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    Please use this identifier to cite or link to this item: http://ir.lib.ncu.edu.tw/handle/987654321/50797


    Title: Androgens as therapy for androgen receptor-positive castration-resistant prostate cancer
    Authors: Chuu,CP;Kokontis,JM;Hiipakka,RA;Fukuchi,J;Lin,HP;Lin,CY;Huo,C;Su,LC
    Contributors: 生命科學系
    Keywords: CELL-CYCLE ARREST;DEPRIVATION THERAPY;ATHYMIC MICE;TUMOR-GROWTH;TESTOSTERONE REPLACEMENT;CARDIOVASCULAR-DISEASE;GENE AMPLIFICATION;PROTEIN EXPRESSION;PROSPECTIVE TRIAL;LNCAP CELLS
    Date: 2011
    Issue Date: 2012-03-27 18:10:20 (UTC+8)
    Publisher: 國立中央大學
    Abstract: Prostate cancer is the most frequently diagnosed non-cutaneous tumor of men in Western countries. While surgery is often successful for organ-confined prostate cancer, androgen ablation therapy is the primary treatment for metastatic prostate cancer. However, this therapy is associated with several undesired side-effects, including increased risk of cardiovascular diseases. Shortening the period of androgen ablation therapy may benefit prostate cancer patients. Intermittent Androgen Deprivation therapy improves quality of life, reduces toxicity and medical costs, and delays disease progression in some patients. Cell culture and xenograft studies using androgen receptor (AR)-positive castration-resistant human prostate cancers cells (LNCaP, ARCaP, and PC-3 cells over-expressing AR) suggest that androgens may suppress the growth of AR-rich prostate cancer cells. Androgens cause growth inhibition and G1 cell cycle arrest in these cells by regulating c-Myc, Skp2, and p27(Kip) via AR. Higher dosages of testosterone cause greater growth inhibition of relapsed tumors. Manipulating androgen/AR signaling may therefore be a potential therapy for AR-positive advanced prostate cancer.
    Relation: JOURNAL OF BIOMEDICAL SCIENCE
    Appears in Collections:[生命科學系] 期刊論文

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