Walker 256 tumor MHC class I expression during the shift from A variant to the immunogenic AR variant

dc.creatorSchanoski, AS
dc.creatorCavalcanti, TC
dc.creatorBarbosa, C
dc.creatorCampos, L
dc.creatorViera-Matos, AN
dc.creatorRettori, O
dc.creatorGuimaraes, F
dc.date2004
dc.date46935
dc.date2014-11-13T23:54:50Z
dc.date2015-11-26T16:03:20Z
dc.date2014-11-13T23:54:50Z
dc.date2015-11-26T16:03:20Z
dc.date.accessioned2018-03-28T22:52:35Z
dc.date.available2018-03-28T22:52:35Z
dc.identifierCancer Letters. Elsevier Sci Ireland Ltd, v. 211, n. 1, n. 119, n. 127, 2004.
dc.identifier0304-3835
dc.identifierWOS:000222476100014
dc.identifier10.1016/j.canlet.2004.01.023
dc.identifierhttp://www.repositorio.unicamp.br/jspui/handle/REPOSIP/76261
dc.identifierhttp://www.repositorio.unicamp.br/handle/REPOSIP/76261
dc.identifierhttp://repositorio.unicamp.br/jspui/handle/REPOSIP/76261
dc.identifier.urihttp://repositorioslatinoamericanos.uchile.cl/handle/2250/1265247
dc.descriptionNovel tumor cell variants can be obtained by serially passaging tumor cells in different media and/or environments. Serial intraperitoneal (ip) passages of the Walker 256 tumor A variant was followed for studying the generation of its regressive AR variant. MHC class I molecule expression was assessed since variations in this molecule would explain changes in tumor cell immunogenicity and therefore, the shift from progressive A variant to the regressive AR variant. Within 25 ip passages all serial repetitions shifted from A to AR variant, which was characterized by a significant increase in red blood cell (R13Q osmotic fragility with marked spleen hypertrophy in the host. In one serial repetition AR tumor cells were rejected tip passage number 36) and immunity against the AR and A variants was conferred. Flow cytometry analysis showed a significant increase in the number MHC class I positive cells in AR variant (n = 15, 14.21 +/- 1.32) compared with A variant (n = 10, 9.10 +/- 1.22). These data provide evidence that the generation of the AR variant could result from factors present in the ip environment leading to an increase in the number of Walker 256 MHC class I positive tumor cells, probably due to immune selection of MHC class I negative tumor cells. (C) 2004 Published by Elsevier Ireland Ltd.
dc.description211
dc.description1
dc.description119
dc.description127
dc.languageen
dc.publisherElsevier Sci Ireland Ltd
dc.publisherClare
dc.publisherIrlanda
dc.relationCancer Letters
dc.relationCancer Lett.
dc.rightsfechado
dc.rightshttp://www.elsevier.com/about/open-access/open-access-policies/article-posting-policy
dc.sourceWeb of Science
dc.subjectAMC class I expression
dc.subjectascitic tumor
dc.subjecttumor cell variants
dc.subjectWalker 256 tumor
dc.subjectNk Cells
dc.subjectRats
dc.subjectAntigens
dc.subjectEscape
dc.subjectFibrosarcoma
dc.subjectLymphocytes
dc.subjectGrowth
dc.subjectAnemia
dc.subjectMice
dc.titleWalker 256 tumor MHC class I expression during the shift from A variant to the immunogenic AR variant
dc.typeArtículos de revistas


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