Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0017638 (glioma)
30,880 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Because of technical difficulties, the pharmacokinetics of neocarzinostatin (NCS) have not been thoroughly evaluated in patients with malignant glioma. The authors produced anti-NCS antibody by immunizing rabbits with NCS and established a means of quantifying tissue levels of NCS with enzyme-linked immunosorbent assay. In one patient given a bolus injection of 1 mg of NCS intra-arterially, the concentration of drug in neoplastic tissue at 25 minutes (0.1136 micrograms/g) was higher than that in blood at 20 minutes and was retained for a longer period. Rapid entry of NCS into the tumor cavity was observed at 5 minutes. In two postoperative cases, NCS applied topically to the tumor site (50 and 100 micrograms) was retained at high levels (0.2941 and 3.33 micrograms/ml) even after 48 hours, although no NCS was detected in blood after 60 minutes. NCS concentrations as low as 1 microgram/ml demonstrated cytocidal effects, and a delay in tumor growth was observed even at an NCS level of 0.1 microgram/ml, despite the fact that the half-life of NCS is extremely short (3 seconds in serum). Because its cytotoxic effect seems to be very rapid, it appears more important to obtain a high initial NCS concentration than to maintain a constant blood level.
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PMID:[Pharmacokinetics of neocarzinostatin in patients with malignant glioma. Quantitative analysis of tissue concentration]. 247 48

Some human tumor cell lines express the c-sis gene, the proto-oncogene of the transforming gene v-sis, and produce platelet-derived growth factor, which may contribute to carcinogenesis by autocrine or paracrine mechanisms. Here we demonstrate that c-sis expression in some human glioma and osteosarcoma cell lines can be blocked by agents that increase cellular cyclic adenosine monophosphate (cAMP). Forskolin, 8-bromocyclic AMP, cholera toxin, and prostaglandin E1 reduced c-sis mRNA in these cells by up to 90%. c-sis transcription rates were reduced by agents that increase cAMP; the stability of c-sis mRNA was unaffected. The possible therapeutic value of blocking the expression of tumor growth factor genes pharmacologically warrants further study.
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PMID:Cyclic AMP blocks expression of the c-sis gene in tumor cells. 254 92

We examined the antitumor effect of recombinant human lymphotoxin (rHuLT) on a xenotransplantable human malignant glioma line. Tumor-bearing nude mice were treated with rHuLT for three weeks following four schedules: intratumoral injection of rHuLT 20,000 units once a week, twice a week, intravenous injection once a week and twice a week. The inhibition rate of tumor growth was 98.8%, 99.1%, 92.1% and 98.8%, respectively. Histologically, necrotic lesions were observed in the tumors of all treated mice. Thrombo-obstructive changes of tumor vessels were also seen in the tumors of mice after intravenous injection of rHuLT. None of the mice died as a result of this treatment in spite of significant body weight loss. These results indicate that rHuLT has a strong antitumor effect on a xenotransplantable human malignant glioma line.
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PMID:Antitumor effect of recombinant human lymphotoxin on a tumor line of human malignant glioma. 258 52

Earlier, we conducted Phase I clinical trials to determine any acute toxicity of adoptive immunotherapy with intralesional injections of autologous lymphocytes expressing lymphokine-activated killer (LAK) activity and recombinant interleukin-2 (rIL-2) in patients with malignant glioma. Within six weeks of craniotomy and intralesional injection of autologous LAK cells plus rIL-2, 3 of 29 patients demonstrated a decline in clinical status and evidence on computed tomographic and magnetic resonance imaging scans of edema and mass of unknown character at the site of previous surgery and immunotherapy. Craniotomy was performed to remove the tissue and reduce intracranial pressure. Microscopic examination of the excised material indicated no new tumor growth within the resected mass, but rather that the tissue had the histological characteristics of a chronic sterile abscess including necrosis, fibrosis, and influx of inflammatory cells. Factors that may have contributed to this reaction in the 3 patients were age, Karnofsky score, the extent of tumor excision, and immune status. All 3 had also been treated with greater than average numbers of rIL-2 activated lymphocytes that demonstrated significant in vitro LAK activity. The results suggest that in patients whose clinical status is good and who are not immunosuppressed by corticosteroids, the dose-limiting toxicity of intraparenchymal immunotherapy with LAK cells plus rIL-2 for glioma may be related to the total, absolute number of activated cells injected, and this toxicity develops over time and is manifested by development of a sterile abscess.
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PMID:Sterile abscesses in glioma patients treated by intraparenchymal injection of lymphokine-activated killer cells and recombinant interleukin-2: case reports. 258 34

It has recently been shown that human T-cell subpopulation can be identified functionally via surface receptors for Fc fragment of immunoglobulins. We detected peripheral blood T-cells bearing the Fc receptor for IgG molecules (T gamma cell) in patients with brain tumors who manifested a variety of immunological abnormalities. We also analyzed immunological values of T gamma cells which were thought to be suppressor and/or a part of killer T cells, comparing with other immunological parameters. The percentage of T gamma cells was significantly higher in patients with malignant brain tumors than in normal controls (6.54 +/- 1.6%). The values of T gamma cells in patients with glioma, metastatic brain tumor, benign brain tumor were 15.4 +/- 4.8%, 14.9 +/- 3.2%, and 8.1 +/- 3.7%, respectively. In the patients with glioma, the values increased in the uncontrolled group compared with the well-controlled group. Furthermore, the values were decreased by surgical removal of the tumor. On immunological study of T gamma cells in the patients with glioma, there was a definite correlation between the values of T gamma cells and ADCC activity. Furthermore, the T gamma cells in the patients showed higher ADCC activity than in normal controls. The values of T gamma cells also correlated with blastogenesis of the peripheral blood lymphocytes by PHA (r = -0.742, p less than 0.001) and Con A (r = -0.662, p less than 0.001). These results suggest that T gamma cells are playing two important roles in patients with glioma such as suppressor function and ADCC activity, and that these cells may change according to the tumor growth.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Clinicoimmunological values of measurement of IgG-Fc receptor positive T cells in the patients with malignant brain tumors]. 293 80

Hematoporphyrin derivative injected directly into a subcutaneous rat glioma resulted in a significant greater tumor growth inhibition than hematoporphyrin derivative injected parenterally upon stimulation by light, Co60 or by combination of the above. The photodynamic effect was analyzed in an in vivo and in an in vitro clonogenic assay. The directly injected hematoporphyrin derivative without external activation inhibited tumor growth to 34%. Light and directly injected HPD inhibited tumor growth to 3%, whereas 4, 8 and 16 Gy of Co60 produced a growth inhibition to 11%, 0.05% and 0.00% respectively. This cytotoxic effect of the ionizing radiation is further potentiated by the addition of light, resulting in a growth inhibition to 0.1%, 0.00% and 0.00% respectively for the three corresponding radiation doses. The direct intratumoral injection of HPD minimizes the side effects and increases the effect of the photodynamic therapy as compared to the parenterally administered HPD. This direct injection modality could be of potential value in the treatment of human gliomas or other tumors.
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PMID:Photodynamic therapy is potentiated by Co60 and intratumoral injection of hematoporphyrin derivative. 297 84

An experimental transplantable canine brain tumor model with the advantages of rapid tumor growth within 10 days and relative safety for the investigator is presently available. The tumor is produced by intracerebral inoculation of cultured cells derived from a canine brain tumor induced by the Schmidt-Ruppin strain of the Rous-Sarcoma virus (SR-RSV). It has potential use as a model in experiments designed to evaluate the effectiveness of chemotherapy and radiotherapy with serial computerized tomography scans. However, characterization of the induced tumor is essential. Ideally, it should have features attributable to glioma and/or neuroectodermal tumors. Utilizing the technique of intracerebral inoculation of cells cultured from the original dog brain tumor induced by SR-RSV, Salcman et al identified the tumor they induced in brains of mongrel puppies as a glioma by light microscopic criteria (Reference). The purpose of our study was to further characterize this experimental tumor by electron microscopic and immunohistochemical techniques. Tumor was induced in 6 mongrel puppies. Stains of the tumor for immunohistochemical reactivity to glial fibrillary acid protein, S-100 protein and 210K neurofilament protein were all negative. With the electron microscope, the intracerebral tumor cells were mostly undifferentiated. They had a few cell processes, occasional punctate adhesions and some microvilli-like structure. The tumor cell nucleus was usually oval shaped and sometimes had nuclear indentations. The cytoplasm contained abundant free ribosomes, some rough endoplasmic reticulum and mitochondria. Collagen fibers and basal lamina were not observed in the intercellular spaces. The capillaries within the tumor were characterized by proliferation of immature endothelial cells which were non-fenestrated.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Brain tumor induced in dogs by intracerebral inoculation of SR-RSV induced cultured tumor cells--electron microscopic study]. 299 91

The vascularization of intracerebral transplantation tumors of the two rat glioma clones RG2 and F98 was studied in various stages of progressive tumor growth by use of biotinylated Ricinus communis agglutinin I (B-RCA I) in avidin-biotin-peroxidase complex (ABC)-histochemistry. The tumors were induced by stereotactic implantation of 1000 glioma cells into the right caudate nucleus of 26 adult CDF-rats and examined after 10, 14, 18, and 21 days following controlled intracardial perfusion of the host animals. Our histochemical results on paraffin sections demonstrate that B-RCA I selectively stains vascular endothelial cells of arteries, veins, and capillaries not only in the normal rat brain but also in the transplantation tumors. Subsequently morphometric measurements of the B-RCA I-stained sections were performed to define the tumor vascularization in quantitative terms. There was an increase in the mean tumor vessel diameters during tumor growth in both transplantation tumor types leading to values about two times above those of the normal rat striatum. On the contrary, the mean vessel density and the mean vessel surface per tumor area were markedly reduced in the late stages of both tumor types when compared to the normal striatum. The RG2 and F98 transplantation tumors differed with regard to the intercapillary distance, which was two times higher in the F98 transplantation tumors than in the RG2 tumors on day 21. In conclusion, B-RCA I is a very sensitive histochemical marker for rat vascular endothelia on paraffin sections. Moreover, this method appears to provide the possibility for qualitative and quantitative study of the development of vasculature in intracerebral transplantation systems including tumors.
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PMID:Vascularization of syngenic intracerebral RG2 and F98 rat transplantation tumors. A histochemical and morphometric study by use of ricinus communis agglutinin I. 320 23

An in vivo model for correlative imaging studies of intracerebral glial tumors and peritumor brain edema has been developed. Adult male and female cats implanted with 1 x 10(6) or 5 x 10(5) 9L glioma cells had parietal tumors of 4 mm or greater in diameter and showed signs of increased intracranial pressure 13.7 +/- 1.9 days or 19.2 +/- 1.3 days after implantation. No immunosuppression was required and the success rate for tumor growth after implantation was 88%. Histologically, the tumor resembles a malignant astrocytoma. The tumor contained the highest water content (85.94%); peritumor white matter was more edematous (73.01%) than white matter in the contralateral hemisphere (69.04%), sham-operated (69.41%) and control brain (68.76%). There was no correlation between the size of the tumor and water content in tumor or white matter. Increased tissue albumin in peritumor white matter indicated blood-brain barrier dysfunction within the tumor and confirmed the vasogenic origin of the edema. Proton magnetic resonance imaging provided good spatial and contrast resolution with increased signal intensity in edematous white matter, decreasing with distance from the tumor. The large brain of this animal model allows the use of serial imaging and regional correlative biochemical measurements in a single animal. Other advantages of this model are its predictability and the short time required to produce tumors with marked peritumor edema.
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PMID:A feline model for experimental studies of peritumor brain edema. 322 Dec 63

The effects of long-term low- and high-dose ibuprofen on tumor growth and permeability were assessed in a glioma model in rats. The rats were treated with ibuprofen (24 mg/kg/day or 96 mg/kg/day) for 24 hours before implantation of C6 astrocytoma spheroids and then for 13 days following implantation. The wet and dry weight of the tumors and protein extravasation were measured by an Evans blue dye technique. Protein extravasation did not appear to be reduced by the treatments when assessed on the basis of tumor dry weight. The treatment significantly reduced the wet weight of the tumors in rats treated with high-dose and low-dose ibuprofen when compared to tumor wet weights in untreated rats. High-dose ibuprofen treatment significantly decreased the dry weight of the tumors compared to that of tumors in untreated control animals. It is hypothesized that the ibuprofen treatment regimen employed inhibits prostaglandin-associated angiogenesis induced by the C6 tumor cell growth and/or the implantation technique, thereby interfering with the ability of the tumors to grow.
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PMID:Effect of ibuprofen on tumor growth in the C6 spheroid implantation glioma model. 337 88


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