Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0017636 (glioblastoma)
 18,345 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This is a paper of new trial of treatment of malignant brain tumor by local injection of bleomycin (BLM). The new method of intraneoplastic BLM injection is as follows: in the cases ended up with subtotal or partial removal of the tumor, Ommaya's device was detained in the tumor bed, and its reservoir was fixed subcutaneous on the skull. 0.1 mg/kg to 0.2 mg/kg of BLM was injected by subcutaneous puncture into the reservoir every other day. Usual total dose of BLM was 30-80 mg. The patients were usually treated with 60Co-irradiation and immunotherapy after local injection of BLM. Twelve patients with malignant brain tumor were treated by the above mentioned new method and a follow-up study was done. One-year survival rate was 50% and three-year survival rate was 25%. Each case of primary sarcoma, medulloblastoma and malignant oligodendroglioma survived for a very long time. However, most of the patients especially those with glioblastoma died of recurrence in about one year or so inspite of temporary improvement of their clinical symptoms and clinical findings. In the autopsy cases of malignant gliomas, similar pathological findings were obtained around the tumor bed. In macroscopical view, the extensive necrotic foci and small haemorrhages were observed around the tumor bed not deeper than 2 to 3 cm from the surface of the cavity, and in the deeper part the tumor tissues were actively proliferating. Microscopically there was a severe coagulation necrosis of tumor cells with haemorrhage, collagenous tissue proliferation, fibrin deposit, increasing capillary vessels and infiltrating lymphocytes and granulocytes. Consequently, the scintillation scanning of BLM labelled 57Co was utilized to make clearance curves of the drugs in the patients with malignant brain tumor. The results were as follows: 57Co-BLM activity in the tumor tissue decreased about 70% 2-4 days after local injection of the drugs, whereas, it decreased about 70% 2-4 hours after intravenous injection of the drugs. From these results it could be presumed that locally injected BLM remained in the tumor tissues for a longer time and killed malignant tumor cells completely. However, an unfavorable fact was that locally injected BLM was retained only within the tumor tissue less than 2-3 cm apart from the cavity, showing no efficacy enough to prevent tumor proliferation in more remote area. In conclusion, the local injection of BLM seems to be very effective for the treatment of malignant brain tumors if it is used together with intravenous or intraarterial injection of other chemotherapeutic drugs.
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PMID:[A new treatment of malignant brain tumor -1: local injection of bleomycin (author's transl)]. 617 6

Activities of pyrimidine nucleoside phosphorylase in brain tumors were measured and their relationship to a clinical course of the patients was investigated. Pyrimidine nucleoside phosphorylase is said to exist more quantitatively in malignant tumors such as Sarcoma 180, Ehrlich ascites carcinoma, Walker 256, and hepatoma, and very little in normal tissues. In brain tumors the activities were measured by bioassay and compared to that of Sarcoma 180. When the activity of Sarcoma 180 was expressed to be 100%, those of brain tumors were as follows: ten cases of normal brain less than 8.5; six cases of glioblastoma 39.3 +/- 30.7; five cases of astrocytoma 22.0 +/- 13.8; five cases of meningioma 22.4 +/- 13.7; two cases of oligodendroglioma 8.1 and 11.3; two cases of sarcoma 94.3 and 145.4; chordoma 48.0; ependymoblastoma 3.7; plexus papilloma 22.5; parotid cancer 43.4; ten cases of metastatic brain tumors from lung cancer 61.5 +/- 41.6; two cases from breast cancer 28.0 and 68.8; that from thyroid cancer 10.0; that from gastric cancer 13.5; malignant melanoma 77.2. In 12 cases of gliomas (glioblastoma, astrocytoma, oligodendroglioma) the mean activity was highest in glioblastoma (39.3), followed by astrocytoma (22.0) and oligodendroglioma (9.7). The postoperative survival time became shorter in gliomas with the higher activities. In metastatic brain tumors from lung, breast, and gastric cancer, the average time from the diagnosis of primary cancer to brain metastasis was shorter in cases with high activities and longer in cases with low activities.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Activities of pyrimidine nucleoside phosphorylase in brain tumors and antitumor effect of 5'-DFUR]. 622 41

The distribution and localization of a glioma-associated antigen defined by monoclonal antibody 81C6 has been examined using human cultured cell lines and tissues. Monoclonal antibody 81C6 was selected from a hybridoma fusion of spleen cells of mice immunized with the glial fibrillary acidic protein-positive human glioma cell line U-251 MG. Results of cell surface radioimmunoassay and absorption analysis demonstrated that 81C6 defined a glioma-mesenchymal extracellular matrix (GMEM) antigen expressed by 14 of 16 gliomas, 1 of 3 neuroblastomas, 1 of 7 melanomas, 2 of 6 sarcoma cell lines, and 8 of 9 cultured fibroblast lines. GMEM was not expressed by carcinoma or by the myeloid-lymphoid cell lines examined. Within the central nervous system, GMEM was expressed in 10 of 11 glioblastomas but was undetected in 5 of 6 astrocytomas and in normal adult and fetal brain by peroxidase-antiperoxidase immunohistology. In glioblastomas, the GMEM antigen was localized to basement membranes of the distinctive glomeruloid endothelial proliferations and hyperplastic blood vessels. The GMEM antigen was also expressed in 3 of 3 glioblastoma cell lines and 6 of 8 glioblastoma biopsy xenografts in athymic nude mice. Among non-central nervous system tissues and tumors, GMEM was found by peroxidase-antiperoxidase immunohistology in normal liver sinusoids, spleen red pulp sinusoids, kidney medullary tubule interstitium, and glomerular mesangium and in association with vascular and stromal elements of several undifferentiated tumors. The GMEM antigen is distinct from previously described forms of fibronectin, laminin, collagen types I to V, hyaluronic acid, chondroitin sulfate, and heparin, as determined by absorption analysis and immunohistological localization in tissues. The expression of GMEM in glioblastoma but not normal brain, association with glioblastoma-proliferative endothelium basement membranes, and expression in glioblastoma cell lines and nude mouse xenografts suggest that GMEM may be a useful marker of gliomas in vivo and in vitro.
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PMID:Human glioma-mesenchymal extracellular matrix antigen defined by monoclonal antibody. 634 60

Secondary malignancies after marrow transplantation have been observed in 20 patients: 19 patients underwent marrow transplantation for the treatment of a hemopoietic malignancy and one for aplastic anemia. All but three were given total body irradiation at doses of 8.0-15.75 Gy as part of the conditioning regimen. Secondary malignancies were composed of three groups: (a) Six patients had recurrence of leukemia (three acute lymphoblastic, two acute myeloblastic, and one chronic myelocytic) in cells of donor origin 62-1074 days after grafting. (b) Eight patients developed lymphoproliferative disorders (four of immunoblastic sarcoma type, one lymphoblastic, one follicular center cell, and one Hodgkin's lymphoma and one acute lymphoblastic leukemia) 54-730 days after grafting. In four of seven patients with appropriate studies these tumors were of donor-cell origin and in three of four tested the cells contained Epstein-Barr virus genome or expressed viral antigens. (c) Six patients developed solid tumors (two glioblastoma multiforme, two adenocarcinomas, one squamous cell carcinoma, and one sarcoma) 347-1875 days after grafting. All but two patients (one with glioblastoma and one with squamous cell carcinoma) have died. These data suggest that patients undergoing marrow transplantation for a hemopoietic malignancy may be at risk of developing secondary malignancies. The etiology appears to be multifactorial, including irradiation, immunosuppression, Epstein-Barr virus infections, and other factors.
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PMID:Secondary malignancies after marrow transplantation. 638 5

Monoclonal antibodies against a human plasminogen activator of M(r) approximately 52,000 (HPA52) were derived by immunization of mice with an impure preparation of the enzyme (urokinase), subsequent hybridization of spleen cells with NSI-Ag4/1 myeloma cells, and cloning of the hybridomas. Selection of mice for hybridization and screening of hybridomas were based solely on direct inhibition of an enzymatic assay of the plasminogen activator with the impure enzyme preparation. A cloned hybridoma produced IgG1 antibodies that bound to and inhibited the enzymatic activity of HPA52 irrespective of whether the HPA52 was derived from urokinase or from human glioblastoma cells, whereas there was no inhibition of or binding to a plasminogen activator of M(r) approximately 70,000 from human melanoma cells or a plasminogen activator of M(r) approximately 36,000 that is a degradation product of HPA52 and present in urokinase. Nor did the anti-HPA52 IgG1 inhibit a murine plasminogen activator of M(r) approximately 48,000 derived from sarcoma virus-transformed cells. By using affinity chromatography with columns of anti-HPA52 IgG1 bound to Sepharose, HPA52 was purified from urokinase to homogeneity as evaluated by NaDodSO(4)/polyacrylamide gel electrophoresis. This study demonstrates that inhibitory monoclonal antibodies against enzymes can be derived with the sole use of impure enzyme preparations and shows how such antibodies subsequently can be used for enzyme purification.
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PMID:Monoclonal antibody that specifically inhibits a human Mr 52,000 plasminogen-activating enzyme. 680 14

Incorporation of the serine protease active site reagent diisopropyl fluorophosphate (DFP) into a plasminogen activator with an Mr of approximately 52000 released from cultured human glioblastoma cells was strongly enhanced by incubation with plasmin. This observation led to the isolation of an inactive form of the enzyme from serum-free conditioned culture fluid by affinity chromatography on a column of a Sepharose-bound monoclonal antibody raised against urokinase. An 831-fold purification was obtained with a yield of 41%. The purified molecule was homogeneous as evaluated by polyacrylamide gel electrophoresis with sodium dodecyl sulfate (NaDodSO4), having one stainable band under nonreducing as well as reducing conditions with an Mr of approximately 52000. It was unable to activate plasminogen, but catalytic amounts of plasmin converted it into active enzyme. After NaDodSO4-polyacrylamide gel electrophoresis, the active enzyme showed one band under nonreducing conditions, but after reduction, two bands with Mr values of approximately 20000 and 32000 were observed. The active enzyme incorporated [3H]DFP into the approximately Mr 32000 band, while no incorporation was observed into the inactive form. These findings show that the Mr 52000 human plasminogen activator exists in a proenzyme form consisting of a single polypeptide chain that by proteolysis between half-cystine residues is converted into the active enzyme consisting of two chains with molecular weights of approximately 20000 and 32000, the active site being on the latter chain. The results are consistent with the active form of the enzyme being identical with the higher molecular weight form of urokinase, and together with recent observations that a murine plasminogen activator is released from sarcoma virus transformed cells as an inactive proenzyme, they suggest that zymogens to plasminogen activators are of more general occurrence.
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PMID:Purification of zymogen to plasminogen activator from human glioblastoma cells by affinity chromatography with monoclonal antibody. 689 Dec 64

Total cellular RNAs from a variety of fresh and culture-derived human hematopoietic neoplastic cell types at various stages of differentiation and human sarcoma, carcinoma, melanoma, and glioblastoma cell lines were enriched for poly(A)- containing sequences, fractionated by gel electrophoresis, and blot hybridized to a cloned DNA probe containing the transforming sequences (v-amv) of avian myeloblastosis virus (AMV), a virus known to cause myeloid leukemias in chickens. Expression of RNA sequences homologous to AMV was detected in all immature myeloid and lymphoid T cells in addition to the single erythroid cell line examined, but not in mature T cells or in B cells, including lymphoblast cell lines derived from patients with Burkitt lymphoma. In addition, induction of the cell line HL60, a promyelocytic leukemia line, to differentiate with dimethyl sulfoxide or retinoic acid resulted in a reduction of the level of expression of the human cellular gene c-amv homologous to v-amv. There was no detectable c-amv mRNA in any of the solid tumor cell lines examined. Thus, expression of the human c-amv gene could be correlated with the stage of differentiation of different hematopoietic cell types determined by morphologic and marker studies. Expression of c-amv could not be correlated with the extent of methylation in HL60 and in HL60 induced to differentiate with dimethyl sulfoxide.
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PMID:Differential expression of the amv gene in human hematopoietic cells. 695 33

For an immunohistochemical analysis of cellular function of tumors, as related to acetylcholine, the antibody to choline acetyltransferase from bovine brain was obtained in guinea pigs. The specificity of the antibody was immunohistochemically studied in the cervical spinal cord of the mouse. And the findings coincided well with the biochemically and histochemically data on the distribution of choline acetyltransferase or acetylcholinesterase in the spinal cord. The choline acetyltransferase activity in the tumor cells at 6-10 days after subculture was 2.26 nmol/1 x 10(5) cells/hr in glioblastoma, 1.77 nmol/1 x 10(5) cells/hr in C-1300 and 1.45 nmol/1 x 10(5) cells/hr in sarcoma and the difference was statistical. In the immunohistochemical cell staining of these tumors, the rate of fluorescence-positive cells was 82.0% in glioblastoma, 37.3% in C-1300 and 4.2% in sarcoma. These findings coincide well with data on the enzymatic activity. The antibody is applicable not only in the field of the immunohistochemistry, but also for a mechanical analysis of cells at the single cell level, as demonstrated by Fluorescence Activated Cell Sorter (FACS).
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PMID:[Immunohistochemical analysis of tumor cells using choline acetyltransferase (author's transl)]. 703 12

A phase I study of intracarotid cis-diamminedichloroplatinum was performed in 11 patients with intracerebral tumors (five glioblastoma, four melanoma, one meningeal sarcoma, and one lung carcinoma) progressing after radiation +/- chemotherapy. The internal carotid artery was temporarily cannulated by a percutaneous transfemoral approach. All patients received i.v. heparin, mannitol, and fluids; seven received dexamethasone, 50 mg i.v., twice the day before and the day of treatment. Intracarotid cis-diamminedichloroplatinum, 60 to 100 mg/sq m in 175 to 250 ml 0.45% NaCl solution with 1000 units heparin, was infused over 1 hr. Six patients received two or more courses (maximum of 6) at 2- to 8-week intervals. Gastrointestinal toxicity was mild to moderate. Ototoxicity was minor. Central nervous system (CNS) toxicity was focal, severe, permanent, and possibly due to embolus in one patient at 75 mg/sq m; focal and reversible in one patient at 100 mg/sq m; and generalized but reversible in one patient at 75 mg/sq m. Possible CNS toxicity was noted in two additional patients. Two patients with CNS toxicity developed permanent ipsilateral retinal toxicity, and one patients without CNS toxicity developed bilateral decreased visual and auditory acuity 2 weeks after his sixth treatment. Renal and hematological toxicity and orbital pain were mild. Response status included: early death, one; probable responses, six (2+ 4+, 6, 6+, 8, and 8+ months); stabilization, two (3+ and 4 months); and failure, two. We recommend cis-diamminedichloroplatinum (60 mg/sq m) every 2 to 4 weeks for Phase II studies. Severe CNS and retinal toxicity are possible.
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PMID:A phase I study of intracarotid artery infusion of cis-Diamminedichloroplatinum(II) in patients with recurrent malignant intracerebral tumors. 719 71

Among the 54946 post-mortem examinations carried out by the Pathological Institute of the Medical Academy of Erfurt in the years 1953 to 1976 with a total of 1491 DNS-tumours (2.7%), the temporal lobe was involved in the following 10 types of tumours: glioblastoma, ependymoma, oligodendroglioma, plexus papilloma, tumour-like gliosis, sarcoma, angioma and angioblastoma, epidermoid tumour, teratoma. Only tumours that had formed in the cerebral tissue proper were evaluated, so that meningiomas and other tumours of the meninges or tumours of the meninges in the middle cranial fossa were left out of consideration. In a total of 949 cases of the above mentioned 10 tumours types, the temporal lobe was involved in 327 (34.5%) cases; these were mainly astrocytomas and glioblastomas (86.5%). Only 63 of the 327 tumours (19.3%) were exclusively located in the temporal lobe. The age peak of the occurrence of temporal lobe tumours was in the 6th decennium. The male showed with 55.4 per cent a slightly greater incidence. CLinically, the left-sided temporal lobe tumours with 79 per cent of the observations were found more frequently than the right-sided ones (67%). Accordingly, left-sided tumours were operated on more frequently (49%) than tumours on the right-hand side (40%).
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PMID:[Localization of brain tumors in autopsy. Part I: Tumors of the temporal lobe]. 734 Mar 11


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