| pubmed-article:19018267 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:19018267 | lifeskim:mentions | umls-concept:C1140680 | lld:lifeskim |
| pubmed-article:19018267 | lifeskim:mentions | umls-concept:C0026882 | lld:lifeskim |
| pubmed-article:19018267 | lifeskim:mentions | umls-concept:C0021467 | lld:lifeskim |
| pubmed-article:19018267 | lifeskim:mentions | umls-concept:C2698872 | lld:lifeskim |
| pubmed-article:19018267 | lifeskim:mentions | umls-concept:C0312418 | lld:lifeskim |
| pubmed-article:19018267 | lifeskim:mentions | umls-concept:C0449438 | lld:lifeskim |
| pubmed-article:19018267 | lifeskim:mentions | umls-concept:C0812241 | lld:lifeskim |
| pubmed-article:19018267 | lifeskim:mentions | umls-concept:C1537502 | lld:lifeskim |
| pubmed-article:19018267 | lifeskim:mentions | umls-concept:C0752313 | lld:lifeskim |
| pubmed-article:19018267 | lifeskim:mentions | umls-concept:C0021469 | lld:lifeskim |
| pubmed-article:19018267 | lifeskim:mentions | umls-concept:C0036667 | lld:lifeskim |
| pubmed-article:19018267 | pubmed:issue | 12 | lld:pubmed |
| pubmed-article:19018267 | pubmed:dateCreated | 2008-12-16 | lld:pubmed |
| pubmed-article:19018267 | pubmed:abstractText | This study examined the status of KRAS and BRAF mutations, in relation to extracellular signal-regulated protein kinase (ERK) activation in 58 ovarian carcinomas to clarify the clinicopathological and prognostic significance of KRAS/BRAF mutations. Somatic mutations of either KRAS or BRAF were identified in 12 (20.6%) out of 58 ovarian carcinomas. The frequency of KRAS/BRAF mutations in conventional serous high-grade carcinomas (4.0% : 1/25) was significantly lower than that in the other histological type (32.3% : 10/31). Phosphorylated ERK1/2 (p-ERK1/2) expression was identified in 18 (38.2%) out of 45 ovarian carcinomas. KRAS/BRAF mutation was significantly correlated with International Federation of Gynecology and Obstetrics (FIGO) stage I, II (P<0.001), and p-ERK1/2 (P<0.001). No significant correlations between KRAS/BRAF mutations or p-ERK1/2 expression and overall survival were found in patients with ovarian carcinoma treated with platinum and taxane chemotherapy (P=0.2460, P=0.9339, respectively). Next, to clarify the roles of ERK1/2 activation in ovarian cancers harbouring KRAS or BRAF mutations, we inactivated ERK1/2 in ovarian cancer cells using CI-1040. Cl-1040 is a compound that selectively inhibits MAP kinase kinase (MEK), an upstream regulator of ERK1/2, and thus prevents ERK1/2 activation. Profound growth inhibition and apoptosis were observed in CI-1040-treated cancer cells with mutations in either KRAS or BRAF in comparison with the ovarian cancer cells containing wild-type sequences. This was evident in both in vitro and in vivo studies. The findings in this study indicate that an activated ERK1/2 pathway is critical to tumour growth and survival of ovarian cancers with KRAS or BRAF mutations. Furthermore, they suggest that the CI-1040-induced phenotypes depend on the mutational status of KRAS and BRAF in ovarian cancers. Therefore, ovarian cancer patients with KRAS or BRAF mutations may benefit from CI-1040 treatment. | lld:pubmed |
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| pubmed-article:19018267 | pubmed:language | eng | lld:pubmed |
| pubmed-article:19018267 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:19018267 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:19018267 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:19018267 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:19018267 | pubmed:month | Dec | lld:pubmed |
| pubmed-article:19018267 | pubmed:issn | 1532-1827 | lld:pubmed |
| pubmed-article:19018267 | pubmed:author | pubmed-author:NakayamaKK | lld:pubmed |
| pubmed-article:19018267 | pubmed:author | pubmed-author:MiyazakiKK | lld:pubmed |
| pubmed-article:19018267 | pubmed:author | pubmed-author:NakayamaNN | lld:pubmed |
| pubmed-article:19018267 | pubmed:author | pubmed-author:IshibashiMM | lld:pubmed |
| pubmed-article:19018267 | pubmed:author | pubmed-author:IidaKK | lld:pubmed |
| pubmed-article:19018267 | pubmed:author | pubmed-author:FukumotoMM | lld:pubmed |
| pubmed-article:19018267 | pubmed:author | pubmed-author:KatagiriAA | lld:pubmed |
| pubmed-article:19018267 | pubmed:author | pubmed-author:YeasminSS | lld:pubmed |
| pubmed-article:19018267 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:19018267 | pubmed:day | 16 | lld:pubmed |
| pubmed-article:19018267 | pubmed:volume | 99 | lld:pubmed |
| pubmed-article:19018267 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:19018267 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:19018267 | pubmed:pagination | 2020-8 | lld:pubmed |
| pubmed-article:19018267 | pubmed:dateRevised | 2010-9-23 | lld:pubmed |
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