dc.creatorSchanoski, Alessandra Soares
dc.creatorCavalcanti, Tereza Cristina
dc.creatorCampos, Cláudia Barbosa Ladeira
dc.creatorViera-Matos, Ana Neuza
dc.creatorRettori, Ovídio
dc.creatorGuimarães, Fernando
dc.date2004-Jul
dc.date2015-11-27T12:58:13Z
dc.date2015-11-27T12:58:13Z
dc.date.accessioned2018-03-29T00:59:09Z
dc.date.available2018-03-29T00:59:09Z
dc.identifierCancer Letters. v. 211, n. 1, p. 119-27, 2004-Jul.
dc.identifier0304-3835
dc.identifier10.1016/j.canlet.2004.01.023
dc.identifierhttp://www.ncbi.nlm.nih.gov/pubmed/15194224
dc.identifierhttp://repositorio.unicamp.br/jspui/handle/REPOSIP/195830
dc.identifier15194224
dc.identifier.urihttp://repositorioslatinoamericanos.uchile.cl/handle/2250/1296063
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 (RBC) osmotic fragility with marked spleen hypertrophy in the host. In one serial repetition AR tumor cells were rejected (ip 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.
dc.description211
dc.description119-27
dc.languageeng
dc.relationCancer Letters
dc.relationCancer Lett.
dc.rightsfechado
dc.rightsCopyright 2004 Elsevier Ireland Ltd.
dc.sourcePubMed
dc.subjectAnimals
dc.subjectCarcinoma 256, Walker
dc.subjectGenetic Variation
dc.subjectHistocompatibility Antigens Class I
dc.subjectMale
dc.subjectRats
dc.subjectRats, Wistar
dc.titleWalker 256 Tumor Mhc Class I Expression During The Shift From A Variant To The Immunogenic Ar Variant.
dc.typeArtículos de revistas


Este ítem pertenece a la siguiente institución