pubmed-article:18097478 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:18097478 | lifeskim:mentions | umls-concept:C0024299 | lld:lifeskim |
pubmed-article:18097478 | lifeskim:mentions | umls-concept:C0087111 | lld:lifeskim |
pubmed-article:18097478 | lifeskim:mentions | umls-concept:C0003374 | lld:lifeskim |
pubmed-article:18097478 | lifeskim:mentions | umls-concept:C1292733 | lld:lifeskim |
pubmed-article:18097478 | pubmed:issue | 1 | lld:pubmed |
pubmed-article:18097478 | pubmed:dateCreated | 2008-1-3 | lld:pubmed |
pubmed-article:18097478 | pubmed:abstractText | The two modes of self-destruction at the cellular level - apoptosis (self-killing) and autophagy (self-eating) - are thought to be tumor suppressive. In particular, germline loss of function of genes involved in autophagy has been associated with tumorigenesis. However, recent studies, including the one by Maclean et al. reported in this issue of the JCI, indicate that autophagy can provide a means for cell survival when nutrients are limiting, such that inhibition of autophagy by the antimalarial drug chloroquine can inhibit tumorigenesis, specifically Myc-induced lymphoma in mice (see the related article beginning on page 79). These findings suggest that a new use of an old drug for cancer prevention may profoundly affect disease outcome. | lld:pubmed |
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pubmed-article:18097478 | pubmed:language | eng | lld:pubmed |
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pubmed-article:18097478 | pubmed:citationSubset | AIM | lld:pubmed |
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pubmed-article:18097478 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:18097478 | pubmed:month | Jan | lld:pubmed |
pubmed-article:18097478 | pubmed:issn | 0021-9738 | lld:pubmed |
pubmed-article:18097478 | pubmed:author | pubmed-author:DangChi VCV | lld:pubmed |
pubmed-article:18097478 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:18097478 | pubmed:volume | 118 | lld:pubmed |
pubmed-article:18097478 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:18097478 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:18097478 | pubmed:pagination | 15-7 | lld:pubmed |
pubmed-article:18097478 | pubmed:dateRevised | 2011-11-2 | lld:pubmed |
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pubmed-article:18097478 | pubmed:year | 2008 | lld:pubmed |
pubmed-article:18097478 | pubmed:articleTitle | Antimalarial therapy prevents Myc-induced lymphoma. | lld:pubmed |
pubmed-article:18097478 | pubmed:affiliation | Division of Hematology, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA. cvdang@jhmi.edu | lld:pubmed |
pubmed-article:18097478 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:18097478 | pubmed:publicationType | Comment | lld:pubmed |
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