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)

The distribution and degree of expression of c-yes-1 gene product in a variety of cell lines, human foetal tissues, and adult normal and malignant tissues were examined using immunohistochemical techniques. A murine monoclonal antibody 1B7 raised against a fusion protein consisting of 64 amino acid residues from the N-terminus of the c-yes-1 gene product and bacterial phosphate-binding protein (PBP) was used. At the ultrastructural level, the c-yes-1 gene product recognised by 1B7 was localised in the cytoplasm. Moderate to strong expression of the c-yes-1 gene product was observed in HT10-80 (fibrosarcoma). IN-1 (malignant lymphoma), Marcus (glioblastoma), TIG-1-20 (foetal skin fibroblast), proximal tubules of foetal and adult kidney, one of four breast cancers, one of four colorectal cancers, 14 of 33 head and neck cancers, 13 of 24 renal cancers, three of 19 lung cancers and one of seven stomach cancers. These results were further confirmed by Western blotting. Histological types showing moderate to strong expression of the c-yes-1 gene product were renal cell carcinoma (13/24) and squamous cell carcinoma (15/38). The fact that the c-yes-1 gene product is expressed preferentially in renal cell carcinoma and squamous cell carcinoma may indicate that it plays an important role.
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PMID:Distribution of c-yes-1 gene product in various cells and tissues. 202 34

This report presents the case of a 74-year-old woman who was simultaneously affected by two highly malignant neoplasms, a metastasizing renal cell carcinoma and a glioblastoma with sarcomatous component. Leptomeningeal metastasis of renal carcinoma is shown to invade the glioblastoma at its margin. Especially in gliomas, "cancer to cancer" phenomenomal are only rarely documented. Support by immunohistochemical data may prove those events to be more frequent than assumed.
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PMID:Metastasis of renal carcinoma colliding with glioblastoma. Carcinoma to glioma: an event only rarely detected. 217 31

The epidermal growth factor receptor binds the mitogens epidermal growth factor and transforming growth factor-alpha. Increased expression of the epidermal growth factor receptor has been noted in many types of tumors and is associated with gene amplification in several including epidermoid carcinoma, lung carcinoma, breast carcinoma and glioblastoma. We have recently observed increased expression of the epidermal growth factor receptor messenger RNA in neoplastic tissue relative to normal kidney tissue from patients with renal cell carcinoma. To determine if epidermal growth factor receptor gene amplification was present in renal cell carcinoma, DNA was extracted from renal cell carcinoma cell lines and from normal kidney and renal cell carcinoma tissues derived from radical nephrectomy specimens from thirty patients. DNA was analyzed by Southern blot hybridization. There was no epidermal growth factor receptor gene amplification detected in the renal cell carcinoma samples studied, indicating the increased epidermal growth factor gene expression observed in renal cell carcinoma does not occur through gene amplification. Unlike other tumors with enhanced epidermal growth factor receptor gene expression, amplification of this gene does not appear to be a common feature of renal cell carcinoma.
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PMID:Epidermal growth factor receptor gene analysis in renal cell carcinoma. 229 52

Purified human natural tumor necrosis factor (n-TNF) was prepared by stimulating human leukemic B cell line (BALL-1) with Sendai virus. The colony formations of all of 18 human cancer-derived abnormal cell lines were suppressed by 10(1)-10(6) U/ml of n-TNF, while n-TNF was nontoxic to all human normal fibroblast cells. This in vitro inhibition of cell growth was reversible. In breast adenocarcinoma MCF7 cells treated with n-TNF a specific decrease of DNA synthesis was observed, and DNA histograms showed a block at G1 in the cell cycle. In vivo studies revealed that n-TNF suppressed the tumor growth of murine Meth A sarcoma, human renal adenocarcinoma (ACHN), malignant melanoma (SK-MEL-28) and glioblastoma (U-373 MG). Isobologram analysis showed that n-TNF synergistically inhibited cell growth in combination with human natural interferon (IFN)-a. In vivo synergism of n-TNF and IFN-a was also found in the U-373 MG tumor model implanted into nude mice.
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PMID:The inhibition of neoplastic cell proliferation with human natural tumor necrosis factor. 303 Sep 86

The purpose of these studies was to examine the antiproliferative properties of 16 recombinant human IFN-alpha B/D hybrids against various human tumor lines of different histological origin and to determine whether any of the hybrid molecules possessed immunomodulating activity that could active antitumor properties in peripheral blood monocytes of normal donors. Hybrids with the B domain at the NH2 terminal end exhibited higher activity for antiviral activity and a higher level of direct antitumor antiproliferative activities as compared with hybrids with the D domain at the NH2 terminal end. The positive hybrids were directly cytostatic to melanoma, glioblastoma, renal carcinoma, colon carcinoma, and prostatic carcinoma cells. Tumor cell sensitivity to IFN-alpha hybrids was independent of sensitivity to IFN-gamma or to Adriamycin. The growth of a normal cell line (human embryo fibroblast) was unaffected by IFN-alpha hybrids but was completely arrested by Adriamycin. Some of the IFN-alpha hybrids were also cytostatic to mouse melanoma, lung carcinoma, and fibrosarcoma cell lines, albeit at lower levels than they were to human cells. The incubation of monocytes with IFN-alpha hybrids with the B domain at the NH2 terminal end was also associated with marked antitumor cytotoxicity. Kinetic studies, however, indicated that this activity was attributable to IFN-alpha carried on monocytes and acting directly on tumor cells. We conclude that recombinant human IFN-alpha B/D hybrids possess potent direct antiproliferative activity against a large variety of human tumor lines.
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PMID:Direct antiproliferative effects of recombinant human interferon-alpha B/D hybrids on human tumor cell lines. 382 90

Host blood lymphocytes undergo accentuated blastic transformation when cultured with tumor cells pretreated with neuraminidase. The effect has been observed in 38 patients with such common solid tumors as bronchus carcinoma, skin melanoma, hypernephroma, or adenocarcinoma of the breast, lung, colon, or rectum. Individual response varied but often exceeded response to allogeneic cells. Three patients with glioblastoma of the brain did not respond. Lymphoblastic transformation was not observed in three of four cultures containing benign tumor or in any cultures containing normal tissue analogues of the malignant tumors. A factor in host blood serum inhibiting lymphoblastic transformation correlated to abnormal elevation of serum-bound sialic acid. This blocking factor differed in specificity from enhancing antibody or serum blocking complexes described by other investigators. Blocking effects were observed when the tumor-cell type of a serum donor differed from the cell type of the culture test tumor. Serum with abnormal elevation of bound sialate from a cancerfree human also non-specifically blocked host response to tumor. The blocking effect could be eliminated by partial enzymatic removal of bound sialic acid from serum glycoproteins.
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PMID:Neuraminidase-mediated augmentation of in vitro immune response of patients with solid tumors. 437 8

Three types of interferon preparation (alpha, beta and gamma) have been used in the treatment of tumours in vivo. At the time of writing no information is available on IFN-gamma treatment of tumour patients. Treatments with IFN-alpha and IFN-beta have been undertaken at many clinical centres. Both types of preparation can exert side effects. Both types have also been able to cause regression of certain tumours in individual patients. At our hospital, IFN-alpha has been given to tumour patients over the last decade. Antitumour effects have been registered on patients with juvenile laryngeal papillomatosis, Hodgkin's disease, myelomatosis, ovarian carcinoma, hypernephroma and glioblastoma. Further study is needed on how therapy with IFN should best be undertaken and also how such treatment compares with other treatments of various tumour diseases. IFN therapy should also be combined with other such treatments.
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PMID:Interferon therapy in neoplastic diseases. 618 85

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

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

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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