pubmed-article:6460831 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:6460831 | lifeskim:mentions | umls-concept:C0027651 | lld:lifeskim |
pubmed-article:6460831 | lifeskim:mentions | umls-concept:C0221102 | lld:lifeskim |
pubmed-article:6460831 | lifeskim:mentions | umls-concept:C0079613 | lld:lifeskim |
pubmed-article:6460831 | lifeskim:mentions | umls-concept:C2355612 | lld:lifeskim |
pubmed-article:6460831 | lifeskim:mentions | umls-concept:C0443211 | lld:lifeskim |
pubmed-article:6460831 | pubmed:issue | 4 | lld:pubmed |
pubmed-article:6460831 | pubmed:dateCreated | 1982-5-21 | lld:pubmed |
pubmed-article:6460831 | pubmed:abstractText | On the basis of preceding studies showing that tumor-induced, T cell-mediated immunosuppression serves as an obstacle to adoptive immunotherapy of the Meth A fibrosarcoma, it was predicted that cyclophosphamide treatment of tumor bearers would remove this obstacle and allow passively transferred immune T cells to cause tumor regression. It was found that infusion of immune spleen cells alone had no effect on tumor growth, and cyclophosphamide alone caused a temporary halt in tumor progression. In contrast, combination therapy consisting of intravenous injection of 100 mg/kg of cyclophosphamide followed 1 h later by intravenous infusion of tumor-immune spleen cells caused small, as well as large tumors, to completely and permanently regress. Tumor regression caused by combination therapy was completely inhibited by intravenous infusion of splenic T cells from donors with established tumors, but not by spleen cells from normal donors. These suppressor T cells were eliminated from the spleen by treating the tumor-bearing donors with 100 mg/kg of cyclophosphamide. Immune T cells, in contrast, were resistant to this dose of cyclophosphamide. These results show that failure of intravenously-infused, tumor-sensitized T cells to cause regression of the Meth A fibrosarcoma growing in its syngeneic or semi-syngeneic host is caused by the presence of a tumor-induced population of cyclophosphamide-sensitive suppressor T cells. | lld:pubmed |
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pubmed-article:6460831 | pubmed:language | eng | lld:pubmed |
pubmed-article:6460831 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:6460831 | pubmed:citationSubset | IM | lld:pubmed |
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pubmed-article:6460831 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:6460831 | pubmed:month | Apr | lld:pubmed |
pubmed-article:6460831 | pubmed:issn | 0022-1007 | lld:pubmed |
pubmed-article:6460831 | pubmed:author | pubmed-author:NorthR JRJ | lld:pubmed |
pubmed-article:6460831 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:6460831 | pubmed:day | 1 | lld:pubmed |
pubmed-article:6460831 | pubmed:volume | 155 | lld:pubmed |
pubmed-article:6460831 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:6460831 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:6460831 | pubmed:pagination | 1063-74 | lld:pubmed |
pubmed-article:6460831 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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pubmed-article:6460831 | pubmed:year | 1982 | lld:pubmed |
pubmed-article:6460831 | pubmed:articleTitle | Cyclophosphamide-facilitated adoptive immunotherapy of an established tumor depends on elimination of tumor-induced suppressor T cells. | lld:pubmed |
pubmed-article:6460831 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:6460831 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
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