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

Seven different tumor cell lines (human melanoma SK MEL 28; hamster melanoma HM29; murine melanomas B16F10 and amelanotic melanoma B16a; human colon carcinoma HCT8; murine colon carcinoma CT26; and murine Lewis lung carcinoma) were treated with thrombin at 0.5-1 unit/ml and examined for their ability to bind to adherent platelets; HM29 was studied for its ability to bind to fibronectin and von Willebrand factor; CT26, B16F1, B16F10, and B16a were studied for their ability to form pulmonary metastasis after i.v. injection of thrombin-treated tumor cells; CT26 was studied for its ability to grow s.c. Five of 7 thrombin-treated tumor cell lines increased their adhesion to adherent platelets 2-to 3-fold. HM29 increased its adherence to fibronectin and von Willebrand factor 2- to 3-fold. CT26, B16F1, B16F10, and B16a increased experimental pulmonary metastasis 10- to 156-fold. Thrombin-treated CT26 cells demonstrated 2-fold greater growth in vivo after s.c. injection. The mechanism of enhanced adhesion of thrombin-treated tumor cells to platelets required the platelet integrin GPIIb-GPIIIa since it could be inhibited by agents known to block adhesion of ligands to GPIIb-GPIIIa (monoclonal antibody 10E5, tetrapeptide RGDS, disintegrin Albolabrin); as well as a "GPIIb-GPIIIa-like" structure on tumor cells since it could be inhibited by treatment of thrombin-treated tumor cells with 10E5 and RGDS. The thrombin effect on tumor cells was optimum at 1 h of incubation with thrombin, did not require active thrombin on the tumor cell surface, and did not require protein synthesis (not inhibited by cycloheximide). Thus, thrombin-treated tumor cells markedly enhance pulmonary metastasis. It is suggested that this may be secondary to thrombin-induced enhanced adhesion as well as growth of tumor cells.
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PMID:Effect of thrombin treatment of tumor cells on adhesion of tumor cells to platelets in vitro and tumor metastasis in vivo. 159 84

The expression of fibronectin (FN) mRNA was studied in histological sections of surgical biopsies from human laryngeal and ectocervical invasive carcinomas of different grading stages by in situ hybridization and image analysis. This approach made it possible to identify the cell types synthesizing FN mRNA in the tissue sections and to compare semi-quantitatively the FN mRNA levels expressed in the different specimens. The carcinoma cells synthesized low levels of FN mRNA, comparable to those detected in control epithelia and connective-tissue fibroblasts. Well-differentiated (G1) laryngeal and ectocervical carcinomas induced the synthesis of FN mRNA--to levels 7 to 13 times higher than in control connective tissues--in the stromal fibroblasts surrounding the tumors. In carcinoma samples analysed, the amount of FN mRNA detected in the stroma decreased in relation to tumor grading (from G1 to G3) and the stromal destruction. FN mRNA was not detectable in the endothelial cells of venules while it was present in large amounts in those surrounding the capillaries present in the stroma. These data indicate that FN, usually observed around carcinomas, is produced by stromal fibroblasts, which are induced to express FN mRNA, presumably in response to diffusible factors produced by the tumor cells, and/or by endothelial cells of the infiltrating capillary vessels. The induction of FN mRNA, inversely proportional to the tumor grading, may be useful in evaluating the invasion potential of the tumor.
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PMID:Study of fibronectin and mRNA in human laryngeal and ectocervical carcinomas by in situ hybridization and image analysis. 161 76

The influence of various normal and malignant human cells on the level of collagen synthesis by human fibroblasts was tested in coculture. As revealed by immunoperoxidase staining, in cocultures with breast adenocarcinoma cells (MCF7, SA52, T47D) fibroblasts synthesized collagen while tumor cells did not. Fibroblasts displayed increased collagen production without change in the overall protein synthesis. Several other types of cells derived from normal human tissues (keratinocytes, normal mammary cells) or from fibrosarcoma, melanoma, cervical carcinoma, choriocarcinoma, or other breast adenocarcinoma (SW613, MDA, BT20) did not affect collagen synthesis of fibroblasts. Although to a lesser extent, this stimulating effect was reproduced by using the conditioned medium (CM) of the active cells but not with CM of the other cell types. A slight stimulation was also obtained when tumoral MCF7 cells and fibroblasts shared the same medium but were physically separated, suggesting that close contact was required for optimal stimulation of collagen synthesis. The collagen synthesis stimulating activity was not related to a modification of fibroblast proliferation rate. The production of collagen types I, III, and VI and fibronectin were increased in cocultures of fibroblasts with MCF7 cells. The increased synthesis of collagen types I and III and fibronectin was paralleled by similar changes in the steady-state level of their mRNAs. On the contrary, the increased production of collagen type VI appeared regulated at a post-transcriptional level.
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PMID:Modulation of collagen and fibronectin synthesis in fibroblasts by normal and malignant cells. 161 29

Fifty-four cases of undifferentiated neuroblastoma (stroma-poor neuroblastoma with undifferentiated histology) were studied immunohistochemically for the presence of S-100 protein-positive cells and extracellular matrix proteins (laminin, type IV collagen and fibronectin). In 30 of the 54 patients, the tumor had S-100 protein-positive cells in the peculiar stroma observed as thick fibrocellular septa (trabecular pattern) or delicate fibrovascular meshwork surrounding small nests of tumor cells (reticular pattern). The tumors were divided into four subgroups according to the stromal patterns: type A showing a predominant "reticular" pattern (14 cases); type B showing a predominant "trabecular" pattern (6 cases); type C showing both "reticular" and "trabecular" patterns (14 cases), and type D lacking either pattern but rich in vascular channels (20 cases). Clinicopathologically, the patients with S-100 protein-positive cells had a more favorable outcome (86.7% 2-year survival rate) than patients without these cells (12.0% 2-year survival rate). It is concluded that the existence of peculiar fibrovascular stroma containing S-100 protein-positive cells and extracellular matrix proteins is correlated with a favorable prognosis in undifferentiated neuroblastomas.
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PMID:S-100 positive undifferentiated neuroblastomas with a special reference to the tumor stroma related to favorable prognosis. 162 90

The effects of cell differentiation on cell adhesion to laminin were studied using the human colon tumor cell line, HT29. HT29 cells were induced to differentiate either by glucose deprivation (HT29glc- vs HT29glc+) or by 2 mM butyrate (HT29glc-+B+). Adhesion was assayed after incubating cell suspensions in microtiter wells previously coated with laminin or other substrates. HT29glc+ cells adhered preferentially to laminin over BSA, fibronectin, and ovalbumin. The adhesion to laminin was greater than 50% of maximum within 15 min. HT29glc- cell adhesion to laminin was consistently lower than that for HT29glc+ or HT29glc+B+ cells. alpha-Lactalbumin (ALA), a modifier of galactosyltransferase (GT) substrate specificity, caused a significant reduction (greater than 50%) in HT29glc+ cell adhesion to laminin when ALA was added to the adhesion incubation mixture. Addition of glucose+ALA to the suspension restored adhesion to laminin. Ovalbumin, a GT substrate, increased adhesion of HT29glc+ and HT29glc- cells to laminin, but lactose, a GT product, did not. The data show that undifferentiated HT29 cells adhere preferentially to laminin over fibronectin and collagen IV and that differentiation of HT29 cells reduces adhesion to laminin. In addition, the data imply that cell adhesion to laminin may be mediated by factors that also modify galactosyltransferase activity.
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PMID:Colonic cancer cell (HT29) adhesion to laminin is altered by differentiation: adhesion may involve galactosyltransferase. 163 32

We have investigated the expression of integrins in C6 glioma, a chemically-induced glial tumor cell line from rat brain. Immunochemical analysis revealed that C6 cells express sets of integrin receptor complexes which immunologically and electrophoretically are indistinguishable from those expressed by normal rat skin fibroblasts. These include the well-characterized fibronectin (alpha 5 beta 1) and the multi-specific laminin, collagen and fibronectin (alpha 3 beta 1) receptors. Assay of cell adhesion indicated that C6 cells adhere to fibronectin-coated surfaces or matrix deposited by the C6 glioma cells (CGM) in an RGD- and divalent cation-dependent fashion. However, anti-fibronectin antibodies, which are able to inhibit fibroblast adhesion to fibronectin, did not inhibit adhesion of the C6 cells to fibronectin or CGM. This may reflect differences in functional properties and/or distribution patterns of integrins in C6 cells and normal fibroblasts.
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PMID:Expression of multiple integrins and extracellular matrix components by C6 glioma cells. 164 Apr 99

Four mouse monoclonal antibodies (PTN63, PTN108, PTN124, PTN514) against the ecto-5'-nucleotidase purified from a human pancreatic adenocarcinoma cell line (PaTu II) have been raised and characterized. All four monoclonal antibodies recognize the protein moiety of the glycosylated ecto-5'-nucleotidase. In competition assays it was demonstrated that three of the antibodies (PTN63, PTN108, PTN514) recognize different epitopes within the protein moiety. Furthermore, PTN108, PTN124, and PTN514 reduced the 5'-nucleotidase AMPase activity in contrast to PTN63 having no inhibitory effect. The antibodies show no cross-reactivity with ecto-5'-nucleotidases from rat liver, bull seminal plasma, chicken gizzard and human peripheral blood cells. When assayed by indirect immunofluorescence the antibodies react with the plasma membrane of human pancreatic tumor cells with varying staining intensity. Immunocytochemistry on paraffin sections of normal human pancreas revealed a prominent staining of the pancreatic duct cells. No staining of the acinar and islet cells could be detected. Thus, 5'-nucleotidase is a marker enzyme for pancreatic duct cells and can be used to determine the origin of pancreatic tumor cells. PTN63 reduced the attachment to fibronectin substratum of a human pancreatic adenocarcinoma tumor cell line possessing a high amount of plasma membrane bound ecto-5'-nucleotidase, but had no effect on a cell line lacking the membrane bound AMPase. In contrast, PTN108 and PTN514, which inhibit the AMPase activity, exhibited no influence on the adhesion of human pancreatic tumor cells to fibronectin substratum.
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PMID:Monoclonal antibodies against 5'-nucleotidase from a human pancreatic tumor cell line: their characterization and inhibitory capacity on tumor cell adhesion to fibronectin substratum. 164 65

The expression and distribution of the extracellular matrix (ECM) in 37 gliomas and 19 meningiomas were studied immunohistochemically by antibodies to type 3, 4 and 6 collagen, fibronectin and laminin. In gliomas the expression of these antigens was more intense and thicker in the tumor vessel walls, and was positively correlated to the malignant degree of the gliomas. This suggests that the thickening of the vessel walls and the increase of their ECM components in gliomas may be one of the causes why gliomas are extremely rare to metastasize to the outside of the cranium. All the above-cited ECM were positive in the fibroblastic type of meningioma, being just located between the tumor cells; whereas in syncytial type they were negative. This indicates that the immunohistochemistry of ECM may be of advantage in differentiating meningioma type.
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PMID:[Immunohistochemical study of extracellular matrices in human glioma and meningioma]. 164 41

Tetranectin (TN) is a human, plasminogen kringle 4 binding plasma protein with ubiquitous cellular distribution and lectin-like characteristics. By means of the peroxidase-antiperoxidase staining technique a polyclonal and a monoclonal antibody were used to demonstrate TN within the intracellular as well as the extracellular compartment of invasive breast carcinoma. Whereas cell associated TN was universal showing only quantitative differences depending of the growth pattern of the tumor, 78 of 133 tumors displayed TN extracellularly as well. The occurrence of this stromal TN immunoreactivity was closely associated with desmoplasia, recognized morphologically by an increase in fibroblastic cells and immunohistochemically by an intense staining for the connective tissue glycoprotein fibronectin (FN). Benign breast tissue displayed a universal, intense cytoplasmic but no extracellular reaction for TN, with the exception of rare foci of granulation tissue and around dilated cysts. Functional studies have shown that human embryonal lung fibroblasts increase their release of TN to the growth medium upon stimulation. The presence of TN extracellularly within fibroblast-rich foci of desmoplasia (and granulation tissue) suggests that a similar increased release of the protein takes place in vivo during active states. Desmoplasia has been found to have a protective effect on tumor cell propagation and metastasis in a murine model. The molecular interactions, which are responsible for this effect, are undoubtedly complex. However, TN may, by its specific binding to kringle 4 of plasminogen and its high affinity for sulphated polysaccharides, add to the understanding of how plasminogen activation is modulated at the local extracellular level.
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PMID:Differences in tetranectin immunoreactivity between benign and malignant breast tissue. 165

Eight cell lines derived from human non-small cell lung carcinomas were used to compare their in vivo invasiveness, in vitro chemoinvasive abilities and type IV collagenase activity. For the evaluation of the in vivo invasive potential, the tumor cells were seeded into deepithelialized rat tracheas and transplanted subcutaneously into nude mice. The invasive behavior of the cells was observed at 4, 8 and 12 weeks and assessed histologically by determination of the levels of penetration of tumor cells into the different layers of the tracheal wall. Except for two cell lines that did not grow at all in vivo, there was a very good correspondence between the levels of in vivo tracheal wall penetration and the in vitro chemoinvasion assay using fibronectin as chemoattractant and Matrigel as barrier. This also correlated very well with the capacity of the cells to secrete type IV collagenase. The in vivo evaluation of invasion using tracheal transplants, although requiring several weeks of experimentation, proved to be very reliable, yielding homogeneous results with little internal variation, and is proposed as a dependable in vivo invasion assay that closely mimics the in vivo human conditions in which most carcinomas develop and eventually invade neighboring tissues.
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PMID:In vivo and in vitro invasiveness of human lung carcinoma cell lines. 165 72


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