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)

A comparative analysis was performed on the electrophysiological properties of 11 neoplastic neurogenic cell culture lines and five other cell lines of different origin (HV1C, rat bile duct carcinoma; BICR/M1RK, rat mammary tumor; HeLa, human cervix carcinoma; 3T3, mouse embryo; REe, rat embryo). Neurogenic lines were derived either from N-ethyl-N-nitrosourea-induced neoplasms of the nervous system or from cultured fetal rat brain cells that had undergone neoplastic transformation in vitro after exposure to N-ethyl-N-nitrosourea in vivo. Electrical membrane excitability was lacking in all neurogenic cells analyzed. Their membrane potential and input resistance values were similar to those of the nonneurogenic lines. Intercellular ionic coupling was consistently observed between cells of a fibroblastoid shape or cells bearing multiple cytoplasmic processes (i.e., all neurogenic lines HV1C, BICR/M1RK, and 3T3). Epithelioid cells (i.e., HeLa, REe, an NV1C subpopulation, and a GV1C1 variant) showed no such intercellular communication. In vivo monolayer cultures on glass coverslips were obtained by a modified i.p. diffusion chamber technique. Under these conditions, the cells (with the exception of a glioma-derived cell line) retained the morphological appearance and electrophysiological properties observed in vitro.
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PMID:Electrophysiological properties of ethylnitrosourea-induced, neoplastic neurogenic rat cell lines cultured in vitro and in vivo. 17 99

Brain tumors are highly resistant to therapy. Their diffuse infiltrative nature and the relative inaccessibility of brain tissue to blood and lymph are barriers to surgical and cytotoxic treatments alike. The purpose of this study was to produce immune cells specifically reactive with an anaplastic rat glioma (RT2) and determine whether those cells could affect tumor progression in the brain. RT2-specific cytotoxic cells were prepared by priming rats in vivo with RT2 tumor cells and Corynebacterium parvum and stimulating the primed lymphocytes in vitro with irradiated RT2 tumor cells and interleukin-2 (IL-2). Cultured cells exhibited a high level of cytotoxicity against RT2, but not C6 (an allogeneic glioma), 3M2N (a syngeneic mammary tumor), or CSE (a syngeneic fibrosarcoma) tumor cells. To generate a model for therapy, rats were injected intracerebrally with RT2, generating progressing brain tumors, which killed untreated rats in approximately 2 weeks. To test the therapeutic potential of the effector cells, tumor-bearing rats were treated by intravenous injection of lymphocytes on Day 5 of tumor growth. Treated rats also received a 5-day course of systemic IL-2 beginning on Day 5. Treatment with IL-2 alone, RT2-primed spleen cells, or RT2-primed spleen cells stimulated in vitro with C6 did not affect rat survival. However, tumor-bearing rats treated with RT2-stimulated lymphocytes exhibited increased survival or were cured. Systemic IL-2 was an essential adjunct, because survival was not affected by treatment with effector cells alone. Therapy initiated on Day 8 of tumor progression lacked effect on survival.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Successful treatment of a malignant rat glioma with cytotoxic T lymphocytes. 140 33

The melanin precursor analogue p-boronophenylalanine (BPA) has been used to deliver 10B to melanoma tissue for boron neuron capture therapy. Uptake studies in tumor models other than melanoma now indicate that BPA is capable of delivering therapeutic amounts of boron to tumors other than melanoma. The KHJJ murine mammary tumor carried s.c. in BALB/c mice, the GS-9L rat glioma carried both s.c. and intracranially in F-344 rats, and the human U-87 MG glioma xenograft carried s.c. in nude mice have all shown significant accumulation of boron in tumor tissue following single p.o. (intragastric) doses of BPA. In this KHJJ mammary tumor, the L isomer of BPA was preferentially accumulated compared to the D isomer, indicative of a carrier-mediated transport process. Double-label, whole-body autoradiographic studies in a pigmented murine melanoma have shown that the boron distribution (from BPA) differs from the distribution of a tritiated melanin precursor (tyrosine). Boron accumulated only in the tumor; labeled tyrosine accumulated in tumor, liver, intestinal epithelium, bone-marrow, and secretory glands. Toxicity studies in mice and rabbits indicate that, even at very high doses, BPA p.o. caused no adverse effect in tissues, on blood chemistry, or on differential leukocyte counts. These data indicate that BPA may be generally useful as a boron delivery agent for boron neutron capture therapy of tumors.
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PMID:Selective delivery of boron by the melanin precursor analogue p-boronophenylalanine to tumors other than melanoma. 229 47

Hematoporphyrin derivative linked by ether bonds (HE) was synthesized by unambiguous procedures in order to compare its properties to hematoporphyrin derivative (HpD). Reverse phase high performance liquid and gel filtration chromatography were used to compare the HE derivatives to HpD. The cellular uptake of HE derivatives was compared to HpD using the WEHI 3B (D+) cell line and was shown to be taken up to a degree and in a manner similar to HpD. The efficiency of HE porphyrins as photosensitizers was compared to HpD using the V79 cell line. HE porphyrins were more efficient in sensitizing the V79 cells than was HpD. The in vivo tumor localizing properties of HE porphyrins were compared to HpD in CBA mice bearing the C6 cerebral glioma, and BALB/c mice bearing the EMT6 mammary tumor. HE derivatives localized in both tumor models as effectively as HpD. We conclude that the properties of ether linked hematoporphyrin derivatives are very similar to properties of HpD.
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PMID:Nature of the tumor-localizing components of hematoporphyrin derivative. 358 Oct 80

Pathological examination was carried out on 16 male Sprague-Dawley rats received single i. v. injection of 60 mg/kg of streptozotocin (SZ) at 5 weeks of age and maintained for 22 months. Insulinoma (63%), renal adenoma (50%), hepatocellular tumor (69%), cholangioma (31%) and Leydig cell tumor (56%) were found in a high incidence, and therefore occurrence of these tumors was considered to be attributable to the treatment with SZ. In addition to these tumors, though in a low incidence, various such tumors as leukemia, reticulum cell sarcoma, mammary tumor and glioma were also found.
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PMID:Neoplastic lesions in streptozotocin-treated rats. 622 53

Human (U251, U87, U343) and rat glioma cell lines (C6, 9L) were examined by the reverse transcriptase-polymerase chain reaction and subsequent nucleotide sequencing analysis to see whether they express wild type (wt)-p53 or mutated form (mut)-p53 messages. Results showed that U87, U343, and C6 cells expressed wt-p53 messages whereas U251 and 9L cells expressed mut-p53 messages. All these cell lines were transfected with wt-p53 cDNA or the s-myc gene linked to the mouse mammary tumor virus (MMTV) promoter. Of several G418-resistant clones obtained from each transfection, a few expressed the s-Myc or wt-p53 proteins. Independent of mutations in the intrinsic p53 gene, the cellular growth in vitro and tumorigenicity in nude mice of these clones were drastically suppressed, the extent of suppression being correlated with the expression level of the transfected gene. Flow-cytometric analysis demonstrated that both p53 and s-Myc arrested the cell cycle at the G1/S boundary. These data suggest that these genes having negative effects on tumor cell proliferation could be used in gene therapy of gliomas, which are caused by alteration of the p53 gene or by some other genetic change.
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PMID:Negative effects of wild-type p53 and s-Myc on cellular growth and tumorigenicity of glioma cells. Implication of the tumor suppressor genes for gene therapy. 780 77

In the present study, the synergistic effect of mild hyperthermia in combination with gene expression of interferon-beta (IFN-beta) was examined in vitro in the human glioma cell line U87MG. The cells transiently expressed the IFN-beta gene under the control of the mouse mammary tumor virus promoter and were then subjected to temperature elevation (41 degrees C for 1 h). In terms of the cell killing effect, the optimum scheme was obtained by transfection for 4 days before hyperthermia, i.e. rate in the time course of IFN-beta gene expression. The relative specific growth rate decreased to 32% compared with the control while it was only 40% under the hyperthermic conditions. These observations suggest that IFNbeta expression was able to enhance the sensitivity of transfected glioma cells to mild hyperthermia.
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PMID:Synergism between mild hyperthermia and interferon-beta gene expression. 1039 72

The inhibitory effects of (E)-5-(2-bromovinyl)-2'-deoxyuridine (BVDU) and its arabinosyl derivative (E)-5-(2-bromovinyl)-1-beta-D-arabinofuranosyluracil (BVaraU) on the growth of both MDA-MB-435 human breast carcinoma and 9L rat gliosarcoma cells expressing the thymidine kinase (tk)-encoding gene of the Varicella zoster virus (VZV) or the Herpes simplex virus (HSV) were evaluated. In vitro, BVDU and BVaraU effectively killed both cell types expressing VZVtk, with 50% inhibitory concentration values ranging from 0.06 to 0.4 microM, whereas ganciclovir (GCV) lacked activity. On HSVtk+ cells, BVDU had high cytotoxic activity, with 50% inhibitory concentration values that were similar to those of GCV, whereas BVaraU was inactive. In vivo, BVDU applied intraperitoneally caused a 50% tumor growth inhibition in nude mice inoculated subcutaneously with VZVtk+ as well as HSVtk+ mammary tumor cells. In mice and at variance with the in vitro results, BVaraU had very little activity against the VZVtk+ mammary cells; GCV had the highest activity on the HSVtk+ cells, resulting in a 50% eradication of the tumors. With the 9L rat gliosarcoma model, the VZVtk/BVDU system completely failed to inhibit the development of VZVtk+ glioma tumors induced subcutaneously in syngeneic rats, although BVDU had a similar 45-minute half-life in both rats and mice. Factors other than degradation of the prodrug and related to the mode of action of these analogs are possibly involved in the observed discrepancies between the in vitro and in vivo results.
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PMID:Comparative in vitro and in vivo cytotoxic activity of (E)-5-(2-bromovinyl)-2'-deoxyuridine (BVDU) and its arabinosyl derivative, (E)-5-(2-bromovinyl)-1-beta-D-arabinofuranosyluracil (BVaraU), against tumor cells expressing either the Varicella zoster or the Herpes simplex virus thymidine kinase. 1077 Jun 29

1,N(6)-Etheno-2-aza-adenosine was synthesized by treating 1,N(6)-etheno-adenosine with alkali, followed by nitrosation. The mechanism of formation of this novel nucleoside was elucidated using adenosine tritiated at C-8 and C-2, and was found to deformylate exclusively at C-2. This new 2-aza nucleoside fluoresces at 494 nm when excited at 358 nm. Toxicity study showed the compound is active in a rat mammary tumor tissue culture line, but inactive in HeLa and Glioma 26 tissue culture lines. It was also found to selectively inhibit the thymidine incorporation into DNA in a rat mammary tumor, but exhibits no ill effect on normal proliferative tissue. The reactive intermediate 3-beta-D-ribofuranosyl-4-amino-5-(imidazol-2-yl) imidazole was identified and was found to be an active agent in tissue culture.
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PMID:Synthesis of 1,N6-etheno-2-aza-adenosine (2-aza-epsilon-adenosine): a new cytotoxic fluorescent nucleoside. 1079 38

Purified field bean protease inhibitor (FBPI) was labeled with 99mTcO4- to ascertain its ability to locate tumors in tumor-bearing rat models. The labeling was done with Sn2+ as a reducing agent and the yield was 95%. It was stable for 2 hr at ambient temperature. The biodistribution study of the intravenously injected radiolabeled FBPI in normal Wistar rats at various time intervals showed a rapid blood clearance from the systemic circulation (approximately 5hr). The complex was predominantly excreted through the renal and the hepatobiliary systems. In vivo distribution and scintiimaging of 99mTc-FBPI were carried out in rats bearing carcinogen-induced mammary tumor or transplanted C6-gliomas. The results obtained were compared with conventional tumor-seeking radiopharmaceuticals such as 99mTc-(V)dimercaptosuccinic acid (DMSA), 201Thallous chloride (TICI) and 99mTc-Citrate. The tumor to muscle (T/M) ratios obtained with 99mTc-FBPI in rat C6 glioma was nearly 2 to 5-fold higher than obtained with all the three conventional tumor-seeking agents. The T/M ratio obtained with 99mTc-FBPI in rat mammary tumor on the other hand appeared to be 2-3-fold higher than noted with 99mTc(V)-DMSA and 201TlCl. The ratio was however comparable with that obtained with 99mTc-Citrate. The study indicated that 99mTc-FBPI has the specific potentials for imaging gliomas and possibly other tumors as well.
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PMID:99mTc-labeled field bean protease inhibitor can function as an efficient tumor detecting agent. 1201 74


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