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

The ability of melanocyte stimulating hormone (MSH), adrenocorticotropic hormone (ACTH), and prostaglandin E1 (PGE1) to stimulate the accumulation of cyclic AMP was examined in intact mouse melanoma cells of varying metastatic potential. F1 cells (low metastatic potential) had significantly greater cyclic AMP levels in response to all three hormones than F5 (intermediate metastatic potential) and F10 (high metastatic potential) cells. The ranking of the response was as follows: MSH, F1 greater than F5 greater than F10, ACTH, F1 greater than F5 greater F10, PGE, F1 greater than F10 greater F5. In contrast to the above, the degree of hormonal stimulation of adenylate cyclase in broken cell preparations was virtually identical in all three melanoma cell lines. Control enzyme activity was depressed in both F5 and F10 relative to F1. The conflicting results between studies of intact vs. broken cell preparations could not be explained by increased cyclic AMP phosphodiesterase activity in F5 and F10 cells. We conclude that as the melanoma cells increase in metastatic potential, there is a significant loss in the ability of their cyclic AMP system to respond appropriately to hormonal stimuli.
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PMID:Hormonal activation of adenylate cyclase in mouse melanoma metastatic variants. 20 54

The control of melanin production, tyrosinase activity, and cell replication by melanocyte-stimulating hormone (MSH) and cyclic AMP (cAMP) was examined in differentially metastasizing B16 mouse melanoma variants. In B16-F1 cells (low metastatic potential), MSH or cAMP greatly elevated tyrosinase activity and melanin content while inhibiting cell replication. The same parameters in B16-F5 cells (intermediate metastatic potential) were altered to a much lesser degree, whereas B16-F10 cells (high metastatic potential) were not significantly affected by MSH or cAMP. Therefore, a correlation exists between loss of hormonal regulation and increased metastatic potential.
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PMID:Control of melanogenesis in mouse melanoma cells of varying metastatic potential. 21 Feb 94

B16 malignant melanoma cell lines transform arachidonic acid and its transient metabolite, prostaglandin endoperoxide H2, into prostaglandin D2. The highly metastatic line, B16 F10, forms less prostaglandin D2 compared to the moderately metastatic parent line, B16 F1. Since platelet aggregation may be one factor involved in B16 metastasis and since prostaglandin D2 inhibits platelet aggregation, this prostaglandin could affect the outcome of platelet-tumour interactions, which may contribute ultimately to metastasis. Arachidonic acid metabolism may be another one of the intrinsic biochemical properties of tumor cells that affects their metastasis. Our results suggest that quantitative release of unusual prostaglandins must be considered in this context.
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PMID:Prostaglandin D2 formation by malignant melanoma cells correlates inversely with cellular metastatic potential. 28 15

Several in vitro properties of two variant cell lines of the B16 melanoma (B16-F10 and B16-BL6) with markedly different spontaneous metastatic behavior were examined. The two cell lines were compared with regard to their in vitro growth rate, ability to migrate, ability to adhere to a variety of substrata, detachment rates, production of plasminogen activator, and cell surface proteins as determined by lactoperoxidase-catalyzed iodination. Growth rates in vitro, attachment rates, and qualitative patterns of cell surface proteins were almost identical. B16-F10 cells (the less spontaneously metastatic line) produced greater amounts of plasminogen activator, were more motile in vitro, and detached more readily from plastic than the more invasive B16-BL6 cells. The study of tumor cell variants, selected for different biologic behavior, is a valuable approach to the elucidation of those mechanisms responsible for their malignant activity.
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PMID:The selection and characterization of an invasive variant of the B16 melanoma. 50 92

The organ distribution, arrest and survival of [125I]5-iodo-2'-deoxyuridine-labeled B16 melanoma cells with low (B16-F1) or high (B16-F10) metastatic potential were studied in a variety of normal and immunosuppressed syngeneic C57BL/6 mice, allogeneic A mice, and athymic nude NIH Swiss mice and their immunocompetent littermates. In addition, the in vitro aggregation properties of these tumor cells with various host organ cells in suspension were examined. Tumor cell arrest and survival following i.v. injection occurred at significantly higher rates in normal mice than in immune-depressed animals irrespective of strain, and, two weeks later, significantly more tumor colonies were found in the normal animals. In syngeneic or allogeneic animals, B16-F10 cells were arrested, survived and formed significantly more gross pulmonary tumors than B16-F1 cells. B16-F10 cells also aggregated in vitro with purified organ cells in suspension obtained from either syngeneic or allogeneic mice at a greater rate than B16-F1 cells. These results indicate that although host properties can affect the arrest and survival of circulating tumor emboli, they do not diminish or abolish the biological differences between the high and low metastatic variant B16 lines.
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PMID:Tumor cell and host properties affecting the implantation and survival of blood-borne metastatic variants of B16 melanoma. 63 82

B16 melanoma variant lines, which resisted lysis by syngeneic lymphocytes, were selected in vitro by repeated exposure of the tumor cells to purified cytotoxic lymphocytes. The resistance of the tumor cells to lysis mediated by syngeneic lymphocytes was not accompanied by a loss or masking of major histocompatibility antigens. Neither the lymphocyte-susceptible B16 (F10) nor the lymphocyte-resistant B16 (F10Lr) cells grew in allogeneic recipients, and both were destroyed in vitro by allogeneic lymphocytes. The resistance to lysis by syngeneic lymphocytes was not accompanied by loss or masking of receptors for macrophage recognition and destruction. F10Lr cells did not protect F10 cells from lymphocyte-mediated lysis in cocultivation experiments. Immunization of syngeneic mice in vivo with B16-F10 cells successfully protected mice against challenge with B16-F10 cells. However, mice immunized with B16-F10Lr cells were not protected against challenge with B16-F10 cells. B16-F10Lr cells were not immunogenic when tested under this condition. Light, scanning, and transmission electron microscopic studies of tumor cell-lymphocyte interaction suggested that the resistance of B16-F10Lr cells to destruction by syngeneic lymphocytes in vitro was due to the masking or absence of tumor-specific antigen(s) present on the lymphocyte-susceptible F10 cells.
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PMID:Mechanism of tumor cell resistance to lysis by syngeneic lymphocytes. 90 34

The hypothesis that abnormalities in intercellular adhesion are a property of metastatic tumors was examined in vitro with B16 melanoma variants that were selected in vivo for increased metastatic behavior. The adhesive characteristics of low (B16-F1), intermediate (B16-F5), and high (B16-F10) metastatic lines were determined by quantitative adhesion assays that measured the rate and degree of attachment of single cells to confluent monolayers of melanoma, BALB/3T3, or virus-transformed 3T3 cells. Intercellular adhesions were monitored by loss of single cells from suspension and adherence of intraperitoneally grown 125I-5-iodo-2'-deoxyuridine-labeled cells to the monolayers, and were affected by time, temperature, and serum concentration. Although there was little difference in adhesive properties between the untransformed and transformed 3T3 cell lines, the more metastatic melanoma variants exhibited higher relative rates and extents of homotypic and heterotypic monolayer attachment compared with lower metastatic lines (B16-F10 greater than B16-F5 greater than B16-F1). The correlation between in vivo and in vitro tumor cell adhesive properties and metastasis was discussed.
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PMID:Determination of adhesive properties of variant metastatic melanoma cells to BALB/3T3 cells and their virus-transformed derivatives by a monolayer attachment assay. 94 56

This report describes the selection and behavior of tumor cells resistant to cytolysis by syngeneic lymphocytes. Two B16 melanoma lines, F1 (low metastasis) and F10 (high metastasis), were cultured with lymphocytes from C57BL/6 mice immunized against B16. The selection procedure involved repeated exposure of the tumor cells to lymphocytes in vitro. After each interaction, the viable tumor cells were trpsinized, replated, and designated lines F1Lr-1 and F10Lr-1. The procedure was repeated five times, yielding lines F1Lr-6 and F10Lr-6, which resisted cytolysis by syngeneic lymphocytes. Mice were given s.c. or i.v. injections of cells from lines F1, F1Lr-6, F10, or F10Lr-6. Tumor growth patterns were the same for all four lines when the cells were injected s.c., however, the incidence of pulmonary metastases differed significantly after i.v. injection. Line F10 cells yielded more pulmonary metastases than an equal number of line F1 cells (p less than 0.01). F1Lr-6 cells yielded significantly fewer metastases than an equal number of lines F1 cells (p less than 0.01). A similar difference between F10Lr-6 and F10 cells was observed. The incidence of artificial metastases after i.v. injection of F10Lr-6 cells was similar to that for F1 cells. The quantitative organ distribution, arrest, and survival of i.v.-injected tumor cells were studied by using [125]-5-iodo-2'-deoxyuridinelabeled cells. There was a significantly greater number of cells from line F10, arrested and able to survive for 14 days in lungs, than cells from line F1. In contrast, cells from either line F1Lr-6 or F10Lr-6 had a lower incidence of arrest and survival than their lymphocyte-sensitive counterparts.
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PMID:Characterization in vivo and in vitro of tumor cells selected for resistance to syngeneic lymphocyte-mediated cytotoxicity. 97 82

The fate of bloodborne malignant melanoma cells selected for their enhanced ability to form lung colonies was examined to determine how specific tumor cells are arrested in certain organs during the experimental metastasis process. After murine B16 melanoma variant tumor cell lines with low (B16-F1) or high (B16-F10) survival and growth potential in vivo were admisistered by iv or intracardiac injections into syngeneic C57BL/6 mice, the quantitative distribution of [125l]5-iodo-2'-deoxyuridine (125IUDR)-labeled cells in the organs and subsequent formation of metastatic lung colonies were assessed. The initial distribution of viable tumor cells was dependent on the route of injection: Soon after iv injection, more 125IUDR-labeled B16 cells were localized in the lungs and fewer in the blood and other organs than after intracardiac injection. However, 1 day after the injection, the number of viable tumor cells in the lungs was independent of the route of injection, and at 14 days the quantity of resulting lung tumor colonies was similar. Variant line B16-F10 cells were better arrested and formed more tumors per input cell than B16-F1, regardless of the injection route. B16-F10 yielded only lung tumor colonies, whereas B16-F1 formed some extrapulmonary tumor growths. The results suggested that the ultimate fate of circulating tumor cells was not determined solely by nonspecific arrest in the capillary bed of the first organ encountered, and that in vivo selection could produce tumor line variants with organs preferences.
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PMID:Organ selectivity for implantation survival and growth of B16 melanoma variant tumor lines. 100 51

Gelatinases/type IV collagenases have been shown to be involved in tumor invasion and metastasis. In this study, we examined the effect of culture medium pH on the secretion of the gelatinases from mouse B16 melanoma cell lines and human tumor cell lines using zymography analysis. The highly metastatic clone F10 of B16 melanoma did not secrete any gelatinase in neutral culture media (pH 7.1-7.3), whereas it secreted a high level of a 103-kDa gelatinase in an initial pH range of 5.4-6.1. The addition of an excess amount of glucose into a neutral culture medium also induced the gelatinase secretion from the cells by decreasing the medium pH during incubation. The extent of the acid-induced gelatinase secretion by the B16 melanoma cell lines was in the order of BL6 greater than F10 greater than F1 much greater than the parent B16 line, in good agreement with the order of their metastatic potentials. Two human cell lines (A549 and HT1080) secreted a higher level of a 90-kDa gelatinase at pH 6.8 compared with pH 7.3. The acid-induced gelatinase secretion from B16-F10 cells was blocked by cycloheximide, indicating that the enzyme induction was due to de novo synthesis. When in vitro tumor cell invasion was assayed in Boyden chambers, B16-F10 cells incubated in an acidic medium exerted a more active migration through type IV collagen gel than those in a neutral medium. These results suggest that the acidic environment formed around tumor tissues may be an important factor in invasion and metastasis of some types of tumors.
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PMID:Induction of 103-kDa gelatinase/type IV collagenase by acidic culture conditions in mouse metastatic melanoma cell lines. 131 66


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