Source:http://linkedlifedata.com/resource/pubmed/id/20514414
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
1
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pubmed:dateCreated |
2010-6-1
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pubmed:abstractText |
In previous research, we focused on the discovery of K-ras biomarkers, and effects of genotoxic carcinogens on their expression were investigated in this study. It is well-known that mutated K-ras gene is involved in approximately 30% of human cancers such as lung cancer. To search for K-ras oncogene-induced modulators in lung tissues of K-ras transgenic mice, we analyzed K-ras-specific genes and proteins related to cancer development, signal transduction, inflammation as well as tumor suppression in a previous study. In this study, we investigated the modulating effects of genotoxic carcinogen treatment on expression of K-ras-dependent modulated genes and proteins in lung tissues of K-ras Tg mice. In order to evaluate candidate K-ras markers modulated by genotoxic stress and to investigate whether a genotoxic carcinogen would enhance or inhibit carcinogenesis in lung tissues of the K-ras Tg mice, the anti-cancer drug melphalan was intraperitoneally injected into K-ras Tg mice every two days for four weeks. RT-qPCR and proteomics analyses were performed in order to confirm whether K-ras-specific biomarkers would be modulated by melphalan treatment in K-ras Tg mice. The decreased adenomas were histopathologically observed and K-ras expression was suppressed in melphalan-treated K-ras Tg mice. Melphalan also recovered the expression of K-ras-dependent modulated biomarkers. These results suggest that melphalan inhibits carcinogenesis via modulating K-ras-specific genes and proteins expressed in the lung tissues of K-ras Tg mice.
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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 |
Jul
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pubmed:issn |
1791-2423
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pubmed:author |
pubmed-author:ChoiHeesookH,
pubmed-author:KimEunjinE,
pubmed-author:KimHeejongH,
pubmed-author:KimJinmanJ,
pubmed-author:LeeSojungS,
pubmed-author:ParkSue-NieSN,
pubmed-author:ParkYoung-HoYH,
pubmed-author:SheenYhunyhongY,
pubmed-author:YoonDo-YoungDY,
pubmed-author:YoonSeok-JooSJ,
pubmed-author:YuDae-YeulDY
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pubmed:issnType |
Electronic
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pubmed:volume |
37
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
219-28
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pubmed:meshHeading |
pubmed-meshheading:20514414-Adenoma,
pubmed-meshheading:20514414-Animals,
pubmed-meshheading:20514414-Antineoplastic Agents, Alkylating,
pubmed-meshheading:20514414-Cell Proliferation,
pubmed-meshheading:20514414-Cluster Analysis,
pubmed-meshheading:20514414-Female,
pubmed-meshheading:20514414-Gene Expression Profiling,
pubmed-meshheading:20514414-Gene Expression Regulation, Neoplastic,
pubmed-meshheading:20514414-Genes, ras,
pubmed-meshheading:20514414-Humans,
pubmed-meshheading:20514414-Lung Neoplasms,
pubmed-meshheading:20514414-Male,
pubmed-meshheading:20514414-Melphalan,
pubmed-meshheading:20514414-Mice,
pubmed-meshheading:20514414-Mice, Transgenic,
pubmed-meshheading:20514414-Models, Biological,
pubmed-meshheading:20514414-Tumor Markers, Biological
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pubmed:year |
2010
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pubmed:articleTitle |
Melphalan inhibits adenoma development through modulating the expression of K-ras-specific markers in K-ras Tg mice.
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pubmed:affiliation |
Department of Bioscience and Biotechnology, Bio/Molecular Informatics Center, Konkuk University, Hwayang-dong 1, Gwangjin-gu, Seoul 143-701, Korea.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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