| pubmed-article:18474871 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:18474871 | lifeskim:mentions | umls-concept:C0238463 | lld:lifeskim |
| pubmed-article:18474871 | lifeskim:mentions | umls-concept:C0017262 | lld:lifeskim |
| pubmed-article:18474871 | lifeskim:mentions | umls-concept:C0752046 | lld:lifeskim |
| pubmed-article:18474871 | lifeskim:mentions | umls-concept:C0547047 | lld:lifeskim |
| pubmed-article:18474871 | lifeskim:mentions | umls-concept:C0205214 | lld:lifeskim |
| pubmed-article:18474871 | lifeskim:mentions | umls-concept:C2911684 | lld:lifeskim |
| pubmed-article:18474871 | lifeskim:mentions | umls-concept:C0185117 | lld:lifeskim |
| pubmed-article:18474871 | pubmed:issue | 20 | lld:pubmed |
| pubmed-article:18474871 | pubmed:dateCreated | 2008-5-21 | lld:pubmed |
| pubmed-article:18474871 | pubmed:abstractText | Although papillary thyroid carcinoma (PTC) displays strong heritability, no predisposing germ-line mutations have been found. We show that a common G/C polymorphism (rs2910164) within the pre-miR-146a sequence reduced the amount of pre- and mature miR-146a from the C allele 1.9- and 1.8-fold, respectively, compared with the G allele. This is matched by a similar decrease in the amount of each pre-miR generated from the corresponding pri-miR-146a in an in vitro processing reaction. The C allele also interfered with the binding of a nuclear factor to pre-miR-146a. The reduction in miR-146a led to less efficient inhibition of target genes involved in the Toll-like receptor and cytokine signaling pathway (TRAF6, IRAK1), and PTC1 (also known as CCDC6 or H4), a gene frequently rearranged with RET proto-oncogene in PTC. In an association study of 608 PTC patients and 901 controls, we found marked differences in genotype distribution of rs2910164 (P = 0.000002), the GC heterozygous state being associated with an increased risk of acquiring PTC (odds ratio = 1.62, P = 0.000007), and both homozygous states protective with odds ratio = 0.42 for the CC genotype (P = 0.003) and odds ratio = 0.69 for the GG genotype (P = 0.0006). Moreover, 4.7% of tumors had undergone somatic mutations of the SNP sequence. Thus, our data suggest that a common polymorphism in pre-miR-146a affects the miR expression, contributes to the genetic predisposition to PTC, and plays a role in the tumorigenesis through somatic mutation. Preliminary evidence suggests that these effects are mediated through target genes whose expression is affected by the SNP status. | lld:pubmed |
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| pubmed-article:18474871 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:18474871 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:18474871 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:18474871 | pubmed:month | May | lld:pubmed |
| pubmed-article:18474871 | pubmed:issn | 1091-6490 | lld:pubmed |
| pubmed-article:18474871 | pubmed:author | pubmed-author:FranssilaKaar... | lld:pubmed |
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| pubmed-article:18474871 | pubmed:author | pubmed-author:JazdzewskiKry... | lld:pubmed |
| pubmed-article:18474871 | pubmed:author | pubmed-author:MurrayElizabe... | lld:pubmed |
| pubmed-article:18474871 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:18474871 | pubmed:day | 20 | lld:pubmed |
| pubmed-article:18474871 | pubmed:volume | 105 | lld:pubmed |
| pubmed-article:18474871 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:18474871 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:18474871 | pubmed:pagination | 7269-74 | lld:pubmed |
| pubmed-article:18474871 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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| pubmed-article:18474871 | pubmed:year | 2008 | lld:pubmed |
| pubmed-article:18474871 | pubmed:articleTitle | Common SNP in pre-miR-146a decreases mature miR expression and predisposes to papillary thyroid carcinoma. | lld:pubmed |
| pubmed-article:18474871 | pubmed:affiliation | Human Cancer Genetics Program, Comprehensive Cancer Center, Ohio State University, 850 Biomedical Research Tower, 460 West 12th Avenue, Columbus, OH 43210, USA. | lld:pubmed |
| pubmed-article:18474871 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:18474871 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
| pubmed-article:18474871 | pubmed:publicationType | Research Support, N.I.H., Extramural | lld:pubmed |
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