| pubmed-article:7478532 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:7478532 | lifeskim:mentions | umls-concept:C0376358 | lld:lifeskim |
| pubmed-article:7478532 | lifeskim:mentions | umls-concept:C0019904 | lld:lifeskim |
| pubmed-article:7478532 | lifeskim:mentions | umls-concept:C1707257 | lld:lifeskim |
| pubmed-article:7478532 | lifeskim:mentions | umls-concept:C0205147 | lld:lifeskim |
| pubmed-article:7478532 | lifeskim:mentions | umls-concept:C0205145 | lld:lifeskim |
| pubmed-article:7478532 | lifeskim:mentions | umls-concept:C0796365 | lld:lifeskim |
| pubmed-article:7478532 | lifeskim:mentions | umls-concept:C1521699 | lld:lifeskim |
| pubmed-article:7478532 | lifeskim:mentions | umls-concept:C1442161 | lld:lifeskim |
| pubmed-article:7478532 | pubmed:issue | 10 | lld:pubmed |
| pubmed-article:7478532 | pubmed:dateCreated | 1995-12-28 | lld:pubmed |
| pubmed-article:7478532 | pubmed:abstractText | Frequent loss of an allele at specific chromosomal regions implicates these regions as sites of tumor suppressor genes (TSG) that become inactivated during tumor progression. We have studied chromosome 8p allele losses in 32 primary human prostate carcinomas with 16 polymorphic microsatellite sequences. Overall, 22 of 32 (69%) informative specimens showed loss of allele in at least one locus. The most frequent losses of heterozygosity (LOH) occurred at the LPL locus (46%) on chromosome 8p22 and at the D8S360 (45%) and NEFL (43%) loci on chromosome 8p21. Homozygous deletions were detected at the LPL and NEFL loci at 8p22 and 8p21, respectively. The minimal region with frequent LOH and homozygous deletion, around the LPL locus, was restricted between the MSR locus and the D8S258 marker, separated by less than 9 cM. The second region was restricted between markers D8S1128 and D8S131 separated by 12 cM. The results suggest the existence of two chromosome 8p sites for candidate TSGs in prostate cancer. | lld:pubmed |
| pubmed-article:7478532 | pubmed:language | eng | lld:pubmed |
| pubmed-article:7478532 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:7478532 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:7478532 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:7478532 | pubmed:month | Nov | lld:pubmed |
| pubmed-article:7478532 | pubmed:issn | 0950-9232 | lld:pubmed |
| pubmed-article:7478532 | pubmed:author | pubmed-author:GlassmanA BAB | lld:pubmed |
| pubmed-article:7478532 | pubmed:author | pubmed-author:SteinJJ | lld:pubmed |
| pubmed-article:7478532 | pubmed:author | pubmed-author:von... | lld:pubmed |
| pubmed-article:7478532 | pubmed:author | pubmed-author:KaganJJ | lld:pubmed |
| pubmed-article:7478532 | pubmed:author | pubmed-author:BabaianR JRJ | lld:pubmed |
| pubmed-article:7478532 | pubmed:author | pubmed-author:TroncosoPP | lld:pubmed |
| pubmed-article:7478532 | pubmed:author | pubmed-author:PistersL LLL | lld:pubmed |
| pubmed-article:7478532 | pubmed:author | pubmed-author:JoeY SYS | lld:pubmed |
| pubmed-article:7478532 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:7478532 | pubmed:day | 16 | lld:pubmed |
| pubmed-article:7478532 | pubmed:volume | 11 | lld:pubmed |
| pubmed-article:7478532 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:7478532 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:7478532 | pubmed:pagination | 2121-6 | lld:pubmed |
| pubmed-article:7478532 | pubmed:dateRevised | 2006-11-15 | lld:pubmed |
| pubmed-article:7478532 | pubmed:meshHeading | pubmed-meshheading:7478532-... | lld:pubmed |
| pubmed-article:7478532 | pubmed:meshHeading | pubmed-meshheading:7478532-... | lld:pubmed |
| pubmed-article:7478532 | pubmed:meshHeading | pubmed-meshheading:7478532-... | lld:pubmed |
| pubmed-article:7478532 | pubmed:meshHeading | pubmed-meshheading:7478532-... | lld:pubmed |
| pubmed-article:7478532 | pubmed:meshHeading | pubmed-meshheading:7478532-... | lld:pubmed |
| pubmed-article:7478532 | pubmed:meshHeading | pubmed-meshheading:7478532-... | lld:pubmed |
| pubmed-article:7478532 | pubmed:meshHeading | pubmed-meshheading:7478532-... | lld:pubmed |
| pubmed-article:7478532 | pubmed:meshHeading | pubmed-meshheading:7478532-... | lld:pubmed |
| pubmed-article:7478532 | pubmed:meshHeading | pubmed-meshheading:7478532-... | lld:pubmed |
| pubmed-article:7478532 | pubmed:year | 1995 | lld:pubmed |
| pubmed-article:7478532 | pubmed:articleTitle | Homozygous deletions at 8p22 and 8p21 in prostate cancer implicate these regions as the sites for candidate tumor suppressor genes. | lld:pubmed |
| pubmed-article:7478532 | pubmed:affiliation | Division of Laboratory Medicine-Hematopathology Program, University of Texas, M.D. Anderson Cancer Center, Houston 77030, USA. | lld:pubmed |
| pubmed-article:7478532 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:7478532 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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| http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:7478532 | lld:pubmed |
