| pubmed-article:10951588 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:10951588 | lifeskim:mentions | umls-concept:C0007634 | lld:lifeskim |
| pubmed-article:10951588 | lifeskim:mentions | umls-concept:C0034678 | lld:lifeskim |
| pubmed-article:10951588 | lifeskim:mentions | umls-concept:C0040132 | lld:lifeskim |
| pubmed-article:10951588 | lifeskim:mentions | umls-concept:C0752312 | lld:lifeskim |
| pubmed-article:10951588 | lifeskim:mentions | umls-concept:C0919532 | lld:lifeskim |
| pubmed-article:10951588 | lifeskim:mentions | umls-concept:C1370600 | lld:lifeskim |
| pubmed-article:10951588 | lifeskim:mentions | umls-concept:C1704259 | lld:lifeskim |
| pubmed-article:10951588 | lifeskim:mentions | umls-concept:C1705987 | lld:lifeskim |
| pubmed-article:10951588 | lifeskim:mentions | umls-concept:C0205263 | lld:lifeskim |
| pubmed-article:10951588 | pubmed:issue | 34 | lld:pubmed |
| pubmed-article:10951588 | pubmed:dateCreated | 2000-8-31 | lld:pubmed |
| pubmed-article:10951588 | pubmed:abstractText | Activating mutations of RAS are thought to be early events in the evolution of thyroid follicular neoplasms. We used a doxycycline-inducible expression system to explore the acute effects of H-RAS12 on genomic stability in thyroid PCCL3 cells. At 2-3 days (first or second cell cycle) there was a significant increase in the frequency of micronucleation. Treatment of cells with YVAD-CHO inhibited RAS-induced apoptosis, but had no effect on micronucleation. The effects of H-RAS(V12) were mediated by activation of MAPK, as treatment with PD98059 at concentrations verified to selectively inhibit MEK1 reduced the frequency of prevalence of cells with micronuclei. In addition, doxycycline-inducible expression of a constitutively active MEK1, but not of a mutant RAC1, mimicked the effects of H-RAS(V12). The effects of H-RAS(V12) on genome destabilization were apparent even though the sequence of p53 in PCCL3 cells was confirmed to be wild-type. Acute activation of H-RAS(V12) evoked a proportional increase in both CREST negative and CREST positive micronuclei, indicating that both clastogenic and aneugenic effects were involved. H-RAS(V12) and activated MEK1 also induced centrosome amplification, and chromosome misalignment. Evidence that acute expression of constitutively activated RAS destabilizes the genome of PCCL3 cells is consistent with a mode of tumor initiation in which this oncogene promotes phenotypic progression by predisposing to large scale genomic abnormalities. | lld:pubmed |
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| pubmed-article:10951588 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:10951588 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:10951588 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:10951588 | pubmed:month | Aug | lld:pubmed |
| pubmed-article:10951588 | pubmed:issn | 0950-9232 | lld:pubmed |
| pubmed-article:10951588 | pubmed:author | pubmed-author:WangJJ | lld:pubmed |
| pubmed-article:10951588 | pubmed:author | pubmed-author:StambrookP... | lld:pubmed |
| pubmed-article:10951588 | pubmed:author | pubmed-author:FabioG PGP | lld:pubmed |
| pubmed-article:10951588 | pubmed:author | pubmed-author:EliseiRR | lld:pubmed |
| pubmed-article:10951588 | pubmed:author | pubmed-author:ShirokawaJ... | lld:pubmed |
| pubmed-article:10951588 | pubmed:author | pubmed-author:OuyangBB | lld:pubmed |
| pubmed-article:10951588 | pubmed:author | pubmed-author:KnaufJ AJA | lld:pubmed |
| pubmed-article:10951588 | pubmed:author | pubmed-author:SaavedraH IHI | lld:pubmed |
| pubmed-article:10951588 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:10951588 | pubmed:day | 10 | lld:pubmed |
| pubmed-article:10951588 | pubmed:volume | 19 | lld:pubmed |
| pubmed-article:10951588 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:10951588 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:10951588 | pubmed:pagination | 3948-54 | lld:pubmed |
| pubmed-article:10951588 | pubmed:dateRevised | 2009-11-19 | lld:pubmed |
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| pubmed-article:10951588 | pubmed:year | 2000 | lld:pubmed |
| pubmed-article:10951588 | pubmed:articleTitle | The RAS oncogene induces genomic instability in thyroid PCCL3 cells via the MAPK pathway. | lld:pubmed |
| pubmed-article:10951588 | pubmed:affiliation | Division of Endocrinology and Metabolism, University of Cincinnati College of Medicine, Ohio 45267, USA. | lld:pubmed |
| pubmed-article:10951588 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:10951588 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
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