Source:http://linkedlifedata.com/resource/pubmed/id/14678517
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
6
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pubmed:dateCreated |
2003-12-17
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pubmed:abstractText |
An association between common chromosome fragile sites and frequent chromosomal deletions in cancer has been observed and led to the hypothesis that genes at fragile sites may play a role in tumor development. In 1996, the human fragile histidine triad gene, FHIT, was identified by positional cloning at 3p14.2, a chromosomal region spanning the carcinogen-sensitive, common fragile site FRA3B. FHIT gene is lost and inactivated in a large fraction of tumors and early in carcinogenesis. A group of ancestral cancerous cells that carry FHIT alterations, expanding in succeeding cell generations, exhibits a hallmark in carcinogenesis scenario.
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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:issn |
1359-4117
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
3
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
291-6
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pubmed:dateRevised |
2006-11-15
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pubmed:meshHeading | |
pubmed:articleTitle |
Alteration of the fragile histidine triad gene early in carcinogenesis: an update.
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pubmed:affiliation |
Center for Molecular Medicine, Jichi Medical School, Tochigi, Japan. hishii@ms.jichi.ac.jp
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pubmed:publicationType |
Journal Article,
Review,
Research Support, Non-U.S. Gov't
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