| pubmed-article:9182976 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:9182976 | lifeskim:mentions | umls-concept:C0013227 | lld:lifeskim |
| pubmed-article:9182976 | lifeskim:mentions | umls-concept:C0334227 | lld:lifeskim |
| pubmed-article:9182976 | lifeskim:mentions | umls-concept:C0596402 | lld:lifeskim |
| pubmed-article:9182976 | lifeskim:mentions | umls-concept:C1325847 | lld:lifeskim |
| pubmed-article:9182976 | lifeskim:mentions | umls-concept:C1511636 | lld:lifeskim |
| pubmed-article:9182976 | lifeskim:mentions | umls-concept:C0332293 | lld:lifeskim |
| pubmed-article:9182976 | pubmed:issue | 11 | lld:pubmed |
| pubmed-article:9182976 | pubmed:dateCreated | 1997-6-30 | lld:pubmed |
| pubmed-article:9182976 | pubmed:abstractText | The transmembrane receptor Fas, together with its protein-binding partner (Fas ligand), is a key regulator of programmed cell death (i.e., apoptosis). Fas and Fas ligand also influence the ability of cytotoxic T lymphocytes and natural killer cells to eliminate tumor cells. However, by inducing apoptosis in activated T cells, the Fas/Fas ligand system may protect some tumor cells from clearance by the immune system. Anticancer drugs enhance Fas ligand expression on the surface of Fas receptor-expressing leukemia cells, thus suggesting that apoptosis caused by these drugs may be mediated via the Fas/Fas ligand system. | lld:pubmed |
| pubmed-article:9182976 | pubmed:language | eng | lld:pubmed |
| pubmed-article:9182976 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:9182976 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:9182976 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:9182976 | pubmed:month | Jun | lld:pubmed |
| pubmed-article:9182976 | pubmed:issn | 0027-8874 | lld:pubmed |
| pubmed-article:9182976 | pubmed:author | pubmed-author:MartinFF | lld:pubmed |
| pubmed-article:9182976 | pubmed:author | pubmed-author:SolaryEE | lld:pubmed |
| pubmed-article:9182976 | pubmed:author | pubmed-author:HammannAA | lld:pubmed |
| pubmed-article:9182976 | pubmed:author | pubmed-author:Dimanche-Boit... | lld:pubmed |
| pubmed-article:9182976 | pubmed:author | pubmed-author:MicheauOO | lld:pubmed |
| pubmed-article:9182976 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:9182976 | pubmed:day | 4 | lld:pubmed |
| pubmed-article:9182976 | pubmed:volume | 89 | lld:pubmed |
| pubmed-article:9182976 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:9182976 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:9182976 | pubmed:pagination | 783-9 | lld:pubmed |
| pubmed-article:9182976 | pubmed:dateRevised | 2006-11-15 | lld:pubmed |
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| pubmed-article:9182976 | pubmed:year | 1997 | lld:pubmed |
| pubmed-article:9182976 | pubmed:articleTitle | Sensitization of cancer cells treated with cytotoxic drugs to fas-mediated cytotoxicity. | lld:pubmed |
| pubmed-article:9182976 | pubmed:affiliation | Contrat Jeune Formation de l'Institut National de la Santé et de la Recherche Médicale (INSERM) 94-08, Unité de Formation et de Recherchede Médecine, Dijon, France. | lld:pubmed |
| pubmed-article:9182976 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:9182976 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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