Please use this identifier to cite or link to this item: https://scholarbank.nus.edu.sg/handle/10635/112026
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dc.titlePromotion of tumor growth by transfecting antisense DNA to suppress endogenous H-2Kk MHC gene expression in AKR mouse thymoma
dc.contributor.authorHui, K.M.
dc.contributor.authorSim, B.C.
dc.contributor.authorFoo, T.T.
dc.contributor.authorOei, A.A.
dc.date.accessioned2014-11-28T02:52:19Z
dc.date.available2014-11-28T02:52:19Z
dc.date.issued1991-08
dc.identifier.citationHui, K.M.,Sim, B.C.,Foo, T.T.,Oei, A.A. (1991-08). Promotion of tumor growth by transfecting antisense DNA to suppress endogenous H-2Kk MHC gene expression in AKR mouse thymoma. Cellular Immunology 136 (1) : 80-94. ScholarBank@NUS Repository.
dc.identifier.issn00088749
dc.identifier.urihttp://scholarbank.nus.edu.sg/handle/10635/112026
dc.description.abstractMany AKR spontaneous thymomas are reported to express different amounts of the major histocompatibility complex class I H-2Kk molecules. Moreover, H-2Kk-deficient AKR tumor cells are found to be more malignant when compared to tumor cells that express abundant levels of the H-2Kk molecules. To corroborate further the role of H-2Kk in tumorigenesis of AKR leukemia, we have, in this study, expressed antisense H-2Kk RNA in a high-H-2Kk-expressing and poorly tumorigenic AKR thymoma cell line 369. The down-regulation of H-2Kk molecules in the transfected 369 clones rendered them more tumorigenic in syngeneic AKR/J mice. The increase in oncogenicity correlates well with a concomitant reduction in their susceptibility to tumor-specific cytotoxic T lymphocytes in vitro. These results suggest the relevance of H-2Kk molecules in the immune surveillance of AKR tumors. © 1991.
dc.sourceScopus
dc.typeArticle
dc.contributor.departmentINSTITUTE OF MOLECULAR & CELL BIOLOGY
dc.description.sourcetitleCellular Immunology
dc.description.volume136
dc.description.issue1
dc.description.page80-94
dc.description.codenCLIMB
dc.identifier.isiutNOT_IN_WOS
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