pubmed-article:11208819 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:11208819 | lifeskim:mentions | umls-concept:C0033325 | lld:lifeskim |
pubmed-article:11208819 | lifeskim:mentions | umls-concept:C0086418 | lld:lifeskim |
pubmed-article:11208819 | lifeskim:mentions | umls-concept:C0032854 | lld:lifeskim |
pubmed-article:11208819 | lifeskim:mentions | umls-concept:C0525037 | lld:lifeskim |
pubmed-article:11208819 | lifeskim:mentions | umls-concept:C1527249 | lld:lifeskim |
pubmed-article:11208819 | lifeskim:mentions | umls-concept:C1561558 | lld:lifeskim |
pubmed-article:11208819 | pubmed:issue | 2 | lld:pubmed |
pubmed-article:11208819 | pubmed:dateCreated | 2001-3-6 | lld:pubmed |
pubmed-article:11208819 | pubmed:abstractText | Mutations in the K-ras gene are frequent in human cancer. ras activation in primary cells results in a cellular senescence phenotype that is precluded by inactivation of p16. At the clinical level, this may imply a differential behavior for tumors with alternative or cooperative activation of K-ras function and impairment of p16 pathways. | lld:pubmed |
pubmed-article:11208819 | pubmed:commentsCorrections | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11208819 | pubmed:language | eng | lld:pubmed |
pubmed-article:11208819 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11208819 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:11208819 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11208819 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11208819 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:11208819 | pubmed:month | Jan | lld:pubmed |
pubmed-article:11208819 | pubmed:issn | 0732-183X | lld:pubmed |
pubmed-article:11208819 | pubmed:author | pubmed-author:GonzálezSS | lld:pubmed |
pubmed-article:11208819 | pubmed:author | pubmed-author:MarcuelloEE | lld:pubmed |
pubmed-article:11208819 | pubmed:author | pubmed-author:ManguesRR | lld:pubmed |
pubmed-article:11208819 | pubmed:author | pubmed-author:PeinadoM AMA | lld:pubmed |
pubmed-article:11208819 | pubmed:author | pubmed-author:GermàJ RJR | lld:pubmed |
pubmed-article:11208819 | pubmed:author | pubmed-author:HermanJ GJG | lld:pubmed |
pubmed-article:11208819 | pubmed:author | pubmed-author:EstellerMM | lld:pubmed |
pubmed-article:11208819 | pubmed:author | pubmed-author:CapellàGG | lld:pubmed |
pubmed-article:11208819 | pubmed:author | pubmed-author:RisquesR ARA | lld:pubmed |
pubmed-article:11208819 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:11208819 | pubmed:day | 15 | lld:pubmed |
pubmed-article:11208819 | pubmed:volume | 19 | lld:pubmed |
pubmed-article:11208819 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:11208819 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:11208819 | pubmed:pagination | 299-304 | lld:pubmed |
pubmed-article:11208819 | pubmed:dateRevised | 2006-11-15 | lld:pubmed |
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pubmed-article:11208819 | pubmed:year | 2001 | lld:pubmed |
pubmed-article:11208819 | pubmed:articleTitle | K-ras and p16 aberrations confer poor prognosis in human colorectal cancer. | lld:pubmed |
pubmed-article:11208819 | pubmed:affiliation | Johns Hopkins Oncology Center, Baltimore, MD, USA. | lld:pubmed |
pubmed-article:11208819 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:11208819 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
pubmed-article:11208819 | pubmed:publicationType | Evaluation Studies | lld:pubmed |
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