Transient inflammatory response induced by apoptotic cells is an important mediator of melanoma cell engraftment and growth

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dc.contributor.author Correa, Mariangela [UNIFESP]
dc.contributor.author Machado, Joel [UNIFESP]
dc.contributor.author Carneiro, Celia Regina Whitaker [UNIFESP]
dc.contributor.author Pesquero, Joao Bosco [UNIFESP]
dc.contributor.author Bader, M.
dc.contributor.author Travassos, Luiz Rodolpho [UNIFESP]
dc.contributor.author Chammas, Roger [UNIFESP]
dc.contributor.author Jasiulionis, Miriam Galvonas [UNIFESP]
dc.date.accessioned 2016-01-24T12:37:47Z
dc.date.available 2016-01-24T12:37:47Z
dc.date.issued 2005-04-10
dc.identifier http://dx.doi.org/10.1002/ijc.20673
dc.identifier.citation International Journal of Cancer. Malden: Wiley-Blackwell, v. 114, n. 3, p. 356-363, 2005.
dc.identifier.issn 0020-7136
dc.identifier.uri http://repositorio.unifesp.br/handle/11600/28247
dc.description.abstract Two murine melanoma cell lines, Toil and Tm5, were derived from a nontumorigenic lineage of pigmented murine melanocytes, melan-a. Both Tm1 and Tm5 are invariably tumorigenic in syngeneic mice when inoculated s.c. in doses higher than 104 cells; 103 or fewer cells rarely give rise to tumors. We demonstrate that subtumorigenic inocula of Tint or Tm5 Cells (103) as well as of a known murine melanoma cell line (B16F10) develop as vigorously growing tumor grafts only when coinoculated with apoptotic, but not necrotic cells. the presence of apoptotic cells correlates with a transient inflammatory infiltrate, composed mainly of neutrophils and macrophages. Kinin B1 receptor-deficient mice, which have impaired transmigration of neutrophils to inflamed tissues, had significant growth inhibition of subtumorigenic doses of melanoma cells coinjected with apoptotic cells. Using the same model, tumor take in athymic mice was similar to that seen in wild-type mice, suggesting that a T cell-dependent inflammatory response is not necessary to promote the survival and growth of subtumorigenic doses of melanoma cells. Taken together, our results describe how tumor engraftment and growth can be profoundly affected by microenvironmental alterations in response to the presence of apoptotic cells. Disrupting the delicate balance between apoptotic cells and leukocyte infiltration may provide potentially important insights for understanding and interfering with tumor cell viability during treatment with either gamma-radiation or apoptosis-inducing drugs. (C) 2004 Wiley-Liss, Inc. en
dc.format.extent 356-363
dc.language.iso eng
dc.publisher Wiley-Blackwell
dc.relation.ispartof International Journal of Cancer
dc.rights Acesso aberto
dc.subject melanoma en
dc.subject inflammation en
dc.subject apoptosis en
dc.subject neutrophil en
dc.subject tumor growth en
dc.title Transient inflammatory response induced by apoptotic cells is an important mediator of melanoma cell engraftment and growth en
dc.type Artigo
dc.rights.license http://olabout.wiley.com/WileyCDA/Section/id-406071.html
dc.contributor.institution Universidade Federal de São Paulo (UNIFESP)
dc.contributor.institution Max Delbruck Ctr Mol Med
dc.description.affiliation Universidade Federal de São Paulo, Dept Micro Imuno Parasitol, Disciplina Imunol, BR-04023062 São Paulo, Brazil
dc.description.affiliation Universidade Federal de São Paulo, Disciplina Biofis, BR-04023062 São Paulo, Brazil
dc.description.affiliation Max Delbruck Ctr Mol Med, Mol Biol Peptide Hormone Grp, Berlin, Germany
dc.description.affiliation Universidade Federal de São Paulo, Unidade Oncol Expt, BR-04023062 São Paulo, Brazil
dc.description.affiliation Universidade Federal de São Paulo, Fac Med, Expt Oncol Lab, BR-04023062 São Paulo, Brazil
dc.description.affiliationUnifesp Universidade Federal de São Paulo, Dept Micro Imuno Parasitol, Disciplina Imunol, BR-04023062 São Paulo, Brazil
dc.description.affiliationUnifesp Universidade Federal de São Paulo, Disciplina Biofis, BR-04023062 São Paulo, Brazil
dc.description.affiliationUnifesp Universidade Federal de São Paulo, Unidade Oncol Expt, BR-04023062 São Paulo, Brazil
dc.description.affiliationUnifesp Universidade Federal de São Paulo, Fac Med, Expt Oncol Lab, BR-04023062 São Paulo, Brazil
dc.identifier.doi 10.1002/ijc.20673
dc.description.source Web of Science
dc.identifier.wos WOS:000227223100004



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