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)

The rational application of chemotherapy in tumors of the central nervous system is discussed in particular the use of the new derivatives of nitrosourea: BCNU (1-3 bis-(2-cloroetil) 1-nitrosourea) and CCNU (cloroetil-cicloesil-nitrosourea). The results of therapy with antimetabolites, alkylating agents, antibiotics, and plant alcaloids, are reported as well as those obtained with radio - sensitizing substances (containing B10 or BUdR, IUdR, FUdR). The results obtained in the United States and in Japan with BCNU and CCNU are considered as well as the personal data of 43 cases treated with BCNU and 10 cases treated with CCNU (including intracranial glial tumors, spinal glial tumors and metastatic tumors of the central nervous system).
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PMID:[The chemotherapy of tumors of the central nervous system (author's transl)]. 18 61

Amethopterin and 5-bromodeoxyuridine (BUdR) were used to induce morphological changes in cloned rat glioma (C6). The expression of S-100 protein, an acidic protein localized in glial cells, and steroid sulfatase, an ubiquitously distributed enzyme found in high concentration in glial cells, were followed during cell growth, from subculture to well into the stationary phase of control and drug-treated cultures. Amethopterin and BUdR differed in their effects on glioma morphology and in the expression of the biochemical parameters. Amethopterin coordinately stimualted both the production of S-100 protein and steroid sulfatase activity when cell division was inhibited during early logarithmic growth phase. BUdR stimulated steroid sulfatase activity but repressed production of S-100 protein. The results are discussed with respect to the mechanism of regulation of the differentiated state of tumor cells.
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PMID:Drug-induced differentiation of a rat glioma in vitro: II. the expression of S-100, a glial specific protein and steroid sulfatase. 64 75

To shed light on the metabolic changes in glioma following therapy, uptake changes among 18F-fluoro-2'-deoxyuridine (18FUdR), 14C-thymidine (dThd), 14C-methionine (Met) and 3H-deoxyglucose (DG) in glioma model after chemotherapy were studied, as a means for interpreting clinical PET results, together with the changes in the bromodeoxyuridine (BUdR) labeling index. 1-(4-amino-2-methyl-5-pyrimidinyl)methyl-3-(-2chloroethyl)-3-nitro sourea hydrochloride (ACNU) was administered intraperitoneally in the tumor-bearing rats and uptake of the tracers or BUdR labeling index in tumor tissue were measured. The metabolic response following chemotherapy was a sharp fall immediately for 14C-dThd and 18FUdR and a moderate fall for 14C-Met whereas there was a fall in 3H-DG from 1 week after chemotherapy. The changes of BUdR labeling index paralleled that in the uptake for dThd and FUdR. These result indicate that PET scans using a variety of tracers in conjunction could be used for clinical diagnosis and evaluation of therapy in glioma cases. 18FUdR is a promising tracer of nucleic acid metabolism to evaluate the proliferative potential of brain gliomas.
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PMID:Metabolic changes of glioma following chemotherapy: an experimental study using four PET tracers. 146 67

The purpose of this study is to clarify the usefulness of 201Tl brain SPECT in the prediction of clinical degree of malignancy. Quantitative evaluation of 201Tl uptake in the tumor was expressed as count ratio of tumor site over contralateral normal region (D/C ratio) on 201Tl SPECT image. Fourteen patients with gliomas received an intravenous administration of bromodeoxyuridine (BUdR) at surgery to label tumor cells in the DNA synthesis phase. BUdR-positive cells in excised tumor specimen were stained with anti-BUdR monoclonal antibody by indirect immunoperoxidase staining. Percentage of labeled cells in relation to the total number of tumor cells in microscopic fields was defined as labeling index (BUdR-LI). D/C ratio in patients with grade IV glioma (198.7 +/- 31.7) was higher than that in patients with grade III glioma (138.3 +/- 33.9) or more low-grade gliomas (94.2 +/- 11.9, p less than 0.001). BUdR-LI in patients with high-grade glioma was also higher than that in patients with low-grade glioma. D/C ratio correlated well (r = 0.753) with BUdR-LI, which is considered to represent proliferative activity of the tumor. D/C ratio does not only correlate well with histological grade of glioma, but with clinical course or prognosis of individual patient with glioma. In conclusion, degree of 201Tl uptake in the tumor may provide non-invasive prediction of malignancy grade of gliomas and accurate estimation of efficacy of the therapy and early detection of recurrence or malignant transformation of the tumors, by delineating viable tumor tissue in patients with gliomas.
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PMID:[Evaluation of 201Tl SPECT in patients with glioma: a comparative study with histological diagnosis, clinical feature and proliferative activity]. 177 Jun 41

The proliferative capacity of brain-tumor cells was analyzed in vitro and in situ using monoclonal antibody (MAb) against deoxyribonucleic acid (DNA) polymerase alpha. For the in vitro studies, two cultured human glioma cell lines were investigated using MAb against DNA polymerase alpha, the MAb Ki-67, a serum against proliferating cell nuclear antigen (PCNA/cyclin), bromodeoxyuridine (BUdR), and an anti-BUdR MAb. During exponential growth of the cells, the percentage of polymerase alpha-positive cells (the "polymerase alpha score") ranged from 72.0% to 77.1%, the Ki-67-positive cells (the "Ki-67 score") ranged from 43.4% to 59.4%, the PCNA/cyclin-positive cells from 30.9% to 41.4%, and the BUdR labeling index from 28.6% to 39.3%. For the in situ studies, tissue from 60 human brain tumors and from two normal human brains was investigated and the polymerase alpha scores and Ki-67 scores were compared. In normal brain tissue, no immunostaining was found by either method. In brain tumors, both the polymerase alpha scores and the Ki-67 scores correlated with the histological grade of malignancy. Polymerase alpha scores were generally higher than Ki-67 scores in the same specimen, especially in malignant brain tumors. These findings suggest that immunostaining of DNA polymerase alpha is a convenient and important new method by which to estimate the cellular proliferation rate of brain tumors. Polymerase alpha scores may be closer to the growth fraction of the individual tumor than the MAb Ki-67 or other scores.
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PMID:Immunohistochemical demonstration of DNA polymerase alpha in human brain-tumor cells. 196 2

A method of identifying thymidylate synthase (TS) at the cellular level was developed using anti-TS monoclonal antibody (M-TS-4), a monoclonal antibody created against purified TS from a HeLa cell line. In HeLa cells and four human glioma cell lines (U-251, U-87, 343-MGA, and SF-188), TS was identified primarily in the cytoplasm. Autoradiographic and flow cytometric studies showed that TS appeared mainly in the G1 phase and subsided early in the S phase; thus, the G1 phase can be divided into TS-positive and -negative fractions. Nuclear TS was not demonstrated unequivocally with M-TS-4, and the relationship between nuclear TS and DNA synthesis could not be determined. Although the percentage of TS-positive cells was larger than the S-phase fraction measured by autoradiography after a pulse of tritiated thymidine or by the immunoperoxidase method using BUdR, the ratios were within a similar range (1.2-1.4) in all cell lines studied. Therefore, the S-phase fraction can be estimated indirectly from the percentage of TS-positive cells measured by M-TS-4. Because the emergence of TS detected by our method is cell cycle dependent, M-TS-4 may be useful for biochemical studies of TS and for cytokinetic analysis.
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PMID:Cell cycle phase dependent emergence of thymidylate synthase studied by monoclonal antibody (M-TS-4). 247 89

Cell proliferation potential was assessed by measuring the labeling indices of the monoclonal antibody Ki-67 and of 5-bromodeoxyuridine (BUdR), and the cellular deoxyribonucleic acid (DNA) content in 48 human brain tumors. The diagnostic and prognostic value of flow-cytometric DNA analysis was also evaluated using ethanol-fixed paraffin-embedded BUdR-labeled specimens; these were the same specimens as were used for measuring the BUdR and Ki-67 labeling indices. Both the Ki-67 and the BUdR labeling indices correlated with the degree of malignancy estimated from conventional histological preparations. The Ki-67 labeling index was 1.7 times greater than the BUdR labeling index. The relationship of DNA aneuploidy to the labeling indices or to morphology in cases of glioma was examined. All of the tumors with an aneuploid line corresponded to malignant glioma classified by histological criteria, although malignant glioma did not always show DNA aneuploidy. In addition, the cases with aneuploid lines showed high BUdR and Ki-67 labeling indices. The cell kinetic data, which indicate the biological character of tumors, allowed prediction of the prognosis of the patients with gliomas. In contrast, despite the presence of an aneuploid line, three of 13 meningiomas showed a benign histological pattern without an aggressive clinical course, and neither the Ki-67 nor the BUdR labeling index was high. These results indicate an unequivocal relationship between DNA aneuploidy and clinical behavior; in general, both labeling indices may prove to be objective indicators of the outcome of patients with brain tumors.
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PMID:Flow-cytometric DNA analysis and immunohistochemical measurement of Ki-67 and BUdR labeling indices in human brain tumors. 253 5

Single and combined treatment of interstitial microwave hyperthermia (HT) and radiation therapy (RT) were delivered to rat glioma models. The animal model tumors were induced by intracerebral inoculation of a small piece of G-XII glioma tissue to 6-8 week-old rats. Heating to about 44 degrees C at the surface of the inserting antenna using a 2450 MHz microwave was carried on for 30 minutes. A single dose of 800 r to the whole head was delivered by deep X-ray apparatus. In combined treatment, heating immediately preceded irradiation. Following treatment, animals were sacrificed at 1, 3, 6, 12, 24, 48, 72 and 96 hours. BUdR was administered intraperitoneally 1 hour before sacrifice. Microscopically, in HT, tumor cells became eosinophilic and separated from each other. Some of them were necrotic. Macrophage infiltration in tumor tissue was recognized after 72 hours. BUdR labelling indices were less than 1% till 24 hours had passed, then became 25% at 48 hours, nearly equal to that of the control animals. In RT, ballooning of the tumor cells was prominent, and some of the tumors became necrotic. Lymphocyte infiltration of the tumor tissue was occasionally seen. BUdR labeling indices decreased slowly; less than 10% in 24 hours, but continued until 96 hours had passed. Combined treatment of HT and RT showed addictive effect of histological changes and suppression of tumor cell growth.
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PMID:[Histopathologic changes and tumor cell kinetics after hyperthermia and/or radiation therapy in a rat glioma model: bromodeoxyuridine (BUdR) labelling index]. 261 5

Bromodeoxyuridine (BUdR), a nonhypoxic radiosensitizing drug, is a halogenated pyrimidine analog that is incorporated into the deoxyribonucleic acid of dividing cells in a competitive process with thymidine; BUdR also sensitizes these cells to radiation therapy. Neurons and glial cells have a very low mitotic rate. They will not incorporate BUdR and will not be sensitized. Bromodeoxyuridine is best delivered intra-arterially because of its regional advantage, calculated to be between 6 and 16. An 8-week BUdR infusion is delivered before and during radiation therapy through a permanently implanted pump with a catheter placed retrograde into the external carotid artery. Eighteen patients with malignant glioma (15 grade IV, and three grade III) were entered into a Phase I dose-escalation protocol with BUdR dosages ranging from 400 to 600 mg/sq m/day. The maximum dose that can be tolerated appears to be 400 mg/sq m/day for 8 weeks. The 18 patients entered in this study have a median Kaplan-Meier estimated survival time (+/- standard error of the mean) of 22 +/- 5 months with 11 patients still alive. Three patients are alive at 30, 29, and 21 months after diagnosis with no evidence of tumor on computerized tomography. There have been no vascular complications. Side effects in all patients have included anorexia, fatigue, ipsilateral forehead dermatitis, blepharitis, iritis, and nail ridging. Myelosuppression requiring dose reduction occurred in one patient. One patient had a Stevens-Johnson syndrome requiring termination of BUdR. It is concluded that intra-arterial BUdR may improve survival times in patients with malignant gliomas.
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PMID:Intra-arterial bromodeoxyuridine radiosensitization and radiation in treatment of malignant astrocytomas. 304 41

The cytokinetic response of cultured glioma cell lines to cis-dichlorodiammine platinum (II) (CDDP) was investigated by flow-cytometry using the BUdR-Hoechst technique. By this technique, the percentage of cells in the various components and the relative phase durations were calculated rapidly and simply. In the presence of CDDP ID50, perturbation of the cell cycle was shown and the cell cycle time was prolonged three times longer than in controls in the GB2 cell line. Comparison of histograms obtained at certain time intervals, cell-cycle perturbation by CDDP such as G2-block with prolongation of the S-phase and further G1 accumulation were demonstrated.
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PMID:[Effect of CDDP on cultured glioma cell lines: analysis of cell kinetics by flow cytometry]. 377 53


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