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Query: UMLS:C0025202 (melanoma)
 69,561 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Conditioned media from cultures of human metastatic Hs294T melanoma cells contain a factor/factors that promote(s) fibroblast-mediated contraction of collagen lattices, and stimulate(s) fibroblast glycosaminoglycan (GAG) synthesis. Complete medium from melanoma cell cultures stimulated fibroblast hyaluronate synthesis 9.3-fold, and sulphated GAG synthesis 2.6-fold, as measured by 3H-glucosamine incorporation. 35SO4 incorporation into sulphated GAGS was essentially unaltered, the net result being a decrease in the degree of sulphation. Fibroblasts synthesized hyaluronate with an increased molecular weight when grown in the presence of the melanoma-cell culture medium, while the molecular weights of heparan and chondroitin sulphates remained essentially unaltered. Our results indicate that the tumour-cell-derived factor(s) stimulate(s) changes in fibroblast glycosaminoglycan synthesis, and that these changes may facilitate tumour cell invasion in vivo.
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PMID:Human melanoma cell-derived factor(s) stimulate fibroblast glycosaminoglycan synthesis. 139 27

Triflavin, an Arg-Gly-Asp (RGD) containing peptide purified from Trimeresurus flavoviridis snake venom, inhibits human platelet aggregation by blocking fibrinogen binding to fibrinogen receptors associated with glycoprotein IIb/IIIa complex. In this study, we show that triflavin (1-30 micrograms/mouse) inhibits B16-F10 melanoma cell-induced lung colonization in C57BL/6 mice in a dose-dependent manner. In vitro, triflavin dose-dependently inhibits adhesion of B16-F10 melanoma cells to extracellular matrices (ECMs; i.e., fibronectin, fibrinogen, vitronectin, and collagen type I). Triflavin is approximately 600-800 times more potent than GRGDS at inhibiting cell adhesion. In addition, triflavin dose-dependently inhibits B16-F10 cell-induced platelet aggregation. These results imply that the inhibitory effect of triflavin on the adhesion of tumor cells to ECMs (e.g., fibronectin, vitronectin and collagen type I) and/or tumor cell-induced platelet aggregation may be partially responsible for its antimetastatic activity in C57BL/6 mice.
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PMID:Triflavin, an Arg-Gly-Asp-containing antiplatelet peptide inhibits cell-substratum adhesion and melanoma cell-induced lung colonization. 139 25

To our knowledge, this is the first pathologic report of interscleral collagen bundle changes occurring as well-defined spindleform lesions randomly interspersed within the sclera. The lesions were observed in an otherwise healthy 75-year-old man whose eye was enucleated because of a uveal malignant melanoma. There are few reports in the literature of focal scleral changes of a predominantly acid mucopolysaccharide nature. The entity we observed in this case differs from these reports by its spindleform appearance, random distribution (not overlying the melanoma) and predominantly vicinal glycol nature. Histopathologic, histochemical, and ultrastructural studies revealed that the lesions were not the result of mucoid degeneration of the scleral collagen and not an abnormal collagen structure.
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PMID:Spindleform scleropathy: collagen changes of the sclera. A pathologic report. 140 57

This study determined the distribution pattern of tumor-associated macrophages (TAM) in murine and human neoplasms growing subcutaneously in nude mice. Seven different human neoplasms (cancers of the breast, kidney, colon, prostate, lung, and skin, and a melanoma) and five different murine neoplasms (carcinomas of the lung, colon, and kidney, melanoma, and fibrosarcoma) were injected into nude mice. The murine tumors also were injected into syngeneic mice. Tumor-associated macrophages in small and large tumors were studied immunohistochemically by the use of several antibodies, including the macrophage-specific F4/80. The pattern of TAM distribution differed between mouse and human tumors. Regardless of histologic classification, TAM were uniformly distributed throughout all the murine neoplasms growing in syngeneic or nude mice. In the human neoplasms, TAM were found on the periphery of the lesions and in association with fibrous septae. The distribution of TAM in murine and human tumors was associated with a pattern of vascularization as determined by antibodies to basement membrane collagen type IV. Because the pattern of TAM distribution in neoplasms influences their antitumor activity, the data question the validity of the nude mouse model for the study of macrophage infiltration into human neoplasms.
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PMID:Different patterns of macrophage infiltration into allogeneic-murine and xenogeneic-human neoplasms growing in nude mice. 144 54

When cells from the human malignant melanoma cell line, UCT-Mel 7, were injected into athymic nude mice, tumours developed that were intensely infiltrated with fibrous tissue. In an attempt to reproduce this desmoplastic response in vitro, we co-cultured fibroblasts with UCT-Mel-7 cells, and observed a 2-fold increase in the rate of fibroblast collagen synthesis. This was associated with an increase in the amount of collagen mRNA present in co-cultured fibroblasts. The stimulation was both dose- and time-dependent, with maximal stimulation at a melanoma cell:fibroblast ratio of 1:1. Analysis of the kinetics of proline incorporation into collagen showed that co-culture affected the maximal rate of proline incorporation; no effect was observed on the concentration of proline required for 50% maximal collagen synthesis. The induction of fibroblast collagen synthesis showed an absolute requirement for close proximity between the fibroblasts and the melanoma cells. No soluble fibrogenic factor released by melanoma was detected.
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PMID:The desmoplastic response: induction of collagen synthesis by melanoma cells in vitro. 153 27

Cellular adhesion receptors termed integrins play an important role in the interaction of cells with extracellular matrix (ECM) during wound healing, development and tumorigenesis. During such events, ECM may become modified or damaged which could alter the types of adhesive signals presented to cells. In this study, cell adhesion and affinity chromatography experiments were performed to determine whether different integrins interact with denatured versus native ECM molecules. Human melanoma cells were found to adhere to denatured versus native type I collagen through different integrins. The cells adhere to denatured collagen through the alpha v beta 3 integrin and this interaction is inhibited by an RGD containing peptide but not by a control peptide. In contrast, adhesion to native type I collagen appears to be mediated by several beta 1 integrins and thus, is not inhibited by either alpha v beta 3 antibodies or the RGD peptide. Affinity chromatography reveals a marked increase in the quantity of alpha v beta 3 isolated on denatured collagen versus native collagen-sepharose. These results suggest that RGD sites in type I collagen may be masked and that they become exposed upon denaturation of the molecule. Wounding of extracellular matrix may, thus, expose RGD sites in collagens that facilitate the interaction of cells with damaged extracellular matrix through RGD binding integrins.
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PMID:Affinity of integrins for damaged extracellular matrix: alpha v beta 3 binds to denatured collagen type I through RGD sites. 154 Jan 51

When human melanoma cells are injected into nude mice they usually give rise to tumours that grow progressively and do not elicit a prominent host response. We have recently developed a melanoma cell line, UCT-Mel 7, that did not show these characteristics. In the first place UCT-Mel 7 showed a consistently unusual, phasic growth pattern. After a short initial period of limited growth (phase 1), the tumour ceased growing and remained static for 2-3 months (phase 2). The tumour then regressed (phase 3) to enter a second period of quiescence (phase 4) which was eventually broken by the emergence of a rapidly growing lethal tumour (phase 5). Of particular interest was the fact that the rate at which the tumours grew correlated closely with their collagen content. During the prolonged, phase 2 plateau, the tumours were intensely desmoplastic; rapidly growing phase 5 tumours, that had escaped from dormancy, contained very little collagen and virtually no reticulin. This cell line helps to fill an important need for an experimental system for the study of desmoplasia, dormancy and progression.
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PMID:Unusual growth characteristics of human melanoma xenografts in the nude mouse: a model for desmoplasia, dormancy and progression. 156 56

Murine B16F10 melanoma cells, adherent to thin films of crosslinked, fluorescein-labeled collagen I, and covered by a thin layer of 0.7% agarose, exhibit a decrease in fluorescence emission in the substratum region immediately beneath adherent cells. The relative diminution in fluorescence intensity is dependent on excitation wavelength and is observed following excitation at 490 nm, but is not observed following excitation at 452 nm. The decrease in fluorescence emission is not due to quenching or concentration effects and is attributed to the decrease in extracellular pH in the substratum region. Fluorescence measurements of (I490/I452) within these substratum regions, correlate with an average extracellular pH of 6.4 +/- 0.2 which drops to pH less than 5 after 5 h. It is suggested that this region is sufficiently acidic to activate secreted or cell-surface acid proteinase enzymes and that the activity of these enzymes may be important in invasiveness by this cell-line.
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PMID:Substratum acidification by murine B16F10 melanoma cultures. 161 Sep 14

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

Tissue from nine human eyes (ages 52-78 yr) was used to investigate the fine structural distribution of collagens I-VI and laminin in the ciliary body using the immunogold antibody labeling technique. The anterior segments of the specimens were normal, and the eyes were removed in treatment of choroidal melanoma. The basement membranes of the ciliary epithelium contained collagens I, III, and IV. Laminin was in greater concentration in the outer part of the nonpigmented epithelial basement membrane, and the distribution suggested a washout effect. The zonular apparatus labeled intensely with laminin. In contrast, laminin was not present in the basement membrane of the myocytes in the ciliary body. These cells were sheathed in a basement membrane that contained types I, III, and IV collagen. Plaque-like structures of slightly different morphology (a, filamentous; b, granular; c, amorphous) were found in the tendinous insertions, and subtypes a and b were strongly labeled with laminin. The basement membranes of the vessels contained types I and IV collagen, but laminin labeling was inconclusive. The major finding was that the lamina densa in the basement membranes of various sites labeled for collagens I, III, and IV. Striated collagen fibrils in the stroma were labeled for types I and III. Collagen subtypes V and VI were not identified in significant quantity in any of the regions examined.
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PMID:Extracellular matrix in aged human ciliary body: an immunoelectron microscope study. 163 52


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