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)

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.
 ...
PMID:Distribution of c-yes-1 gene product in various cells and tissues. 202 34

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.
 ...
PMID:Epidermal growth factor receptor gene analysis in renal cell carcinoma. 229 52

Interferon-gamma-induced tryptophan metabolism of human macrophages was compared to ten human neoplastic cell lines of various tissue origin and to normal dermal human fibroblasts. Tryptophan and metabolites were determined in supernatants of cultures, after incubation for 48 h, by high-performance liquid chromatography with ultraviolet and fluorescence detection. With the exception of two cell lines (Hep G 2, hepatoma and CaCo 2, colon adenocarcinoma) in all of the ten other cells and cell lines tryptophan degradation was induced by interferon-gamma. Five of these ten formed only kynurenine (SK-N-SH, neuroblastoma; T 24, J 82, bladder carcinoma; A 431, epidermoid carcinoma; normal dermal fibroblasts), three formed kynurenine and anthranilic acid (U 138 MG, glioblastoma; SK-HEP-1, hepatoma; A 549, lung carcinoma). Only one line, A 498 (kidney carcinoma) showed the same pattern of metabolites as macrophages (kynurenine, anthranilic acid and 3-hydroxyanthranilic acid). Interferon-gamma regulated only the activity of indoleamine 2,3-dioxygenase. All other enzyme activities detected were independent of interferon-gamma, as shown by the capacity of the cells to metabolize L-kynurenine or N-formyl-L-kynurenine. Increasing the extracellular L-tryptophan concentration resulted in a marked induction of tryptophan degradation by macrophages. Contrarily, a significant decrease of the tryptophan degrading activity was observed when the extracellular L-tryptophan concentration was increased 2-fold with SK-N-SH, T 24 and J 82, 4-fold with A 431 and A 549 and 10-fold with U 138 MG and SK-HEP-1. The activity was unaffected by extracellular L-tryptophan with dermal fibroblasts and A 498. Though interferon-gamma was the most potent inducer of tryptophan metabolism, interferon-alpha and/or -beta showed small but distinct action on some of the cells. In all cells which reacted to interferon-gamma by enhanced expression of class I and/or class II major histocompatibility complex antigens tryptophan degradation was also inducible. These results demonstrate that induction of indoleamine 2,3-dioxygenase is a common feature of interferon-gamma action, that the extent of this induction is influenced by extracellular L-tryptophan concentrations and that indoleamine 2,3-dioxygenase is the only enzyme in the formation of 3-hydroxyanthranilic acid from tryptophan which is regulated by interferon-gamma.
 ...
PMID:Characteristics of interferon induced tryptophan metabolism in human cells in vitro. 250 Sep 76

Between December 1986 and December 1988, the Italian Cooperative Group on AIDS-Related Tumours documented 49 HIV-related tumours other than malignant lymphomas (ML) and Kaposi's sarcomas (KS), predominantly among HIV-infected intravenous drug abusers (IVDA). Of 12 germinal testicular tumours collected, six were seminomas, two of which were pure embryonal and the other four embryonal mixed. Cervical carcinoma was observed in nine IVDAs (intraepithelial in eight and advanced, with rapid progression, in one). Lung cancer associated with HIV infection was reported in eight patients, of whom four had an adenocarcinoma, two a small cell carcinoma, one an epidermoid carcinoma and one a mesothelioma. All patients with non-small-cell-lung cancer (SCLC) were at stage III, while those with SCLC and mesothelioma had limited disease. Five out of eight presented with limited disease at onset. The median age was low; lung cancer occurred predominantly in young adults, of whom all but one were smokers. Three patients could not be treated; four died while on treatment because of progression of the neoplasia and one died of an overdose. Acute lymphoblastic leukaemia (ALL) was diagnosed in five patients. The immunophenotype was always Burkitt-like (L3), and acute myeloblastic leukaemia (M2) was diagnosed in one. Of the central nervous system (CNS) tumours, two cases of glioblastoma and one of medulloblastoma were described. Two cases of young adults with multiple myeloma and two cases of colorectal carcinoma were also reported. One case of chronic lymphocytic leukaemia, one anorectal carcinoma, one oral carcinoma, one pancreatic carcinoma, one thymoma, one kidney carcinoma, one malignant melanoma and thyroid carcinoma were also found.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Unusual malignant tumours in 49 patients with HIV infection. 250 49

Two established human tumor cell lines, epidermoid carcinoma line A431 and glioblastoma line SF268, were studied to compare the interaction of each with epidermal growth factor (EGF). SF268 cells bound [125I] EGF with 35-40 fold higher affinity than did the A431 cells. The EGF binding sites of both lines were photoaffinity labeled using 2,4-NAPS-[125I] EGF, a photoreactive derivative of EGF. Extracts of photolysed cells analyzed by SDS-PAGE showed a difference between the two cell lines in the high molecular weight component corresponding to the EGF receptor. EGF in a dose range from 0.3-200 nM had no effect on thymidine incorporation by SF268 cells, whereas thymidine incorporation by A431 cells was markedly inhibited by EGF.
 ...
PMID:Epidermal growth factor receptors in the human glioblastoma cell line SF268 differ from those in epidermoid carcinoma cell line A431. 299 56

Human tumor cells such as melanoma or glioblastoma are intrinsically radioresistant on an average than cells of more common tumors in radiotherapy such as squamous cell carcinoma or adenocarcinoma. Mean inactivation dose (D) for glioblastoma A-7 cells was 3.1 Gy for cells growing exponentially, but was 4.3 Gy for cells grown in large spheroids with hypoxic cells and PLD recovery. The D for cells of squamous cell carcinoma was about 2.1 Gy. This indicates that local control of the radioresistant tumors may be achieved if a drug showing an enhancement ratio of about 2.0. Data on our experiments with others in the literature indicate that drugs which selectively sensitize hypoxic cells and inhibit PLD recovery may be useful to increase the therapeutic ratio. Experimental evidence on a nitrosourea, ACNU has been presented for such mechanisms of the action. Multivariate analysis with Cox's model on malignant gliomas of 209 patients indicated that a significant increase in the survival time was obtained in the radiotherapy combined with ACNU.
 ...
PMID:[Biological basis for combined radio-chemotherapy in radioresistant tumors]. 319 20

Metastatic brain tumors very often cause severe brain edema. We examined ultrastructural findings of capillaries of these tumors and discussed the causes of cerebral edema as compared with those of glioblastoma which were previously reported. Four specimens were examined: two adenocarcinomas from the lung, one squamous cell carcinoma from the lung and one adenocarcinoma from the breast. These replicas and ultrathin sections were examined by transmission electron microscope. The following characteristic structures were detected; the capillary endothelium was proliferated, had marked infolding, and an increased number of pinocytotic vesicles and vacuoles. Short and elongate intercellular junctions were present. No open junction was detected. The basal lamina lost its three layered appearance and was irregular in width. Among these, an appearance of capillary fenestration was the most conspicuous features and observed in almost all capillaries. Two different pathogenesis for making vasogenic edema are proposed in metastatic brain tumor and glioblastoma. The frequent fenestration of the former and activated pinocytotic vesicles of the latter are responsible for extravasation of the edema fluid. The differences in distribution patterns of fenestration in metastatic brain tumor cannot be identified with respect to histological types.
 ...
PMID:[Ultrastructure of capillary permeability in human brain tumor--Part 6: Metastatic brain tumor with brain edema]. 339 12

A murine monoclonal antibody, VM-1, which binds to basal cells of normal human epidermis, reduces the ability of human squamous cell carcinoma cells (SCL-1) derived from the skin to attach and spread on collagen by about 50% and causes cell rounding. Similar effects have been previously shown using normal human keratinocytes. The attachment of cell lines derived from human lung squamous cell carcinomas (SW1271 and SW900), melanoma A375, glioblastoma 126, and fibrosarcoma HT1080 is also inhibited by this antibody. VM-1 antibody does not bind to normal human fibroblasts, benign nevus cells, or the human B-cell-derived line 8866. VM-1 antibody inhibits the growth of SCL-1 cells in vitro as measured by cell numbers and [3H]thymidine ([3H]TdR) incorporation. It is not cytolytic in the presence of complement as measured by 51Cr release. Repeated treatment of SCL-1 cells with VM-1 antibody significantly reduces the proportion of SCL-1 cells that attach to collagen. In addition, after treatment of SCL-1 cells with VM-1 antibody, several proteins can no longer be demonstrated by gel electrophoresis of the cell-free supernatant. The VM-1 antibody effect on attachment and spreading is partially reversed by pretreatment of the collagen surface with laminin and fibronectin, but not with the carbohydrates chondroitin-6-sulfate or hyaluronic acid or with the protein lysozyme. By fluorescence staining, the antigen recognized by VM-1 antibody is membrane-bound and Triton X-100 extractable. The VM-1 antigen is excluded from Bio-Sil TSK-400 and sediments at about 10.5 S. It has a covalent molecular weight on the order of 10(6). Proteinase K digestion produces VM-1 antibody reactive fragments, assumed to be polysaccharides, with a polydisperse molecular weight distribution in the range 5000 to 30,000. The VM-1 antigen is partially lost from solution on boiling and is no longer detectable in the aqueous or organic phase after chloroform-methanol extraction. The properties of the VM-1 antigen are consistent with those of a proteoglycan involved in attachment and spreading of keratinocytes and certain tumor cells on collagen.
 ...
PMID:Inhibition of attachment and growth of tumor cells on collagen by a monoclonal antibody. 369 49

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.
 ...
PMID:Secondary malignancies after marrow transplantation. 638 5

The replication of measles virus in human neural and nonneural cell lines in terms of growth and cytopathic effect was affected by treatment of the cells with papaverine, which increases endogenous cyclic AMP. Suppression of virus growth was most prominent in neuroblastoma cells, followed by that in epidermoid carcinoma and glioblastoma cells, whereas the suppressive effect was relatively weak in oligodendroglioma cells. The papaverine-induced suppression of virus growth in neuroblastoma cells was studied in detail. The suppression that occurred was dependent on the dose of papaverine and was reversible. By treatment with 10 microM papaverine, virus-cell interactions were modified as follows: (i) early replication steps such as adsorption, penetration, and uncoating of the virus were not affected; (ii) synthesis of viral RNAs, including genomic RNA and mRNA, was inhibited; (iii) translation of viral proteins from mRNA was not blocked; and (iv) glycosylation and transport of viral glycoproteins to the cell membrane were not inhibited, but phosphorylation was blocked. The significance of suppressed virus replication in neural cells is discussed in relation to the persistence mechanisms of measles virus in the central nervous system.
 ...
PMID:Effect of papaverine treatment on replication of measles virus in human neural and nonneural cells. 670 72


1 2 3 4 5 6 7 8 9 10 Next >>