pubmed-article:11322829 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:11322829 | lifeskim:mentions | umls-concept:C0162597 | lld:lifeskim |
pubmed-article:11322829 | lifeskim:mentions | umls-concept:C1710082 | lld:lifeskim |
pubmed-article:11322829 | lifeskim:mentions | umls-concept:C1880177 | lld:lifeskim |
pubmed-article:11322829 | pubmed:issue | 2 | lld:pubmed |
pubmed-article:11322829 | pubmed:dateCreated | 2001-4-27 | lld:pubmed |
pubmed-article:11322829 | pubmed:abstractText | The majority of studies of neoplastic transformation have focused attention on events that occur within transformed cells. These cell autonomous events result in the disruption of molecular pathways that regulate basic activities of the cells such as proliferation, death, movement and genomic integrity. Other studies have addressed the microenvironment of tumor cells and documented its importance in supporting tumor progression. Recent work has begun to expand on these initial studies of tumor microenvironment and now provide novel insights into the possible initiation and progression of malignant cells. This review will address the transforming effect of stromal cells on epithelial components. | lld:pubmed |
pubmed-article:11322829 | pubmed:keyword | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11322829 | pubmed:keyword | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11322829 | pubmed:language | eng | lld:pubmed |
pubmed-article:11322829 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11322829 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:11322829 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:11322829 | pubmed:month | Apr | lld:pubmed |
pubmed-article:11322829 | pubmed:issn | 1044-579X | lld:pubmed |
pubmed-article:11322829 | pubmed:author | pubmed-author:TlstyT DTD | lld:pubmed |
pubmed-article:11322829 | pubmed:copyrightInfo | Copyright 2001 Academic Press. | lld:pubmed |
pubmed-article:11322829 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:11322829 | pubmed:volume | 11 | lld:pubmed |
pubmed-article:11322829 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:11322829 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:11322829 | pubmed:pagination | 97-104 | lld:pubmed |
pubmed-article:11322829 | pubmed:dateRevised | 2006-11-15 | lld:pubmed |
pubmed-article:11322829 | pubmed:meshHeading | pubmed-meshheading:11322829... | lld:pubmed |
pubmed-article:11322829 | pubmed:meshHeading | pubmed-meshheading:11322829... | lld:pubmed |
pubmed-article:11322829 | pubmed:meshHeading | pubmed-meshheading:11322829... | lld:pubmed |
pubmed-article:11322829 | pubmed:meshHeading | pubmed-meshheading:11322829... | lld:pubmed |
pubmed-article:11322829 | pubmed:meshHeading | pubmed-meshheading:11322829... | lld:pubmed |
pubmed-article:11322829 | pubmed:meshHeading | pubmed-meshheading:11322829... | lld:pubmed |
pubmed-article:11322829 | pubmed:year | 2001 | lld:pubmed |
pubmed-article:11322829 | pubmed:articleTitle | Stromal cells can contribute oncogenic signals. | lld:pubmed |
pubmed-article:11322829 | pubmed:affiliation | Department of Pathology, UCSF Comprehensive Cancer Center, University of California, San Francisco 94143-0506, USA. ttlsty@itsa.ucsf.edu | lld:pubmed |
pubmed-article:11322829 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:11322829 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
pubmed-article:11322829 | pubmed:publicationType | Research Support, U.S. Gov't, Non-P.H.S. | lld:pubmed |
pubmed-article:11322829 | pubmed:publicationType | Review | lld:pubmed |
pubmed-article:11322829 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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