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Query: UMLS:C0027627 (metastases)
 103,950 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Three lines of B16 melanoma cells (B16-F1, B16-F10 and B16-BL6) were examined for motility in the micropore filter assay and for synthesis in culture of the basal lamina glycoprotein laminin. All three lines synthesized laminin as judged by the incorporation of [35S]methionine into immunoreactive laminin and secreted (or shed) laminin into the culture medium as indicated by biosynthetic labeling studies and enzyme-linked immunosorbent assays. Immunoreactive laminin was also seen on the surface of the cells as indicated by immunofluorescence staining and by complement-mediated killing. Analysis of [35S]methionine-labeled laminin immunoprecipitates by sodium dodecylsulfate-polyacrylamide gel electrophoresis (SDS-PAGE) both with and without reduction of intersubunit disulfide bonds revealed that all three cell lines produced a similar array of laminin forms, and that the Mr = 950 kD laminin molecule (but not the uncombined subunits) was secreted into the culture medium. Laminin biosynthesis appeared to be limited by the availability of the Mr = 400 kD A subunit as shown by the intracellular accumulation of excess B subunit in the form of uncombined B subunit (Mr = 200 kD) and as a disulfide-linked B dimer (Mr = 400 kD). The motility of all three cell lines was stimulated four- to five-fold by the addition of either exogenous laminin from the EHS sarcoma or culture medium from the B16 cells containing the secreted laminin. The stimulated motility was inhibited by antilaminin serum. These observations suggest that the laminin synthesized by the B16 melanoma cells themselves may facilitate their motility.
Clin Exp Metastasis
PMID:Laminin production by murine melanoma cells: possible involvement in cell motility. 353 34

To test the hypothesis that genetic instability correlates with malignant potential, we compared the rate of generation of marker chromosomal abnormalities in clones of B16 F1 and B16 F10 murine melanoma. These rates were estimated through an adaptation of fluctuation analysis of Luria and Delbruck (S. E. Luria and M. Delbruck, Genetics, 28: 491-511, 1943). The highly metastatic F10 line showed the same degree of marker chromosomal instability as the poorly metastatic F1 line (0.01 variants/cell/generation). When subclones of a karyotypically unstable F10 clone were compared with those of a more stable F10 clone, both groups caused the same number of pulmonary metastases, thus demonstrating a further lack of correlation of malignant potential with the level of genomic instability. Since measurements based on marker chromosomes may not truly reflect all of the changes detectable by G-banding, we also analyzed the G-banded karyotypes of the cell lines and their clones (chromatid or chromosomal breaks were not considered in this study). The F10 clones possessed an additional copy of chromosome 1 and also a significantly higher prevalence of the translocation t(9,12) when compared with the F1 clones. Rather than general rates of major karyotypic change determining tumor progression, we suggest the importance of other genetic or epigenetic mechanisms, particularly subtle nonrandom genetic or molecular changes, as the determining factors for malignant potential.
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PMID:Rate of generation of major karyotypic abnormalities in relationship to the metastatic potential of B16 murine melanoma. 359 40

Two widely used B16 melanoma cell lines of low and high lung colonizing potential (B16-F1 and B16-F10) were compared in their ability to induce platelet aggregation. The results of these experiments showed a reproducible difference in platelet aggregating activity of these two cell lines which directly correlated with their lung colonizing potentials. However, when clones were derived from these heterogeneous cell lines and tested for experimental metastatic potential, platelet aggregating ability and Met-72 expression, no correlation could be attached to the platelet aggregating activity of the clones. Results of these experiments provide direct evidence that platelet aggregation is not an accurate index of experimental metastatic potential of tumor cell clones, nor is it an essential trait of all metastatic cells. The ability of tumor cells to induce platelet aggregation is examined and discussed in the context of cellular heterogeneity.
Clin Exp Metastasis
PMID:The lack of correlation between experimental metastatic potential and platelet aggregating activity of B16 melanoma clones viewed in relation to tumor cell heterogeneity. 359 70

B700 is a melanoma-specific glycoprotein antigen, with a m.w. of 65,000 and an isoelectric point of 4.5; this antigen has been shown to bear significant sequence homology to a normally occurring protein, serum albumin. The production of B700 is apparently restricted to all the murine melanomas tested, since a variety of other transformed and untransformed cell lines do not contain detectable levels of this antigen. The capacity of B700 to function as a tumor-specific transplantation antigen (TSTA) is demonstrated in this study. This activity has been titrated, and it is shown that mice immunized with B700 are able to significantly inhibit the growth of B16 F10 melanomas after subcutaneous challenge; immunized mice can also inhibit the establishment and growth of experimental metastases in the lungs after i.v. challenge with B16 melanoma cells. The TSTA was found to cross-protect also against challenge with two other murine melanoma lines, JB/RH and K1735, but was specific in that the growth of two nonmelanoma lines (RBL-5 leukemia and MCA-105 sarcoma) was not affected. B700 is also shown in this study to be unrelated to other known murine tumor antigens, or to murine leukemia virus antigens. It is further shown that mice immunized with B700 produced antibodies specific to B700 that were not cross-reactive with albumins from various mammalian sources.
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PMID:Murine melanoma-specific tumor rejection activity elicited by a purified, melanoma-associated antigen. 371 69

The effect of murine alpha/beta interferon (IFN) on experimental metastasis was investigated using B16-F10 melanoma cells. Since the outcome of metastasis of blood-borne tumor cells is mainly determined within the first 24 h after i.v. inoculation of tumor cells, i.p. injection of IFN was focused on this critical early phase. The inhibition of pulmonary metastases by IFN was found to be maximal when given 3 h prior to tumor cell inoculation, while mice with 24-h and 12-h pretreatment and simultaneous IFN treatment also showed a reduction in metastases, but to a lesser extent. However, mice receiving IFN 2 h after tumor cell inoculation did not show any reduction. Tumor cells cultured for 24 h in IFN-containing medium showed no reduction in metastases. Administration of anti-asialo GMl prior to IFN treatment was found to eliminate the inhibitory effect of IFN 3 h pretreatment. However, natural killer (NK) cell activity in vitro measured at 3 h, 13 h and 24 h after IFN administration was enhanced to the same extent, not paralleling the inhibitory effect on pulmonary metastases. These data indicate that prepared host status against blood-borne tumor cells is established by IFN pretreatment, being maximal when injected several hours prior to tumor cell inoculation, and that this effect is substantially dependent on NK cell activity, though the implication of other factors is not excluded.
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PMID:Time-dependent suppression of melanoma metastases and natural killer cell activation by interferon. 374 Sep 43

Expression of a tumor-associated antigen, recognized by a monoclonal antibody (MoAb 135-13C) to lung carcinoma cells, has been studied in cloned Lewis lung carcinoma (3LL) and in B16 melanoma (F1 and F10) tumor lines endowed with different metastatic potentials. MoAb 135-13C recognizes a protein complex (tumor-specific Mr 180,000 protein) that appears on the cell surface of several murine lung carcinomas but is not detected on normal cells in culture. Standard metastatic variants of B16 melanoma (F1 and F10) and two variant sublines of 3LL (M1087 and BM21548) together with the parental line of 3LL have been used for these experiments. The two cloned variant lines derived from 3LL have been shown to retain high (M1087) and low (BM21548) metastatic phenotypes during in vivo passaging. We found that all three cell lines of 3LL bind monoclonal antibody specifically, but one cell variant with higher metastatic potential shows a higher capacity to bind MoAb 135-13C than did the other variant. Similarly we found that B16 F10 cells bind higher amounts of MoAb 135-13C than did B16 F1 cells. In addition the analysis of the amounts of MoAb 135-13C bound to the cell surface of several other in vitro and in vivo tumor lines with different metastatic capacity demonstrates that all tumor lines which express high ability to colonize to the lung also express, on the cell surface, higher amounts of tumor-specific Mr 180,000 protein. The sodium dodecyl sulfate-polyacrylamide gel electrophoresis autoradiograms of immunoprecipitates from cell lysates of 3LL and B16 tumor lines demonstrate that MoAb 135-13C specifically precipitated three proteins banding at molecular weights of 204,000, 134,000, and 116,000. We conclude that MoAb 135-13C recognizes a surface protein complex which is present in higher amounts in 3LL and B16 cells which possess higher capacity to metastasize to the lung.
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PMID:Expression of tumor antigen correlated with metastatic potential of Lewis lung carcinoma and B16 melanoma clones in mice. 375 21

We studied the patterns of spontaneous regional lymph node metastases of three variants (F1, F10, and BL6) of the B16 melanoma in C57BL/6 mice and related the incidence to primary tumor size and pulmonary metastases. The incidence of regional lymph node and pulmonary metastases correlated with increasing primary tumor size (p less than or equal to 0.0001). The incidence of pulmonary metastases in mice whose regional lymph nodes did not contain tumor also correlated with increasing primary tumor size (p less than or equal to 0.0001). This propensity for direct hematogenous spread was more apparent in BL6 tumors than in F1 and F10 tumors (p less than or equal to 0.0001). BL6 tumors also metastasized to regional nodes at smaller primary tumor sizes (p less than or equal to 0.04). Heterogeneous variants that metastasize earlier to regional lymphatic and hematogenous sites dictates the natural history of the primary tumor. Whether prophylactic lymphadenectomy for melanomas is therapeutic may depend on dissemination-related phenotypic characteristics.
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PMID:Spontaneous regional lymph node metastases of three variants of the B16 melanoma: relationship to primary tumor size and pulmonary metastases. 376 73

An attempt has been made to determine whether changes in the host environment due to ageing or sex differences can influence the metastatic mode of malignant tumours. B16-F10 melanoma cells with a high pulmonary metastasizing potential were injected into the outer ear of C57BL/6 mice; the growth of primary tumour and metastasis of the cervical node were assessed every two days, and the number of lung compared; and in the second young male and female mice were used. The rate of growth of primary tumours was found to be comparable between young and ole mice. Metastasis in the cervical lymph node occurred earlier in old than in young mice. Lung metastases occurred earlier in old than in young mice, but their growth was slower in old than in young mice. Metastasis in the cervical node occurred earlier in males than in females. More lung metastases were found in male than in female mice.
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PMID:Change in the metastatic mode of B16 malignant melanoma in C57BL/6 mice with ageing and sex. 383 Aug 85

Human recombinant interferon alpha A/D (alpha A/D) was examined for its antitumor activity in several mouse tumor models using metastatic tumors, such as B16 melanoma F1, BL6 and F10, UV2237m fibrosarcoma, and K1735m melanoma. Therapeutic treatment with alpha A/D reduced the incidence of pulmonary metastasis and inhibited the tumor growth resulting in an increase of the mean survival time. Since alpha A/D also showed a prophylactic activity against the metastasis, its antitumor activity was suggested to be due to augmentation of the host defense systems. This was confirmed by the fact that alpha A/D inhibited the in vivo growth and incidence of pulmonary metastasis of B16 F1 sublines regardless of their sensitivity to the direct antiproliferative activity of the IFN in vitro.
Clin Exp Metastasis
PMID:Antitumor and antimetastatic activities of human recombinant interferon alpha A/D. 384 Oct 37

Murine B16 melanoma sublines have been sequentially selected in vivo for low (B16-F1) or high (B16-F10) lung, high ovary (B16-O10) or high brain (B16-B15b) colonization, and in vitro for enhanced tissue invasion (B16-BL6). These B16 sublines were tested in vitro in a syngeneic organ adhesion/invasion assay to determine differences in tumor and/or host tissue properties that might account for preferential metastasis to certain sites. Tissues used were murine C57BL/6 lung, ovary and heart. In 8 independent experiments high lung-colonizing B16-F10 cells bound to and infiltrated into lung tissue better than ovary or heart tissue, while high ovary-colonizing B16-O10 cells attached to and invaded into ovary tissue at higher rates than lung or heart tissue. Only highly tissue-invasive B16-BL6 cells were able to invade heart tissue within 18 h in the experiments. The results suggest that organ metastatic colonization preferences by malignant cells may be determined, in part, by differences in the abilities of metastatic tumor cells to attach to and invade target tissue.
Invasion Metastasis 1985
PMID:Preferential organ attachment and invasion in vitro by B16 melanoma cells selected for differing metastatic colonization and invasive properties. 399 11


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