Abstract
Prostate cancer remains a leading cause of death in men despite increased capacity to diagnose at earlier stages. After prostate cancer has become hormone independent, which often occurs after hormonal ablation therapies, it is difficult to effectively treat. Prostate cancer may arise from mutations and dysregulation of various genes involved in regulation signal transduction (e.g., PTEN, Akt, etc.,) and the cell cycle (e.g., p53, p21(Cip1), p27(Kip1), Rb, etc.,). This review focuses on the aberrant interactions of signal transduction and cell cycle genes products and how they can contribute to prostate cancer and alter therapeutic effectiveness.
Publication types
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Research Support, N.I.H., Extramural
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Research Support, Non-U.S. Gov't
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Review
MeSH terms
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Antineoplastic Agents / therapeutic use
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Carcinoma / drug therapy
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Carcinoma / metabolism
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Carcinoma / therapy*
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Cell Cycle Proteins / antagonists & inhibitors*
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Cell Cycle Proteins / physiology
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Drug Resistance, Neoplasm
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Humans
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MAP Kinase Signaling System / drug effects
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Male
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Prostatic Neoplasms / drug therapy
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Prostatic Neoplasms / metabolism
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Prostatic Neoplasms / therapy*
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Proto-Oncogene Proteins c-akt / antagonists & inhibitors
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Signal Transduction / drug effects*
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Tumor Suppressor Protein p53 / antagonists & inhibitors
Substances
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Antineoplastic Agents
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Cell Cycle Proteins
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Tumor Suppressor Protein p53
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Proto-Oncogene Proteins c-akt