pubmed-article:10050867 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:10050867 | lifeskim:mentions | umls-concept:C1140680 | lld:lifeskim |
pubmed-article:10050867 | lifeskim:mentions | umls-concept:C0030705 | lld:lifeskim |
pubmed-article:10050867 | lifeskim:mentions | umls-concept:C0012854 | lld:lifeskim |
pubmed-article:10050867 | lifeskim:mentions | umls-concept:C0043297 | lld:lifeskim |
pubmed-article:10050867 | lifeskim:mentions | umls-concept:C1511022 | lld:lifeskim |
pubmed-article:10050867 | lifeskim:mentions | umls-concept:C0004083 | lld:lifeskim |
pubmed-article:10050867 | pubmed:issue | 4 | lld:pubmed |
pubmed-article:10050867 | pubmed:dateCreated | 1999-3-9 | lld:pubmed |
pubmed-article:10050867 | pubmed:abstractText | Most human female cells contain two X chromosomes, only one of which is active. The process of X-chromosome inactivation, which occurs early in development, is usually random, producing tissues with equal mixtures of cells having active X chromosomes of either maternal or paternal origin. However, nonrandom inactivation may occur in a subset of females. If a tumor suppressor gene were located on the X chromosome and if females with a germline mutation in one copy of that suppressor gene experienced nonrandom X-chromosome inactivation, then some or all of the tissues of such women might lack the wild-type suppressor gene function. This scenario could represent a previously unrecognized mechanism for development of hereditary cancers. We investigated whether such a mechanism might contribute to the development of hereditary ovarian cancers. | lld:pubmed |
pubmed-article:10050867 | pubmed:commentsCorrections | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:10050867 | pubmed:commentsCorrections | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:10050867 | pubmed:language | eng | lld:pubmed |
pubmed-article:10050867 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:10050867 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:10050867 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:10050867 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:10050867 | pubmed:month | Feb | lld:pubmed |
pubmed-article:10050867 | pubmed:issn | 0027-8874 | lld:pubmed |
pubmed-article:10050867 | pubmed:author | pubmed-author:SoodA KAK | lld:pubmed |
pubmed-article:10050867 | pubmed:author | pubmed-author:BullerR ERE | lld:pubmed |
pubmed-article:10050867 | pubmed:author | pubmed-author:SkillingJ SJS | lld:pubmed |
pubmed-article:10050867 | pubmed:author | pubmed-author:LallasTT | lld:pubmed |
pubmed-article:10050867 | pubmed:author | pubmed-author:BuekersTT | lld:pubmed |
pubmed-article:10050867 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:10050867 | pubmed:day | 17 | lld:pubmed |
pubmed-article:10050867 | pubmed:volume | 91 | lld:pubmed |
pubmed-article:10050867 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:10050867 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:10050867 | pubmed:pagination | 339-46 | lld:pubmed |
pubmed-article:10050867 | pubmed:dateRevised | 2006-11-15 | lld:pubmed |
pubmed-article:10050867 | pubmed:meshHeading | pubmed-meshheading:10050867... | lld:pubmed |
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pubmed-article:10050867 | pubmed:meshHeading | pubmed-meshheading:10050867... | lld:pubmed |
pubmed-article:10050867 | pubmed:meshHeading | pubmed-meshheading:10050867... | lld:pubmed |
pubmed-article:10050867 | pubmed:year | 1999 | lld:pubmed |
pubmed-article:10050867 | pubmed:articleTitle | Association between nonrandom X-chromosome inactivation and BRCA1 mutation in germline DNA of patients with ovarian cancer. | lld:pubmed |
pubmed-article:10050867 | pubmed:affiliation | Department of Pharmacology, The University of Iowa Hospitals and Clinics, Iowa City 52242-1009, USA. richard-buller@uiowa.edu | lld:pubmed |
pubmed-article:10050867 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:10050867 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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