Disease relevance of F10

• Using the B16/F10 murine melanoma (B16) as a model for CNS tumor, we show that vaccination with bone marrow-generated DCs, pulsed with either B16 cell extract or B16 total RNA, can induce specific cytotoxic T lymphocytes against B16 tumor cells [1].
• The mean and variance of the numbers of resultant B16 F1 and B16 F10 melanoma metastases strongly correlated with the power function (r2 greater than 0.8) [2].
• A strong correlation was found between the basal levels of membrane-bound protein kinase C and the ability of B16 melanoma cell sublines (F10, F1, and BL6) to metastasize to the lung after intravenous injection [3].
• DFMO administration did not inhibit the experimental metastases induced as a result of i.v. injection of B16 melanoma (line F10) tumor and Lewis lung carcinoma cells into the tail vein [4].
• 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 [5].

High impact information on F10

• The exponent b was 1.4 +/- 0.1 and 1.6 +/- 0.2 for the F1 and F10 melanomas, respectively, indicating a clustering of metastases within certain mice [2].
• By treating with tumor-promoting phorbol esters for 1 hr, the low-metastasizing F1 cells exhibited both translocation of protein kinase C from cytosol to plasma membrane and an increase in metastasis to a level comparable to the (untreated) highly metastatic subline F10 [3].
• F10 vesicle-modified F1 cells reverted to their original arrest behavior and metastatic capacity after removal of F10 vesicle components from the plasma membrane [6].
• The therapeutic efficacy of free ET-18-OCH3 and ELL-12 was investigated against i.p. P388 leukemia, Lewis lung cancer lung metastases, and B16/F10 melanoma (lung tumor nodules) in mice [7].
• B16 sublines selected for various organ colonization properties differentially expressed gp90, bound 125I-labeled transferrin, and responded differently to purified transferrin in proliferation assays in relation to their metastatic properties (B15b greater than O13 greater than F10 greater than F1) [8].

Chemical compound and disease context of F10

• Three levels of 1,3-bis(2-chloroethyl)-1-nitrosourea (10, 15, and 20 mg/kg) were coadministered to mice bearing the L1210 leukemia or the B16/F10 melanoma with each of the deoxyribonucleosides (2 g/kg) [9].
• It was found that thymidine did not increase the cytotoxicity of BCNU for B16/F10 melanoma cells in vitro [10].
• The aim of this work was the in vitro study of either 8-Cl-cAMP or TR effects on B16/F10 and B16/C3 mouse melanoma cell growth and cell death [11].
• An alpha-mannosidase inhibitor, mannostatin A, from Streptoverticillium verticillus var. quintum inhibited chemotactic invasion of mouse B16/F10 melanoma cells in the Boyden chamber assay [12].
• Levan (polyfructose), an immunomodulatory polysaccharide, has been found to exert opposite effects on the growth of the F10 variant of B16 melanoma [13].

Biological context of F10

• The cDNA encoding murine coagulation factor X (fX) was isolated and reconstructed from a lambdaZap cDNA library generated from murine liver mRNA [14].
• All protein domains of human and rat fX are strictly conserved in mouse fX [14].
• By contrast, Cf10, Col4a1, Col4a2, and D8H13S35 mapped near the centromere of mouse Chr 8, defining a new conserved linkage [15].
• 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 [5].
• The highly metastatic F10 line showed the same degree of marker chromosomal instability as the poorly metastatic F1 line (0.01 variants/cell/generation) [5].

Anatomical context of F10

• Analysis of the metastatic properties of clones isolated from mouse B16 melanoma cell lines (B16-F1 and F10) shows extensive cellular heterogeneity and the presence of subpopulations that have widely differing metastatic abilities [16].
• 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 [17].
• The Ig kappa L chain synthesized by the mouse hybridoma line F10 forms large fibrils in the lumen of the endoplasmic reticulum [18].
• The efficiency of receptor-mediated entry of pseudotyped virus carrying the surface protein (SU) of clone A8, a neuropathogenic variant of Friend murine leukemia virus (FrMLV), to rat glial cell line F10 was 1 order of magnitude greater than that of pseudotyped virus carrying SU of nonneuropathogenic FrMLV clone 57 [19].
• Preincubation with 50 micrograms/ml Ac-LDL in F10 medium had no effect on LDL oxidation by either LDLR-/- or C57B6 macrophages [20].

Associations of F10 with chemical compounds

• Although the five cysteine residues of the aberrant kappa-chain are in the normal positions, they display an unusual gel pattern when the intrachain disulfide bonds are opened with 2-ME; that is, the intrachain disulfide bonding pattern of F10 kappa-chain seems to be unusual [18].
• 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 [21].
• Upon loading with the antimalarial drug chloroquine, the MAb F10-bearing liposomes effectively controlled not only the chloroquine-susceptible but also the chloroquine-resistant P. berghei infections in mice [22].
• Part of the core aldehydes accumulated within the cells.Our study demonstrates that i) J774 macrophages are able to promote/accelerate core aldehyde formation in HAM's F10 medium, and ii) that core aldehyde formation rates can be increased by stimulation of the cells with PMA, and, although to a lesser extent, with LPS [23].
• The suitability of liposomes as drug carriers in the treatment of drug-resistant rodent malaria was examined after covalently attaching F(ab')2 fragments of a mouse monoclonal antibody (MAb), MAb F10, raised against the host cell membranes isolated from the Plasmodium berghei-infected mouse erythrocytes, to the liposome surface [22].

Regulatory relationships of F10

• The p53 in F10 cells appears to be as functional as that in NIH3T3 cells because irradiation-induced expression of p53-target genes was comparable in both cells [24].
• Proto-oncogene c-fos was found to be highly expressed in F10 lines by an in situ hybridization technique and also in F10 lung metastatic nests by immunofluorescent staining with anti-c-fos antibody [25].
• Inhibition of recombinant interferon-gamma-induced Ia antigen expression by shed B16 F10 melanoma cell membrane vesicles [26].
• We have examined this by comparing its cytotoxic effects in B16/F10 and B16/F10-differential deficient (-DD) mouse melanoma cells that express high and low levels of tyrosinase activity respectively [27].

Other interactions of F10

• In this study, the authors examined the efficacy of treating central nervous system (CNS) tumors by transfecting poorly immunogenic B16/F10 melanoma cells with interleukin (IL)-2, IL-4, or granulocytemacrophage-colony stimulating factor (GM-CSF) gene, and using these cells to deliver the cytokine locally at the site of the CNS tumor [28].
• The possible relationship between GSH and the ability of Bcl-2 to prevent cell death was studied in B16M cells with high (F10) and low (F1) metastatic potential [29].
• It induced fibronectin expression but not E-cadherin expression in B 16/F10 cells [30].
• BL6 cells differ from F10 cells by an alteration of the gene encoding the B56gamma regulatory subunit of protein phosphatase 2A (PP2A), which results in mRNA encoding a truncated variant of the subunit (deltagamma1) [24].
• Production of GM3 in F10 melanomas treated with IL-2 for 4 days increased, and, if the treatment was continued for 7 days, minor components of gangliosides, such as GM2, GM1, and GD1a, appeared only in F1 melanomas, while the increase of production of GM3 disappeared in both melanomas [25].

Analytical, diagnostic and therapeutic context of F10

• Both F10 and BL6 sublines of B16 mouse melanoma cells are metastatic after intravenous injection, but only BL6 cells are metastatic after subcutaneous injection [31].
• F10Lr cells did not protect F10 cells from lymphocyte-mediated lysis in cocultivation experiments [17].
• Previously, we described common or shared tumor-specific transplantation antigens on the murine malignant melanomas B16 F10, K1735, JB/RH, and JB/MS [32].
• We utilized two independent approaches: (1) in silico mapping based on sequence similarity between human multiple sclerosis susceptibility regions and rodent EAE quantitative trait loci and (2) linkage mapping in an F10 (DA x PVG.AV1) rat advanced intercrossed line [33].
• The F10 tumor grew rapidly after subcutaneous injection in all strains of mice [34].

References