Vitiligo-related pigment cell differentiation antigens are expressed on malignant melanoma cells following phenotypic reversion induced by contact inhibitory factor

Lipkin, George; Naughton, Gail K.; Rosenberg, Martin; Bystryn, Jean‐Claude

doi:10.1111/j.1432-0436.1985.tb00510.x

Cited by 10 publications

(3 citation statements)

References 10 publications

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“…The earliest evidence that the melanoma malignant phenotype is reversible epigenetically was the finding that a ''contact-inhibitory factor'' present in culture medium of a revertant line of melanoma cells could restore in vitro growth control (contact-, serum-, and anchorage-dependent growth) to melanoma cells (Lipkin and Knecht, 1974;Lipkin et al, 1986), cause early G 1 growth arrest (Lipkin and Knecht, 1976), reorganize the actin cytoskeleton (Higgins et al, 1988), induce synthesis of pigment differentiation antigens (Lipkin et al, 1985), and upregulate class I major histocompatibility antigens (Lipkin and Meruelo, 1992), increasing lysis by cytotoxic (CD8) T lymphocytes (unpublished data). It also suppressed both angiogenesis (Lipkin et al, 2001) and metastasis (unpublished data), and led to permanent regression of tumors treated in situ (Lipkin et al, 1989).…”

Section: Melanoma Cell Plasticitymentioning

confidence: 99%

Plasticity of the Cancer Cell: Implications for Epigenetic Control of Melanoma and Other Malignancies

Lipkin

2008

Journal of Investigative Dermatology

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Current treatments of many advanced malignancies, including melanoma, have failed to significantly reduce mortality rates, necessitating newer approaches. There is now abundant evidence that cancer cells, given the appropriate environmental and molecular context, are capable of remarkable plasticity, including complete reversal of the malignant phenotype. Such reprogramming involves both extrinsic and intrinsic factors and can occur via three routes: perturbations of extracellular matrix-cell receptor interactions, modulation of intracellular signaling pathways, and exploitation of epigenetic inheritance. Studies demonstrate the potential for producing dramatic changes in structural, biochemical, immunological, and functional properties of a broad spectrum of tumor cell types, including melanoma, leading to growth arrest, differentiation, senescence, or self destruction. Translating the promise inherent in tumor cell plasticity to the clinical arena remains a major challenge, but it is likely that a variety of epigenetic methods will play an increasingly important and effective role in the future control of malignant melanoma and other cancers.

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Section: Melanoma Cell Plasticitymentioning

confidence: 99%

Plasticity of the Cancer Cell: Implications for Epigenetic Control of Melanoma and Other Malignancies

Lipkin

2008

Journal of Investigative Dermatology

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“…More recently, we have found in collaboration with Drs. G. Lipkin and M. Rosenberg, at the NYU Medical Center, that vitiligo antigens can be induced in nonpigmented hamster melanoma cells by treatment with a factor which causes them to differentiate towards a normal phenotype (26), even though they remain depigmented. This observation suggests that the vitiligo antigens are markers for the terminal differentiation of melanocytes.…”

Section: Characterization Ofvitiligo Antigenmentioning

confidence: 99%

The Significance of Vitiligo Antibodies

Bystryn

Naughton

1985

The Journal of Dermatology

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“…CIF, a diffusible substance found in the conditioned medium of revertant (contact-inhibited) hamster melanocytic cells (Lipkin and Knecht, 1974), mediates certain changes in morphology, growth and differentiation of various cultured tumor cells. Such alterations include: (a) restoration of contact inhibition, (b) regain of anchorage-and serum-dependent proliferation, (c) induction of pigment-cell differentiation antigens on mouse and hamster melanoma cells, and (d) reduced susceptibility of human melanoma, colon carcinoma, and erythroleukemia cells to lysis by NK cells Knecht, 1974, 1976;Lipkin et al, 1978Lipkin et al, , 1985Lipkin et al, , 1986Nabi et al., 1986). CIF reduces cell proliferation by initiating a GI arrest, or at least a prolongation of this cell-cycle phase (Lipkin and Knecht, 1976).…”

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confidence: 99%

Contact‐inhibitory factor induces alterations in the distribution and content of specific cytoskeletal elements in an established line of rat hepatic tumor cells

Higgins

Lipkin

Rosenberg

et al. 1987

Intl Journal of Cancer

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Established 72/22 rat hepatic epithelial tumor cells, which possess intracellular aggregates of intermediate-sized filaments resembling Mallory-body-like inclusions, were used to assess changes in tumor cell growth and morphology associated with exposure to contact-inhibitory factor (CIF). CIF reduced 72/22 proliferative rate, increased mean population doubling time by 42%, lowered culture saturation densities to 34-50% of control values and inhibited formation of dense foci. These proliferative changes were due to an apparent prolongation of the G1 phase of the cell cycle during the period of CIF exposure. CIF concomitantly induced a marked increase (by 70%) in cell spreading and loss of both the usual tight (epithelioid) cell juxtaposition and typical ordered colony structure characteristic of untreated populations. However, CIF exposure failed to achieve complete cytoarchitectural "normalization" in 72/22 cells (i.e., dispersal of the Mallory-body-like aggregate of intermediate filaments and restoration of a more typical hepatocytic phenotype). Most obvious was a reduction in the integrity of the peripheral band of microfilaments (a structure involved in the maintenance of epithelial cell shape) and a decrease in the content of desmoplakin (a protein component of desmosomal plaques). Changes in these major structural elements appear to be critical events in development of the pleomorphic phenotype and reduced substratum adhesiveness observed during treatment. CIF-related fragmentation of peripheral band structures was not reflected in changes in either the total cellular or cytoskeletal-associated actin contents. The morphologic changes observed under conditions of CIF exposure closely paralleled induced decreases in the cellular content of the actin-associated membrane skeleton protein p35. These data collectively suggest that CIF may act to alter the composition of the cortical skeleton in cultured liver tumor cells.

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Vitiligo-related pigment cell differentiation antigens are expressed on malignant melanoma cells following phenotypic reversion induced by contact inhibitory factor

Cited by 10 publications

References 10 publications

Plasticity of the Cancer Cell: Implications for Epigenetic Control of Melanoma and Other Malignancies

Plasticity of the Cancer Cell: Implications for Epigenetic Control of Melanoma and Other Malignancies

The Significance of Vitiligo Antibodies

Contact‐inhibitory factor induces alterations in the distribution and content of specific cytoskeletal elements in an established line of rat hepatic tumor cells

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