Abstract
The murine Pten prostate cancer model described in this study recapitulates the disease progression seen in humans: initiation of prostate cancer with prostatic intraepithelial neoplasia (PIN), followed by progression to invasive adenocarcinoma, and subsequent metastasis with defined kinetics. Furthermore, while Pten null prostate cancers regress after androgen ablation, they are capable of proliferating in the absence of androgen. Global assessment of molecular changes caused by homozygous Pten deletion identified key genes known to be relevant to human prostate cancer, including those "signature" genes associated with human cancer metastasis. This murine prostate cancer model provides a unique tool for both exploring the molecular mechanism underlying prostate cancer and for development of new targeted therapies.
Publication types
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, Non-P.H.S.
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Animals
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Cell Division
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Gene Deletion*
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Gene Expression Profiling
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Humans
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Male
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Mice
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Mice, Knockout
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Neoplasm Metastasis
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PTEN Phosphohydrolase
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Phosphoric Monoester Hydrolases / genetics*
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Prostatic Hyperplasia / genetics*
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Prostatic Hyperplasia / pathology
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Prostatic Intraepithelial Neoplasia / genetics
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Prostatic Intraepithelial Neoplasia / pathology
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Prostatic Neoplasms / genetics*
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Prostatic Neoplasms / pathology
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Protein Serine-Threonine Kinases*
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Proto-Oncogene Proteins / genetics
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Proto-Oncogene Proteins c-akt
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Tumor Suppressor Proteins / genetics*
Substances
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Proto-Oncogene Proteins
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Tumor Suppressor Proteins
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Protein Serine-Threonine Kinases
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Proto-Oncogene Proteins c-akt
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Phosphoric Monoester Hydrolases
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PTEN Phosphohydrolase
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PTEN protein, human