

The magnitude of DNA modulation in rat 9L gliosarcoma cells after a brief exposure to bromodeoxyuridine (BrdU) was studied by assaying colony-forming efficiency (CFE) and the number of sister chromatid exchanges (SCEs) per metaphase. The CFE assay showed that a 1-hr exposure to BrdU, at concentrations ranging from 10 to 1000 microM, produced a maximum cell kill of 5%. After a 2-hr exposure to 20 microM BrdU, the surviving fraction was 0.99, and even at a BrdU concentration of 1000 microM, 77% of the 9L cells survived. Compared with control cultures, the relative number of SCEs per metaphase in treated cultures was increased after a 1-hr exposure to BrdU at concentrations of 100 microM or more and after a 2-hr exposure to concentrations of 20 microM or more; no increase was observed in cells treated for 30 min with BrdU at concentrations up to 1000 microM. When the treated cells were allowed to grow in BrdU-free growth medium, the number of SCEs per metaphase returned to the control level within 24 hr, even after exposure to BrdU at concentrations as high as 1000 microM. These results demonstrate that exposure to BrdU at concentrations of up to 1000 microM for 30 min, 100 microM for 1 hr, and 20 microM for 2 hr causes little modulation of DNA.

Animals↗
PubMed1985

Extraneural metastases in gliosarcoma: a case report and review of the literature.

This report details the case of an 11-year-old girl with gliosarcoma and her rapid demise after a brief asymptomatic postcraniotomy period. The discussion that follows is a collective review of the several aspects illustrated by the case history. Special attention is directed toward the pathological features of this histological variant of glioblastoma multiforme. The topic of extraneural metastasis is reviewed with regard to frequency, mechanisms, sites, and prognosis.

Biopsy↗
PubMed1986

Synergistic effect of methotrexate and radiation on gliosarcoma in tissue culture and in rats.

In vitro and in vivo studies were performed on rat gliosarcoma cells (RT-9) to investigate the synergistic effect of methotrexate and radiation against malignant brain tumors. For in vitro study, RT-9 cells were cultured on microtiter plates and treated with methotrexate, radiation, or both. For in vivo study, the cells were implanted into the cerebrums of CD-Fischer rats, and intraperitoneal methotrexate, whole brain radiation, or both were given. Although synergistic suppression of cell growth with combined therapy was observed in the in vitro study, synergism was less clearly demonstrated in tumor-bearing rats because of systemic toxicity of the therapy.

Animals↗
PubMed1987

Gliosarcoma with chromosome abnormalities in a neonate exposed to heptachlor.

A neonate with a cerebral gliosarcoma was found to have chromosome abnormalities in tissue culture of the tumor, but normal karyotyping of peripheral blood. Similarities to and differences from chromosome abnormalities found in other human gliomas are noted. Unusual exposure of the child to heptachlor during prenatal development and the neonatal period suggests the need for further studies on the role of toxins in oncogenesis.

Animals↗
PubMed1992

Establishment of a new cell line derived from a human gliosarcoma.

A permanent cell line, GI-1, was established from a human gliosarcoma, and its characteristics were investigated. The original tumor was a mixture of two different neoplasms which had components of both glioma and sarcoma. The established cell line expressed various mesenchymal antigens, but not neuroepithelial antigens. It was noted, however, that the cell line produced tumors with the morphological features of human glioma after inoculation in athymic mice. The contrast of the pathological characteristics in tissue culture and in xenograft was unique, and this finding suggests that the GI-1 cell line may have the features of both glioma and sarcoma.

Aneuploidy↗
PubMed1992

Mechanism of interferon gamma-induced protection of human gliosarcoma cells from lymphokine-activated killer lysis: division of lymphokine-activated killer cells into natural killer- and T-like cells.

The mechanism by which interferon gamma (IFN-gamma) decreases the susceptibility of the established cultured gliosarcoma line Gl-1 to lymphokine-activated killer (LAK) lysis was analyzed. The results of monolayer depletion and lectin-dependent cellular cytotoxicity assays by LAK cells revealed that the resistance to LAK lysis of IFN-gamma-treated Gl-1 cells is manifested at the stage of LAK cell target recognition alone. We have also divided LAK cells into populations of phenotypically natural killer (NK)- and T-like cells with monoclonal antibodies and complement, respectively. We have used these cells to examine the mechanism of IFN-gamma-induced protection of Gl-1 cells from LAK lysis in cold target inhibition, monolayer depletion, and direct binding assays. The results revealed that NK-like cells do not recognize IFN-gamma-treated Gl-1 cells as efficiently as they do untreated targets, whereas T-like cells show the opposite tendency. In conclusion, we have demonstrated that the IFN-gamma induced protection of tumor cells from LAK lysis is predominantly regulated by the target recognition of NK-like cells. On the other hand, IFN-gamma-treated tumor cells may bind to T-like cells but fail to trigger them to initiate further stages for lysis as effectively as NK-like cells.

Cell Division↗
PubMed1991

[Establishment of ACNU-resistant rat gliosarcoma cell lines and their characteristics].

One of the most serious problems in cancer chemotherapy is the acquired drug resistance of tumor cells. In order to investigate the mechanism of acquired resistance to 1-(4-amino-2-methyl-5-pyrimidinyl)methyl-3-(2-chloroethyl)-3-nitrosourea hydrochloride (ACNU), nine resistant cells were isolated from rat gliosarcoma 9L cells and characterized. ACNU-resistant cells were easily isolated after a single treatment even with low-dose ACNU (5 micrograms/ml). However, in spite of repeatedly high-pressure dose of ACNU, more than 30 fold increase to parental 9L cell resistance was not achieved. At this time, further increase in selection pressure resulted in cell death. The resistant ratios of these resistant cells were stable in the absence of ACNU for more than 1 year. Luria and Delbrück's fluctuation test indicated that the appearance of ACNU-resistant cells occurred spontaneously at a rate of (4.40-8.02) x 10(-7)/cell/generation. In karyotypic analysis, the mode was higher in the resistant cells than in 9L cells, but a homogeneously staining region or double minute chromosome, which was considered to be a result of gene amplification, was not observed. In growth kinetics, all the resistant cells except R1 and R12 cells had higher saturation density and plating efficacy than parental 9L cells. These findings seemed to be due to cellular modification associated with ACNU resistance.

Animals↗
PubMed1984

Selective peripancreatic sarcoma metastases from primary gliosarcoma. Case report.

Two phenomena associated with malignant gliomas are: 1) the ability to metastasize systemically, and 2) the capacity to induce sarcomatous transformation within the supportive mesenchyma. An unusual case is presented of selective metastases of the sarcomatous elements of a mixed gliosarcoma. Immunohistochemical cell staining with glial fibrillary acidic protein was used to confirm the presence of abnormal glial elements in the primary brain tumor as well as the absence of such glial elements in the abdominal metastases.

Brain Neoplasms↗
PubMed1985

Effect of hematoporphyrin derivative photoradiation therapy on survival in the rat 9L gliosarcoma brain-tumor model.

Intracerebral tumors were produced in 99 rats by stereotaxic implantation of 9L gliosarcoma brain-tumor cells. Hematoporphyrin derivative (HPD), 10 or 20 mg/kg, was administered as an intravenous bolus 24 or 48 hours before irradiation of the tumor region with light from an argon pumped-dye laser (632 nm). Laser light, at a dose of 30, 60, or 200 joules/sq cm, was delivered through a craniectomy 10 or 13 days after tumor implantation. Survival times were significantly prolonged in rats exposed to laser light at a dose of 200 joules/sq cm 24 hours after administration of HPD, 20 mg/kg.

Animals↗
PubMed1988

Specific cytotoxic activity of T lymphocyte clones derived from a patient with gliosarcoma.

Eleven lymphocyte clones were established from the peripheral blood lymphocytes of a patient with gliosarcoma by means of autologous tumor stimulation and the limiting-dilution technique with recombinant interleukin-2. Ten of the 11 clones were cytotoxic against the autologous tumor cell line GI-1. Seven of the 10 clones were also cytotoxic against allogeneic brain-tumor lines and HeLa cells, one clone was cytotoxic against several target cells, and two clones were specifically cytotoxic against GI-1 and allogeneic brain-tumor cells. One of the 11 clones was not cytotoxic against any target cells tested. Lymphokine-activated killer cells induced by recombinant interleukin-2 alone exhibited cytotoxic activity against all target tumor cells tested. Surface phenotypic analysis revealed that all lymphocyte clones expressed CD3 antigen, some expressed CD4 antigen, and others expressed CD8 antigen. These clones seemed to be antigen-specific cytotoxic T lymphocyte clones. Analysis with these antigen-specific cytotoxic T lymphocyte clones may be useful in the elucidation of tumor-specific or tumor-associated antigens on autologous tumor cells.

Antigens↗
PubMed1989

The effect of interleukin-2 on the blood-brain barrier in the 9L gliosarcoma rat model.

Carbon-14-labeled aminoisobutyric acid was used to determine local blood-to-tissue transfer constants in 22 Fischer rats with intracerebral 9L gliosarcomas that received either high-dose parenteral interleukin-2 (IL-2) or a control injection. In tumor and peritumoral tissue, the transfer constants in the IL-2-treated animals (89.6 +/- 14.6 and 35.8 +/- 6.0, respectively, mean +/- standard error of the mean) were larger (p less than 0.05) than in control animals (61.4 +/- 6.4 and 14.6 +/- 2.2, respectively). In contrast, in normal frontal and occipital tissue contralateral to the tumor-bearing hemisphere, there was no significant difference between the transfer constants in IL-2-treated and control animals. Furthermore, treatment of animals with IL-2 excipient caused no change in permeability as compared to animals treated with Hanks' balanced salt solution. Parenteral injection of IL-2 increases blood-brain barrier disruption in tumor-bearing rat brain but does not increase the vascular permeability of normal brain. Methods to prevent this increased tumor vessel permeability are required before parenteral IL-2 can be used safely for the treatment of primary or metastatic brain tumors.

Animals↗