期刊
INTERNATIONAL JOURNAL OF BIOCHEMISTRY & CELL BIOLOGY
卷 39, 期 9, 页码 1562-1568出版社
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.biocel.2007.01.005
关键词
prostate cancer; androgen receptor
资金
- NCI NIH HHS [K01 CA094223, K01 CA094223-05] Funding Source: Medline
- NIA NIH HHS [R01 AG023145, R01 AG023145-03] Funding Source: Medline
- NATIONAL CANCER INSTITUTE [K01CA094223] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE ON AGING [R01AG023145] Funding Source: NIH RePORTER
Prostate cancer is the most common, non-dermatologic cancer in men. Since prostate cancer is highly associated with increased age, the incidence of this disease is expected to increase as the population ages. In its initial stages prostate cancer depends upon the actions of androgen, and androgen deprivation therapy induces tumor regression. Currently, androgen deprivation is achieved by either surgical or chemical androgen blockade. Unfortunately, nearly all prostate cancer patients develop tumors that grow despite androgen blockade and ultimately relapse. Many alterations in prostate cancer cells contribute to this state. Although chemotherapy induces short remissions in some patients, there are no curative therapies for metastatic disease. This review summarizes our current understanding in androgen signaling and the mechanisms that allow tumor cells to bypass androgen manipulation therapy. The identification of novel survival pathways and effector molecules that drive androgen independent growth is necessary to develop effective therapies for advanced prostate cancers. (c) 2007 Elsevier Ltd. All rights reserved.
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