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rdf:type |
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lifeskim:mentions |
umls-concept:C0017398,
umls-concept:C0037083,
umls-concept:C0087111,
umls-concept:C0334227,
umls-concept:C0346647,
umls-concept:C0599894,
umls-concept:C0679199,
umls-concept:C0871261,
umls-concept:C1521991,
umls-concept:C1704632,
umls-concept:C1706817,
umls-concept:C1710082,
umls-concept:C2911692
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pubmed:issue |
2
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pubmed:dateCreated |
2008-1-23
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pubmed:abstractText |
Pancreatic cancer is a deadly cancer with limited sensitivity to gemcitabine. Molecular targeting of critical signaling pathways [nuclear factor kappa-B (NF-kappaB), PI3K/AKT, and mitogen-activated protein kinase (MAPK)] in combination with gemcitabine may improve sensitivity. We hypothesize that pancreatic cancer cell genetics and signaling response to treatment correlate with efficacy of gemcitabine-based molecular targeting strategies.
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/2-(4-morpholinyl)-8-phenyl-4H-1-benz...,
http://linkedlifedata.com/resource/pubmed/chemical/Antimetabolites, Antineoplastic,
http://linkedlifedata.com/resource/pubmed/chemical/Antineoplastic Agents,
http://linkedlifedata.com/resource/pubmed/chemical/Chromones,
http://linkedlifedata.com/resource/pubmed/chemical/Curcumin,
http://linkedlifedata.com/resource/pubmed/chemical/Deoxycytidine,
http://linkedlifedata.com/resource/pubmed/chemical/Enzyme Inhibitors,
http://linkedlifedata.com/resource/pubmed/chemical/Morpholines,
http://linkedlifedata.com/resource/pubmed/chemical/NF-kappa B,
http://linkedlifedata.com/resource/pubmed/chemical/Proto-Oncogene Proteins c-akt,
http://linkedlifedata.com/resource/pubmed/chemical/gemcitabine
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pubmed:status |
MEDLINE
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pubmed:month |
Feb
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pubmed:issn |
1091-255X
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pubmed:author |
|
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pubmed:issnType |
Print
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pubmed:volume |
12
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
288-96
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pubmed:dateRevised |
2009-11-19
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pubmed:meshHeading |
pubmed-meshheading:18049840-Adenocarcinoma,
pubmed-meshheading:18049840-Antimetabolites, Antineoplastic,
pubmed-meshheading:18049840-Antineoplastic Agents,
pubmed-meshheading:18049840-Blotting, Western,
pubmed-meshheading:18049840-Cell Proliferation,
pubmed-meshheading:18049840-Chromones,
pubmed-meshheading:18049840-Curcumin,
pubmed-meshheading:18049840-Deoxycytidine,
pubmed-meshheading:18049840-Dose-Response Relationship, Drug,
pubmed-meshheading:18049840-Drug Synergism,
pubmed-meshheading:18049840-Drug Therapy, Combination,
pubmed-meshheading:18049840-Electrophoretic Mobility Shift Assay,
pubmed-meshheading:18049840-Enzyme Inhibitors,
pubmed-meshheading:18049840-Humans,
pubmed-meshheading:18049840-MAP Kinase Signaling System,
pubmed-meshheading:18049840-Morpholines,
pubmed-meshheading:18049840-NF-kappa B,
pubmed-meshheading:18049840-Pancreatic Neoplasms,
pubmed-meshheading:18049840-Proto-Oncogene Proteins c-akt,
pubmed-meshheading:18049840-Tumor Cells, Cultured
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pubmed:year |
2008
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pubmed:articleTitle |
Pancreatic cancer cell genetics and signaling response to treatment correlate with efficacy of gemcitabine-based molecular targeting strategies.
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pubmed:affiliation |
Department of Surgery, Indiana University School of Medicine, Indianapolis, IN 46202, USA.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, Non-P.H.S.,
Research Support, Non-U.S. Gov't
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