| pubmed-article:11606364 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:11606364 | lifeskim:mentions | umls-concept:C0534628 | lld:lifeskim |
| pubmed-article:11606364 | lifeskim:mentions | umls-concept:C0007112 | lld:lifeskim |
| pubmed-article:11606364 | lifeskim:mentions | umls-concept:C0596087 | lld:lifeskim |
| pubmed-article:11606364 | lifeskim:mentions | umls-concept:C1527148 | lld:lifeskim |
| pubmed-article:11606364 | lifeskim:mentions | umls-concept:C1882417 | lld:lifeskim |
| pubmed-article:11606364 | pubmed:issue | 20 | lld:pubmed |
| pubmed-article:11606364 | pubmed:dateCreated | 2001-10-18 | lld:pubmed |
| pubmed-article:11606364 | pubmed:abstractText | We have performed association studies between a novel coding single nucleotide polymorphism (D104N) in endostatin, one of the most potent inhibitors of angiogenesis, and prostate cancer. We observed that heterozygous N104 individuals have a 2.5 times increased chance of developing prostate cancer as compared with homozygous D104 subjects (odds ratio, 2.4; 95% confidence interval, 1.4-4.16). Modeling of the endostatin mutant showed that the N104 protein is stable. These results together with the observation that residue 104 is evolutionary conserved lead us to propose that: (a) the DNA segment containing this residue might contain a novel interaction site to a yet unknown receptor; and (b) the presence of N104 impairs the function of endostatin. | lld:pubmed |
| pubmed-article:11606364 | pubmed:language | eng | lld:pubmed |
| pubmed-article:11606364 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11606364 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:11606364 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:11606364 | pubmed:month | Oct | lld:pubmed |
| pubmed-article:11606364 | pubmed:issn | 0008-5472 | lld:pubmed |
| pubmed-article:11606364 | pubmed:author | pubmed-author:SuzukiOO | lld:pubmed |
| pubmed-article:11606364 | pubmed:author | pubmed-author:Moreira-Filho... | lld:pubmed |
| pubmed-article:11606364 | pubmed:author | pubmed-author:OlivaGG | lld:pubmed |
| pubmed-article:11606364 | pubmed:author | pubmed-author:AlvesV AVA | lld:pubmed |
| pubmed-article:11606364 | pubmed:author | pubmed-author:SimpsonAA | lld:pubmed |
| pubmed-article:11606364 | pubmed:author | pubmed-author:SoaresFF | lld:pubmed |
| pubmed-article:11606364 | pubmed:author | pubmed-author:MoreiraE SES | lld:pubmed |
| pubmed-article:11606364 | pubmed:author | pubmed-author:Passos-BuenoM... | lld:pubmed |
| pubmed-article:11606364 | pubmed:author | pubmed-author:di LoretoCC | lld:pubmed |
| pubmed-article:11606364 | pubmed:author | pubmed-author:CamargoAA | lld:pubmed |
| pubmed-article:11606364 | pubmed:author | pubmed-author:IughettiPP | lld:pubmed |
| pubmed-article:11606364 | pubmed:author | pubmed-author:SertiéA LAL | lld:pubmed |
| pubmed-article:11606364 | pubmed:author | pubmed-author:GodoiP HPH | lld:pubmed |
| pubmed-article:11606364 | pubmed:author | pubmed-author:ZorickTT | lld:pubmed |
| pubmed-article:11606364 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:11606364 | pubmed:day | 15 | lld:pubmed |
| pubmed-article:11606364 | pubmed:volume | 61 | lld:pubmed |
| pubmed-article:11606364 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:11606364 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:11606364 | pubmed:pagination | 7375-8 | lld:pubmed |
| pubmed-article:11606364 | pubmed:dateRevised | 2008-11-21 | lld:pubmed |
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| pubmed-article:11606364 | pubmed:year | 2001 | lld:pubmed |
| pubmed-article:11606364 | pubmed:articleTitle | A polymorphism in endostatin, an angiogenesis inhibitor, predisposes for the development of prostatic adenocarcinoma. | lld:pubmed |
| pubmed-article:11606364 | pubmed:affiliation | Centro de Estudos do Genoma Humano, Departamento de Biologia, Instituto de Biociências, USP, São Paulo 05508-900, Brasil. | lld:pubmed |
| pubmed-article:11606364 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:11606364 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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