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

Thomsen-Friedenreich (T) antigenic specificity as determined with human serum anti-T was found in reactive form in breast adenocarcinomata but not in healthy and generally not in benign breast tissues. T-antigenic specificity was demonstrable in all metastatic breast carcinoma lesions. T specificity was also present in adeno- and squamous cell carcinomata from other organs; it was not found in the four melanomata, one glioblastoma, and seven benign non-breast tumors. Breast carcinoma patients but not healthy people showed cellular immunity to T antigen in vivo and in vitro. Most striking was the delayed-type cutaneous hypersensitivity reaction that was positive in over 85% of the ductal breast carcinoma patients tested, negative in over 94% benign breast disease patients, and in all presumably healthy individuals investigated. T antigen is readily available from healthy red blood cells in uncontaminated form, and free of HL-A and Australia antigens.
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PMID:Breast cancer patient's cell-mediated immune response to Thomsen-Friedenreich (T) antigen. 624 84

Continued monitoring of a family for new malignant tumors has revealed diverse immunological and neoplastic disorders during a 15-year period. In 1966, the proband developed lymphoma. In 1975, his antibody titers to Epstein-Barr virus (EBV) became elevated, and again, he developed a malignant lymphoma. He also had borderline hypo-immunoglobulin A, died of glioblastoma multiforme in 1977, and at autopsy, had adenomatous colonic polyps. His eldest brother has normal immunoglobulin levels, but developed immune thrombocytopenia in 1973 and had elevated EBV antibody titers in 1980. Another brother had hypo-immunoglobulin A, thymoma in 1965, and adenomas and adenocarcinoma of the colon. Two other brothers succumbed to glioblastoma in 1968 and 1969. The father of the proband had bronchiectasis in 1952, hypo-immunoglobulin M documented in 1972, and elevated EBV antibody titers 5 years preceding development of a malignant lymphoma. The latter contained 10 EBV genome equivalents/cell by EBV viral DNA/DNA reassociation kinetics analysis. The proband's grandmother had died of an immunoglobulin G-secreting myeloma in 1977, and his grandfather had borderline low immunoglobulin M, elevated EBV antibody titers, and hypopharyngeal carcinoma in 1980. Predisposition to oncogenesis in this family was probably inherited.
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PMID:Diverse familial malignant tumors and Epstein-Barr virus. 627 70

Monoclonal antibodies raised against B 16 melanoma cells in syngeneic mice were functionally screened for their ability to inhibit cell adhesion in tissue culture. Three of these antibodies (16/43, 16/77, 16/82), when preinjected into C57BL/6 mice, markedly reduced the number of experimental lung metastases produced by B 16 cells, possibly by interference with their adhesion to the lung endothelia. We now report that these monoclonal antibodies block in vitro attachment of the majority of human melanoma cell lines tested and also of carcinoma, neuroblastoma, and glioblastoma cells from both mice and humans but untransformed cell lines such as 3T3 mouse or MRC-5 human fibroblasts are not affected. The antibodies also react with mouse teratocarcinoma stem cells (F9, PCC4) but not with differentiated teratocarcinoma lines (PYS-2, 944). Furthermore, the antiadhesion activity of the antibodies could be quantitatively absorbed by intact human and mouse tumor cells but not by untransformed cells, suggesting that the corresponding antigens may represent tumor-associated cell surface components. Correspondingly, the antigens were found on simian virus 40-transformed 3T3 mouse fibroblasts and are expressed in a temperature-sensitive fashion in chicken fibroblasts transformed with a temperature-sensitive Rous sarcoma virus. On "immunoblots" of NaDodSO4-containing gels the three selected antibodies (16/43, 16/82, 19/1) were absorbed by antigens with molecular weights of 40,000 and 50,000.
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PMID:Monoclonal antibodies that prevent adhesion of B 16 melanoma cells and reduce metastases in mice: crossreaction with human tumor cells. 631 31

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

In this paper we review the current data on the role of potentially lethal damage (PLD) recovery in human tumour cell lines, both in vitro and in vivo. In the case of cell lines studied in vitro, the mean recovery ratios found were higher for cells derived from tumours of low curability (glioblastoma, hypernephroma, osteosarcoma, melanoma) than for cells derived from tumours of high curability (breast carcinoma, neuroblastoma). Experiments were performed in vivo only with tumours of low and intermediate curability (melanoma, adenocarcinoma of the colon, pancreatic tumour). Although fragmentary and obtained only with established cell lines, these results argue in favour of the occurrence of PLD repair in human tumour, the amplitude of this repair being, in certain cases, sufficient to explain the incurability of a tumour by radiation therapy.
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PMID:Potentially lethal damage repair as a possible determinant of human tumour radiosensitivity. 650 62

Cytoplasmic estrogen receptor (ER) and progesterone receptor (PR) proteins were measured by a dextran-coated charcoal absorption technique in 19 intracranial tumors (10 meningiomas, two acoustic neurinomas, two glioblastomas, one primary tumor of neuroectodermal origin, one hemangioblastoma, one metastasis of carcinoma, one chordoma, and one pituitary adenoma). Positive PR values (greater than or equal to 10 fmol/mg of protein) were found in nine meningiomas (90% of these tumors), in the chordoma, in one glioblastoma, and in the hemangioblastoma, whereas positive ER values were recorded only in the pituitary adenoma and in one glioblastoma. Evidence of PR in meningiomas might explain their predominance in women. A possible pharmacological therapy, based on these findings, is discussed.
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PMID:Estrogen and progesterone receptors in intracranial tumors. 650 43

In normal conditions, neuron-specific enolase (NSE) is histochemically demonstrable only in neurons and cells of the amine precursor uptake and decarboxylation (APUD) system. This has been found not to be true for neoplastic cells. Several types of CNS tumors, including glioblastoma, astrocytoma, oligodendroglioma, ependymoma, medulloblastoma, pineocytoma , meningioma, and choroid plexus papilloma, focally stained positively for NSE. Reactive astrocytes were also frequently positive. In the peripheral nervous system, neuroblastoma, ganglioneuroma, and paraganglioma stained positively for NSE. A number of non-APUD tumors were focally positive. These included schwannoma, carcinoma and fibroadenoma of the breast, renal cell carcinoma, giant cell tumor of the tendon sheath, and chordoma. Caution should be exercised in relying on the immunohistochemical demonstration of NSE as a diagnostic marker in those tumors that do not belong to the APUD cell system. It seems of little value as evidence of differentiation in CNS tumors.
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PMID:Immunohistochemical demonstration of neuron-specific enolase in neoplasms of the CNS and other tissues. 654 18

The hybridoma technique was used to generate monoclonal antibodies against a wide spectrum of melanoma-associated surface antigens. Mice were immunized against the human melanoma lines Mel A-375, SK Mel-25, and Mel S-5 (subclone of SK Mel-25), which differ with respect to a number of biological and biochemical properties. Spleen cells were fused with P3 X 63-AG8.653 myeloma cells. Twenty hybridomas producing antibodies that were negative on platelets, leukocytes, and monocytes but positive on melanoma cells were isolated and recloned. The specificity of antibodies was investigated on 30 human melanoma and nonmelanoma lines. Five groups of antibodies could be distinguished by their reactivity (1) with few melanoma lines and embryonic fibroblasts; (2) with melanoma, neuroblastoma, and teratoma; (3) with melanoma, neuroblastoma, glioblastoma, teratoma, and carcinoma; (4) with melanoma, teratoma, and carcinoma; and (5) with melanoma, neuroblastoma, teratoma, glioblastoma, carcinoma, embryonic fibroblasts, and B-lymphoblastoid cells. The antigen expression was qualitatively and quantitatively different from cell line to cell line. No evidence for melanoma-specific antigens was found. Eight antibodies were isolated detecting phenotypic differences on sublines of SK Mel-25.
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PMID:Detection of phenotypic differences on human malignant melanoma lines and their variant sublines with monoclonal antibodies. 655 61

Estrogen and progesterone receptors have been measured in 13 intracranial tumors (eight meningiomas, two acoustic neurinomas, one primary tumor of neuroectodermal origin, one giant-celled glioblastoma, and one metastasis of carcinoma). Evidence is provided of the presence of progesterone receptors in meningiomas (87.5%). We could not find clear evidence of estrogen receptors in any tumor of this series. Presence of progesterone receptors in meningiomas suggests an explanation for the greater incidence of these tumors in women and their rapid growth during pregnancy.
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PMID:Estrogen- and progesterone-receptor proteins in intracranial tumors. 682 87

Within the Special Research Group of Department of Health and Welfare, seven research subgroups which are testing different types of interferon supplied from each seven companies are organized at the time of October 1982. Out of these subgroups, two groups, Toray company group (IFN-beta) and Sumitomo company group (HLBI-alpha), have made clinical trials on 123 cases and 120 cases respectively. Other groups are still under preparation. 6 cases with complete response and 23 cases with partial response by IFN-beta, and 0 cases with complete response and 13 cases with partial response by HLBI-alpha are observed. Over all responded disease are such as glioblastoma, medulloblastoma, melanoma and cutaneous T-cell lymphoma with local injection, and hypernephroma, bladder carcinoma, medulloblastoma, multiple myeloma, and adult T-cell leucaemia with systemic administration.
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PMID:[Current status and problems of cancer treatment with interferon]. 687 30


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