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Query: UMLS:C0027651 (tumor)
 685,946 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Samples of 35 tumors from the head and neck region (25 squamous cell, 2 basal cell, 5 parotid, 3 melanoma, and 1 lymphosarcoma) were cultured after dispersement with either trypsin or collagenase treatment. Growth was established in 14 (40%). Cultured tumor cells were then used as target cells in in vitro assays of patients' cellular and humoral immunity to their own or similar tumors. Preliminary data suggest this may be a reliable method of monitoring responses in patients receiving immunotherapy for head and neck malignancies.
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PMID:Tissue-cultured head and neck tumors: their use in in vitro assays of immune response. 19 78

The surface topologies of mouse adrenal cortex tumor cells of primary or clonal origin grown as monolayer cell cultures were observed by scanning electron microscopy following their exposure to substances that effect steroid release and/or cell rounding. ACTH induced cell rounding with a concomitant profuse development of fine microvilli in a non-synchronously dividing cell population. This was less pronounced with other steroidogenic substances and absent in EGTA or trypsin-treated cells. Morphological alterations occurred most rapidly with cAMP and least rapidly with dbcAMP. The rapid development of fine microvilli with ACTH is proposed to be a specific hormone mediated response.
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PMID:Scanning electron microscopy of induced cell rounding of mouse adrenal cortex tumor cells in culture. 20 10

A previous report from this laboratory showed that binding of iodine-labeled human choriogonadotropin to Leydig tumor cells is not a reversible process (Ascoli, M., and Puett, D. (1978) J. Biol. Chem. 253, 4892--4899). Most of the cell-bound hormone was found to be degraded to 3'-monoiodotyrosine before being released from the cells, and the degradation process could be inhibited by the lysosomotropic agents NH4Cl, chloroquine, and Triton WR-1339. It is reported herein that the degradation of receptor-bound human choriogonadotropin is an energy-dependent process, which can be inhibited by compounds that interfere with glycolysis or oxidative phosphorylation (e.g. NaF, NaN3, NaCN, and 2-deoxyglucose). Hormone degradation is also inhibited by some protease inhibitors such as the chloromethyl ketones of lysine and phenylalanine, but not by specific trypsin inhibitors (e.g. p-aminobenzamidine and p-tosyl-L-arginine methyl ester). With the exception of NH4Cl, it was found that the compounds which inhibit hormone degradation also inhibit hormone-stimulated steroidogenesis. However, the present results involving dose dependency, and those given in the following paper (Ascoli, M. (1978) J. Biol. Chem. 253, 7839--7843), indicate that these two phenomena are not related.
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PMID:Inhibition of the degradation of receptor-bound human choriogonadotropin by lysosomotropic agents, protease inhibitors, and metabolic inhibitors. 21 38

The chromosomes of metastatic cells and polyploid levels in the bone marrow of 26 patients with small cell anaplastic carcinoma were studied by direct bone marrow preparation and trypsin-Giemsa banding. Eighteen of these patients had received no tumor therapy and 8 had had chemotherapy and/or radiation therapy; 18 patients, including 5 who had received therapy, had karyotypic abnormalities with or without elevation of the polyploid level. Modal numbers and chromosome abnormalities were highly variable in treated and untreated patients. Modes ranged from hypodiploid to polyploid, but polyploid modes were the most frequently observed abnormal modes. Polyploid modes were not seen, however, in post-therapy patients with the exception of one who had received radiation therapy to the mediastinum for only 4 days prior to withdrawal of the specimen for chromosome analysis. Ten patients had elevated polyploid levels that ranged from 4.24 to 44.8% and always occurred in conjunction with karyotypic abnormalities. Both aneusomy (abnormal number) of normal chromosomes and structural aberrations (markers) occurred frequently. Some markers were consistent within an individual, but other variable aberrations were also typically present. Very few markers were common to 2 or more patients. The no. 1 chromosome participated in marker formation in 14 of the 18 patients with karyotypic abnormalities. Of the 26 patients, 5 were negative for metastasis to the marrow by pathologic examination but positive by cytogenetic diagnosis, whereas none were positive by pathologic examination and negative by cytogenetic diagnosis; this demonstrated that cytogenetics may be used as a rapid adjunct diagnostic procedure for the detection of metastasis in the marrow.
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PMID:Cytogenetic diagnosis of cancer: abnormalities of chromosomes and polyploid levels in the bone marrow of patients with small cell anaplastic carcinoma of the lung. 21 65

Antibodies to fibronectin and to distinct types of procollagens and collagens were used in immunofluorescent staining to localize these proteins in cell cultures. Normal human skin or lung fibroblasts produced a fibrillar pericellular matrix in which fibronectin and procollagen (types I and III) showed extensive codistribution. Fibronectin and procollagen were synthesized by the same cells as judged by double-stain immunofluorescence. Pericellular procollagen was specifically digested with collagenase without an effect on the fibrillar distribution of matrix fibronectin. Brief treatment with trypsin removed both matrix proteins. The human tumor cell lines HT-1080 (fibrosarcoma) and RD (rhabdomyosarcoma) produced little or no matrix fibronectin or procollagen. At sites of cell contact, simian virus 40-transformed lung fibroblasts (VA13) produced small amounts of pericellular fibrillar matrix fibronectin that codistributed with procollagen type I. Intracellular fibronectin and procollagen were visualized in all of these human sarcoma cell lines. When chicken embryo fibroblasts infected with a T class mutant (NY68) of Rous sarcoma virus temperature-sensitive for transformation were maintained at the nonpermissive temperature (41 degrees ) the cells had normal phenotype and a fibrillar matrix containing fibronectin and procollagen was present. At the permissive temperature (35 degrees ), the cells showed transformed phenotype and the matrix was lost. The failure to produce a pericellular fibronectin/collagen matrix may account for several phenotypic characteristics of transformed cultured fibroblasts.
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PMID:Codistribution of pericellular matrix proteins in cultured fibroblasts and loss in transformation: fibronectin and procollagen. 21 6

The specificity of human skin collagenase and of an enzyme from an invasive tumor were studied by using types I, II, III, IV, and V (AB) collagen as substrates. Human skin collagenase degraded types I, II, and III collagen, producing the characteristic 3/4 and 1/4 cleavage products, but failed to degrade type IV or V collagen. Collagenase prepared from the invasive tumors showed maximal activity after trypsin treatment. The tumor enzyme degraded type IV (basement membrane) collagen, producing fragments consistent with a single cleavage site but did not attack types I, II, III, and V collagen. Because type IV collagen prepared by pepsinization of placenta was also digested, it is likely that cleavage of type IV collagen by the tumor collagenase occurs within a largely helical domain. A type IV collagenase could play a significant role in tumor metastases and in normal tissues where basement membrane turnover takes place.
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PMID:Preferential digestion of basement membrane collagen by an enzyme derived from a metastatic murine tumor. 22 20

The tumor promoter phorbol myristate acetate (PMA) induces the production of the serine protease plasminogen activator (PA) in cultures of normal chick embryo fibroblasts (CEF) and synergistically enhances PA production in Rous sarcoma virus-transformed chick embryo fibroblasts (RSVCEF). Following PMA treatment of serum-free RSVCEF cultures, PA induction is accompanied by distinct morphological changes, including enhanced cell clustering and the formation of dense cellular aggregates. These alterations in the morphology of the PMA-treated transformed cells are inhibited by several protease inhibitors, including leupeptin, NPGB, SBTI, benzamidine and DFP, the specific inhibitor of serine enzymes. A number of protease inhibitors are ineffective in preventing the PMA-induced morphological changes; these include inhibitors of trypsin, chymotrypsin, elastase, thrombin and, most importantly, plasmin. The use of a fluorescent substrate to assay PA directly demonstrated that the pattern of inhibiton of PA activity correlates exactly with the inhibition of morphological changes. The of 3H-DFP to label and characterize serine zymes in the culture fluid from PMA-treated cells further indicated that PA is the serine protease responsible for the morphological changes. Thus PA itself can catalytically alter cellular behavior in culture independent of plasminogen, until not its only known natural substrate.
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PMID:Phorbol ester-induced morphological changes in transformed chick fibroblasts: evidence for direct catalytic involvement of plasminogen activator. 22 74

Explanted tumour cells are much more sensitive to the deleterious effects of routine trypsinization than are the parent 3T3 or SV40 transformed established cell lines. This differential sensitivity causes the disappearance of tumour-derived cells when grown in co-culture with untransformed 3T3 cells and accounts in some tumor explants for the emergence of trypsin-resistant varient cells which have lost tumour-specific properties.
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PMID:Selective effects of trypsinization on established and tumour-derived mouse 3T3 cells. 22 89

A specific marker for an immature population of thymus cells in the rat was shown by the rosette formation between thymus cells and guinea pig erythrocytes. This method was used to classify murine leukemia virus-induced rat lymphomas. Eight of nine Gross virus-induced rat lymphoma lines, which originated in the thymus, formed rosettes; whereas Friend, Rauscher, or Moloney virus-induced rat lymphoma lines, which originated in either the thymus, spleen, or mesenteric lymph nodes, did not form rosettes. The percentage of the total cells which formed rosettes in the Gross lymphoma lines decreased with in vivo passages. If the tumor cells were exposed to trypsin treatment, then the tumor cells would form rosettes. Lymphoma lines which lacked rosette-forming cells did not show rosette formation after trypsin treatment. An immunofluorescence test showed that none of the lymphoma lines induced by Gross, Friend, Rauscher, or Moloney viruses carried the surface immunoglobulin characteristic of B-cells. These results suggest that Gross lymphomas may be derived from the thymic cortex and that Friend, Rauscher, or Moloney lymphomas may be derived from either mature thymus cells (non-rosette-forming cells) or from a subpopulation of the B-cell series which does not have the surface immunoglobulin G receptor.
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PMID:A thymus cell marker in murine leukemia virus-induced lymphomas of rats. 22 24

Histophysiology, ultrastructure, chemical analyses of transplants and implants of Dunn and Ridgway mouse osteosarcomas demonstrate that tumorigenesis is a manifestation of deranged morphogenesis in developing mesenchymal cell populations. The end product of development is defective, incompletely calcified, disorganized bone without any inclusions of bone marrow tissue. When Dunn osteosarcoma is freeze-dried and then implanted, the tumor is resorbed and replaced by deposits of normal cartilage, bone, and bone marrow. Freeze-dried Ridgway osteosarcoma is replaced only by a fibrous connective tissue scar. Disaggregated Dunn tumor osteoblasts synthesize a trypsin-labile collagenase-resistant cell surface localized bone morphogen. Tumor matrix stroma, prepared by sequential chemical extraction of soluble non-collagenous proteins also contains significant quantities of the same bone morphogen. Tumor tissue pulverized to particle size as small as 44 micrometer3 transmitted bone morphogen more rapidly than intact tumor tissue. The total tumor cell and stroma mediated bone morphogen produces three times more normal bone than normal cortical bone matrix. Our working hypothesis is that a normal bone morphogenetic polypeptide (BMP) is synthesized by Dunn osteosarcoma cells and retained by the tumor matrix stroma. Neither the mechanism of transmission nor the mesenchymal cell receptor sites of BMP are known.
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PMID:An osteosarcoma cell and matrix retained morphogen for normal bone formation. 27 29


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