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A NEW CAUSE AND POSSIBLE TREATMENT FOR PROSTATE CANCER
Author(s) -
Lardy Henry A.,
Miyamoto H.,
Marwah P.,
Marwah A.,
Chang C.
Publication year - 2006
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.20.4.a464-b
Subject(s) - prostate cancer , antiandrogens , androstenediol , androgen receptor , testosterone (patch) , androgen , dihydrotestosterone , medicine , prostate , endocrinology , antiandrogen , cancer research , cancer , hormone , androstenedione
Normal growth of the prostate and the malignant growth of prostate cancer (CaP) are dependent on androgen (e.g. testosterone) stimulation. Consequently, treatment of CaP by androgen ablation (administering antiandrogens or castration) stops cancer growth but, after a period of remission, growth is renewed and is not susceptible to antiandrogen therapy. This phase of the disease is termed “androgen‐independent”. It is the androgen‐independent growth that must be blocked to conquer CaP. In 1998 we found that androstenediol (Adiol) is an androgen and that its effects are not inhibited by the drugs currently used to treat CaP. Adiol is produced in the adrenals and accumulates in the prostate to concentrations that maximally transactivate the androgen receptor. In a search for inhibitors of Adiol we have made many new steroids; three are effective vs both Adiol and dihydrotestosterone. ADEK is the most suitable for therapy. It is non‐toxic in rats and inhibits growth of the prostate and seminal vesicles. Supported by the authors (U.W.) and the George Whipple Professor Endowment (U.R.).