Phenotypic Properties of 3T3 Cells Transformed in vitro with Polyoma Virus and Passaged Once in Syngeneic Animals

Langer, Adit Ben-Baruch; Emmanuel, Noam; Even, Jos; Fridman, Wolf H.; Gohar, Ofra; Gonen, Bosmat; Katz, Ben‐Zion; Ran, Maya; Smorodinsky, Nechama I.; Witz, Isaac P.

doi:10.1016/s0171-2985(11)80646-7

Cited by 11 publications

(3 citation statements)

References 7 publications

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“…Nevertheless, it was suggested as a possible cause-and-effect relationship between the increase in tumorigenicity of non-hematopoietic PyV-transformed cells passaged in vivo and the acquisition of FcγR expression by these cells [51]. Subsequent studies using PyV-induced mouse tumors transfected with vector encoding mouse FcγRIIB1 confirmed these results.…”

Section: Ectopic Expression Of Fcγr On Non-hematopoietic Tumor Cellsmentioning

confidence: 91%

Fc gamma receptors and cancer

Cassard

Cohen-Solal

Camilleri-Broët

et al. 2006

Springer Semin Immun

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FcgammaRs are a family of heterogeneous molecules that play opposite roles in immune response and control the effector functions of IgG antibodies. In many cancers, IgG antibodies are produced that recognize cancer cells, form immune complexes and therefore, activate FcgammaR. The therapeutic efficacy of monoclonal IgG antibodies against hematopoietic and epithelial tumors also argue for an important role of IgG antibodies in anti-tumor defenses. Since the 1980s, a series of lines of evidence in experimental models and in humans strongly suggest that FcgammaR are involved in the therapeutic activity of monoclonal IgG antibodies by activating the cytotoxic activity of FcgammaR-positive cells such as NK cells, monocytes, macrophages and neutrophils and by increasing antigen presentation by dendritic cells. Since many cell types co-express activating and inhibitory FcgammaR, the FcgammaR-dependent effector functions of IgG anti-tumor antibodies are counterbalanced by the inhibitory FcgammaRIIB. In addition, some tumor cells express FcgammaR either constitutively, such as B cell lymphomas or ectopically, such as 40% of human metastatic melanoma. The tumor FcgammaR isoform is preferentially FcgammaRIIB, which is functional at least in human metastatic melanoma. This review summarizes these data and discusses how FcgammaRIIB expression may influence the anti-tumor immune reaction and how beneficial or deleterious this expression could be for the efficiency of therapeutics based on monoclonal anti-tumor antibodies.

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Section: Ectopic Expression Of Fcγr On Non-hematopoietic Tumor Cellsmentioning

confidence: 91%

Fc gamma receptors and cancer

Cassard

Cohen-Solal

Camilleri-Broët

et al. 2006

Springer Semin Immun

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“…The work in our laboratory focuses on tumor-CMF interactions trying to identify genes whose expression is altered (induced/upregulated or silenced/downregulated) by CMF-mediated signaling as low malignancy tumor cells progress to a high malignancy phenotype [Zusman et al, 1996a;Katz et al, 1994Katz et al, , 1994Katz et al, -1995Witz et al, 1996;Halachmi and Witz, 1989;Ben-Baruch et al, 1992;Ran et al, 1991]. The approach undertaken has been to screen for microenvironmentregulated gene-products differentially expressed by tumor cells expressing either a high or a low malignancy phenotype [Katz et al, 1994;Witz et al, 1996;Halachmi and Witz, 1989].…”

Section: Microenvironment-regulated Genes and The Involvement Of Murimentioning

confidence: 99%

“…The approach undertaken has been to screen for microenvironmentregulated gene-products differentially expressed by tumor cells expressing either a high or a low malignancy phenotype [Katz et al, 1994;Witz et al, 1996;Halachmi and Witz, 1989]. By using a combined in vitro/in vivo murine model system developed in our laboratory [Halachmi and Witz, 1989], we were the first to show that certain highly tumorigenic murine tumor cells express de novo receptors for the Fc portion of IgG (Fc␥RIIB1), whereas low tumorigenic tumor cells did not [Zusman et al, 1996a,b;Witz et al, 1996;Ben-Baruch et al, 1992;Ran et al, 1991]. Gene transfer experiments indicated that Fc␥RIIB1 was causally involved in enhancing the tumorigenicity phenotype of the tumor cells and that the cytoplasmic domain of the receptor was the key player in this enhancement [Zusman et al, 1996a,b].…”

Section: Microenvironment-regulated Genes and The Involvement Of Murimentioning

confidence: 99%

Differential expression of genes by tumor cells of a low or a high malignancy phenotype: The case of murine and human Ly-6 proteins

Witz¹

2000

J. Cell. Biochem.

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Progression of tumor cells toward a high malignancy phenotype and metastasis is a multi-event cascade involving inter alia alterations in the expression of various genes. The focus of our laboratory is on genes whose altered expression may lead, directly or indirectly, to an increased malignancy phenotype. The identification of such genes and the evaluation of the consequences of their altered expression is essential for attempts to halt tumor progression and prevent metastasis formation. Published work originating in our laboratory showed that members of the murine Ly-6 supergene family are involved in the progression of certain mouse tumors. The expression level of several members of this family was higher on highly malignant cells than on tumor cells expressing a lower malignancy phenotype. Sorting by flow cytometry of tumor cells to subpopulations expressing either high or low levels of Ly-6E.1 yielded correspondingly cells expressing a high or a low malignancy phenotype. The high malignancy, high Ly-6E.1-expressing cells also expressed high levels of the receptor for urokinase plasminogen activator (uPAR), whereas low malignancy, low Ly-6E.1-expressing cells also expressed low levels of uPAR. Transfection studies indicated that uPAR was causally involved in conferring a high malignancy phenotype upon tumor cells expressing high levels of Ly-6E.1. E48 is a human homologue of the murine ThB protein, a member of the Ly-6 supergene family (but distinct from the Ly-6E.1 protein mentioned above) and expressed on head and neck squamous carcinoma cells. Experiments currently in progress are aimed to find out whether E48 is involved in the progression of such cancer cells. Using the differential display technology, it was shown that ligation of E48 on tumor cells by the corresponding antibodies (serving as a surrogate for an as yet unidentified E48 ligand) upregulates an enzyme (FX) involved in the biosynthesis of GDP-L-fucose. Fucose is an essential component of certain selectin ligands.

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