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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
24
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pubmed:dateCreated |
2004-12-29
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pubmed:abstractText |
As kinase inhibitors transition from the laboratory to patients, it is imperative to develop biomarkers that can be used in the clinic. The primary objectives are to identify patients most likely to benefit from molecularly targeted therapies and to document modulation of the drug target. Constitutive activation of the phosphoinositide 3-kinase (PI3K) pathway and its downstream effectors, as a result of PTEN loss or by other mechanisms, occurs in a high proportion of prostate cancers, making it an ideal template for the design of clinical trials involving PI3K pathway inhibitors. Prostate cancers also present unique organ-specific challenges, in that tumors are heterogeneous and diagnostic tissue is extremely limited.
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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/AKT1 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Antibodies, Monoclonal,
http://linkedlifedata.com/resource/pubmed/chemical/PTEN Phosphohydrolase,
http://linkedlifedata.com/resource/pubmed/chemical/PTEN protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Phosphatidylinositol 3-Kinases,
http://linkedlifedata.com/resource/pubmed/chemical/Phosphoric Monoester Hydrolases,
http://linkedlifedata.com/resource/pubmed/chemical/Protein-Serine-Threonine Kinases,
http://linkedlifedata.com/resource/pubmed/chemical/Proto-Oncogene Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Proto-Oncogene Proteins c-akt,
http://linkedlifedata.com/resource/pubmed/chemical/Ribosomal Protein S6 Kinases,
http://linkedlifedata.com/resource/pubmed/chemical/Tumor Suppressor Proteins
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pubmed:status |
MEDLINE
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pubmed:month |
Dec
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pubmed:issn |
1078-0432
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:day |
15
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pubmed:volume |
10
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
8351-6
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pubmed:dateRevised |
2010-11-18
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pubmed:meshHeading |
pubmed-meshheading:15623612-Antibodies, Monoclonal,
pubmed-meshheading:15623612-Down-Regulation,
pubmed-meshheading:15623612-Enzyme Activation,
pubmed-meshheading:15623612-Gene Expression Regulation, Enzymologic,
pubmed-meshheading:15623612-Gene Expression Regulation, Neoplastic,
pubmed-meshheading:15623612-Humans,
pubmed-meshheading:15623612-Male,
pubmed-meshheading:15623612-PTEN Phosphohydrolase,
pubmed-meshheading:15623612-Phosphatidylinositol 3-Kinases,
pubmed-meshheading:15623612-Phosphoric Monoester Hydrolases,
pubmed-meshheading:15623612-Phosphorylation,
pubmed-meshheading:15623612-Prostate,
pubmed-meshheading:15623612-Prostatic Neoplasms,
pubmed-meshheading:15623612-Protein-Serine-Threonine Kinases,
pubmed-meshheading:15623612-Proto-Oncogene Proteins,
pubmed-meshheading:15623612-Proto-Oncogene Proteins c-akt,
pubmed-meshheading:15623612-Ribosomal Protein S6 Kinases,
pubmed-meshheading:15623612-Signal Transduction,
pubmed-meshheading:15623612-Tumor Suppressor Proteins
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pubmed:year |
2004
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pubmed:articleTitle |
Antibody-based profiling of the phosphoinositide 3-kinase pathway in clinical prostate cancer.
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pubmed:affiliation |
Department of Pathology and Laboratory Medicine, David Geffen School of Medicine, University of California-Los Angeles, Los Angeles, California 90095, USA.
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pubmed:publicationType |
Journal Article,
Comparative Study,
Research Support, U.S. Gov't, P.H.S.,
Research Support, U.S. Gov't, Non-P.H.S.,
Research Support, Non-U.S. Gov't
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