| pubmed-article:11309271 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:11309271 | lifeskim:mentions | umls-concept:C0006826 | lld:lifeskim |
| pubmed-article:11309271 | lifeskim:mentions | umls-concept:C0031437 | lld:lifeskim |
| pubmed-article:11309271 | pubmed:issue | 8 | lld:pubmed |
| pubmed-article:11309271 | pubmed:dateCreated | 2001-4-19 | lld:pubmed |
| pubmed-article:11309271 | pubmed:abstractText | We have proposed that an early step in tumor progression is the expression of a mutator phenotype resulting from mutations in genes that normally function in the maintenance of genetic stability. There is new and strong experimental evidence that supports the concept of a mutator phenotype in cancer. As technologies for chromosomal visualization and DNA advance, there are increasing data that human cancer cells contain large numbers of mutations. First, I will review the concept of a mutator phenotype. Second, I will present the recent evidence that individual cancer cells contain thousands of mutations. Third, I will explore potential target genes that are required for maintenance of genetic stability in normal cells and ask if they are mutated in cancer cells. Fourth, I will address the timing of a mutator phenotype; is it an early event during tumor progression? Do tumors already contain cells that harbor mutations rendering them resistant to most chemotherapeutic agents? Lastly, I will speculate on the theoretical and practical implication of a mutator phenotype in cancer and consider the possibility of cancer prevention by delay, i.e., a reduction in mutation rates early during carcinogenesis might slow the progression of tumors. | lld:pubmed |
| pubmed-article:11309271 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11309271 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11309271 | pubmed:language | eng | lld:pubmed |
| pubmed-article:11309271 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11309271 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:11309271 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:11309271 | pubmed:month | Apr | lld:pubmed |
| pubmed-article:11309271 | pubmed:issn | 0008-5472 | lld:pubmed |
| pubmed-article:11309271 | pubmed:author | pubmed-author:LoebL ALA | lld:pubmed |
| pubmed-article:11309271 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:11309271 | pubmed:day | 15 | lld:pubmed |
| pubmed-article:11309271 | pubmed:volume | 61 | lld:pubmed |
| pubmed-article:11309271 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:11309271 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:11309271 | pubmed:pagination | 3230-9 | lld:pubmed |
| pubmed-article:11309271 | pubmed:dateRevised | 2007-11-14 | lld:pubmed |
| pubmed-article:11309271 | pubmed:meshHeading | pubmed-meshheading:11309271... | lld:pubmed |
| pubmed-article:11309271 | pubmed:meshHeading | pubmed-meshheading:11309271... | lld:pubmed |
| pubmed-article:11309271 | pubmed:meshHeading | pubmed-meshheading:11309271... | lld:pubmed |
| pubmed-article:11309271 | pubmed:meshHeading | pubmed-meshheading:11309271... | lld:pubmed |
| pubmed-article:11309271 | pubmed:meshHeading | pubmed-meshheading:11309271... | lld:pubmed |
| pubmed-article:11309271 | pubmed:year | 2001 | lld:pubmed |
| pubmed-article:11309271 | pubmed:articleTitle | A mutator phenotype in cancer. | lld:pubmed |
| pubmed-article:11309271 | pubmed:affiliation | Departments of Pathology and Biochemistry, The Joseph Gottstein Memorial Cancer Research Laboratory, University of Washington, Seattle, WA 98195-7705, USA. laloeb@u.washington.edu | lld:pubmed |
| pubmed-article:11309271 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:11309271 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:11309271 | pubmed:publicationType | Review | lld:pubmed |
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