Source:http://linkedlifedata.com/resource/pubmed/id/17270245
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
4
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pubmed:dateCreated |
2007-3-19
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pubmed:abstractText |
A radiation etiology is well known in thyroid carcinogenesis. RET oncogene rearrangement is the most common oncogenic alteration in Chernobyl-related papillary thyroid cancer (PTC). To find the characteristic alteration associated with RET rearrangements in radiation-induced thyroid cancers, we analyzed the RET oncogene by fluorescence in situ hybridization. The fluorescence in situ hybridization technique has the possibility of detecting RET rearrangements at a single-cell level regardless of the specific fusion partner involved and directly reveals RET copy number on a per-cell basis. Our study demonstrated RET amplification in all 3 cases of radiation-associated thyroid cancers but not in sporadic well-differentiated PTC (n = 11). Furthermore, RET amplification was observed in all 6 cases of sporadic anaplastic thyroid cancers (ATCs). The frequency of RET amplification-positive cells was higher in ATC (7.2%-24.1%) than in PTC (1.5%-2.7%). The highest frequency of RET amplification-positive cells was observed among ATC cases with a strong p53 immunoreactivity. In conclusion, we found RET amplification, which is a rare oncogenic aberration, in thyroid cancer. This report is the first one to suggest the presence of RET amplification in PTC and ATC. RET amplification was correlated with radiation-associated, high-grade malignant potency, and p53 accumulation, suggesting genomic instability. RET amplification might be induced by a high level of genomic instability in connection with progression of thyroid carcinogenesis and, subsequently, be associated with radiation-induced and/or high-grade malignant cases.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
Apr
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pubmed:issn |
0046-8177
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
38
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
621-8
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pubmed:dateRevised |
2009-11-19
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pubmed:meshHeading |
pubmed-meshheading:17270245-Adult,
pubmed-meshheading:17270245-Aged,
pubmed-meshheading:17270245-Aged, 80 and over,
pubmed-meshheading:17270245-Carcinoma, Papillary,
pubmed-meshheading:17270245-Female,
pubmed-meshheading:17270245-Gene Amplification,
pubmed-meshheading:17270245-Humans,
pubmed-meshheading:17270245-In Situ Hybridization, Fluorescence,
pubmed-meshheading:17270245-Male,
pubmed-meshheading:17270245-Middle Aged,
pubmed-meshheading:17270245-Neoplasms, Radiation-Induced,
pubmed-meshheading:17270245-Proto-Oncogene Proteins c-ret,
pubmed-meshheading:17270245-Reverse Transcriptase Polymerase Chain Reaction,
pubmed-meshheading:17270245-Thyroid Neoplasms
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pubmed:year |
2007
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pubmed:articleTitle |
RET oncogene amplification in thyroid cancer: correlations with radiation-associated and high-grade malignancy.
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pubmed:affiliation |
Tissue and Histopathology Section, Division of Scientific Data Registry, Atomic Bomb Disease Institute, Nagasaki University Graduate School of Biomedical Sciences, Nagasaki 852-8523, Japan. moemoe@nagasaki-u.ac.jp
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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