| Comparison of ras-responsive gene enhancers in pancreatic tumor cells that express either wild-type or mutant K-ras. | |
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MedLine Citation:
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PMID: 19254697 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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There is a pressing need for new therapies to treat pancreatic cancer. In principle, this could be achieved by taking advantage of signaling pathways that are active in tumor, but not normal, cells. The work described in this study set out to determine whether the activities of three enhancers, which have been reported to be highly responsive to activated ras, differ in pancreatic tumor cells that express wild-type versus constitutively active mutant forms of K-ras. Surprisingly, the three enhancers are active in four different pancreatic tumor cell lines that express either normal K-ras gene or mutant K-ras. Moreover, reducing the concentration of serum in the growth medium from 10% to 0.5% had relatively little effect on the strength of any of the enhancers, although it drastically affected cell growth. Importantly, our studies also indicate that MEK is active in pancreatic tumor cells that possess wild-type as well as mutant K-ras, even when cultured in medium that severely limits cell growth. These findings support the hypothesis that the Ras/Raf/Mek/Erk pathway may be constitutively active even in pancreatic tumor cells that express wild-type K-ras. |
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Authors:
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Phillip J Wilder; Harini Chakravarthy; Michael A Hollingsworth; Angie Rizzino |
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Publication Detail:
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Type: Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't Date: 2009-02-28 |
Journal Detail:
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Title: Biochemical and biophysical research communications Volume: 381 ISSN: 1090-2104 ISO Abbreviation: Biochem. Biophys. Res. Commun. Publication Date: 2009 Apr |
Date Detail:
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Created Date: 2009-03-30 Completed Date: 2009-04-28 Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 0372516 Medline TA: Biochem Biophys Res Commun Country: United States |
Other Details:
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Languages: eng Pagination: 706-11 Citation Subset: IM |
Affiliation:
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Eppley Institute for Research in Cancer and Allied Diseases, University of Nebraska Medical Center, Omaha, 68198-6805, USA. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Culture Media Enhancer Elements, Genetic / genetics* Humans Mutation Pancreatic Neoplasms / genetics* Proto-Oncogene Proteins p21(ras) / genetics* Signal Transduction ras Proteins / metabolism* |
| Grant Support | |
ID/Acronym/Agency:
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CA36727/CA/NCI NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Culture Media; EC 3.6.5.2/Proto-Oncogene Proteins p21(ras); EC 3.6.5.2/ras Proteins |
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