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pubmed-article:19330028 | lifeskim:mentions | umls-concept:C0015576 | lld:lifeskim |
pubmed-article:19330028 | lifeskim:mentions | umls-concept:C0025202 | lld:lifeskim |
pubmed-article:19330028 | lifeskim:mentions | umls-concept:C0026882 | lld:lifeskim |
pubmed-article:19330028 | lifeskim:mentions | umls-concept:C0623362 | lld:lifeskim |
pubmed-article:19330028 | lifeskim:mentions | umls-concept:C1417213 | lld:lifeskim |
pubmed-article:19330028 | lifeskim:mentions | umls-concept:C0936012 | lld:lifeskim |
pubmed-article:19330028 | pubmed:issue | 5 | lld:pubmed |
pubmed-article:19330028 | pubmed:dateCreated | 2009-4-28 | lld:pubmed |
pubmed-article:19330028 | pubmed:abstractText | A mutational analysis of the matrix metalloproteinase (MMP) gene family in human melanoma identified somatic mutations in 23% of melanomas. Five mutations in one of the most commonly mutated genes, MMP8, reduced MMP enzyme activity. Expression of wild-type but not mutant MMP8 in human melanoma cells inhibited growth on soft agar in vitro and tumor formation in vivo, suggesting that wild-type MMP-8 has the ability to inhibit melanoma progression. | lld:pubmed |
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pubmed-article:19330028 | pubmed:language | eng | lld:pubmed |
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pubmed-article:19330028 | pubmed:citationSubset | IM | lld:pubmed |
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pubmed-article:19330028 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:19330028 | pubmed:month | May | lld:pubmed |
pubmed-article:19330028 | pubmed:issn | 1546-1718 | lld:pubmed |
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pubmed-article:19330028 | pubmed:issnType | Electronic | lld:pubmed |
pubmed-article:19330028 | pubmed:volume | 41 | lld:pubmed |
pubmed-article:19330028 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:19330028 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:19330028 | pubmed:pagination | 518-20 | lld:pubmed |
pubmed-article:19330028 | pubmed:dateRevised | 2011-9-28 | lld:pubmed |
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pubmed-article:19330028 | pubmed:year | 2009 | lld:pubmed |
pubmed-article:19330028 | pubmed:articleTitle | Analysis of the matrix metalloproteinase family reveals that MMP8 is often mutated in melanoma. | lld:pubmed |
pubmed-article:19330028 | pubmed:affiliation | National Human Genome Research Institute, National Institutes of Health, Bethesda, Maryland, USA. | lld:pubmed |
pubmed-article:19330028 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:19330028 | pubmed:publicationType | Research Support, N.I.H., Extramural | lld:pubmed |
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