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    Testosterone, prolactin, and oncogenic regulation of the prostate gland. A new concept: Testosterone-independent malignancy is the development of prolactin-dependent malignancy!

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    Author
    Costello, L.C.
    Franklin, R.B.
    Date
    2018
    Journal
    Oncology Reviews
    Publisher
    Page Press Publications
    Type
    Review
    
    Metadata
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    See at
    https://dx.doi.org/10.4081/oncol.2018.356
    Abstract
    Hormone-independent malignancy is a major issue of morbidity and deaths that confronts prostate cancer. Despite decades of research, the oncogenic and hormonal implications in the development and progression of prostate malignancy remain mostly speculative. This is largely due to the absence and/or lack of consideration by contemporary clinicians and biomedical investigators regarding the established implications of the co-regulation of testosterone and prolactin in the development, maintenance, metabolism and functions of the prostate gland. Especially relevant is the major metabolic function of production of high levels of citrate by the peripheral zone acinar epithelial cells. Citrate production, along with growth and proliferation by these cells, is regulated by co-existing testosterone and prolactin signaling pathways; and by the oncogenic down-regulation of ZIP1 transporter/zinc/citrate in the development of malignancy. These relationships had not been considered in the issues of hormone-dependent malignancy. This review provides the relevant background that has established the dual role of testosterone and prolactin regulation of the prostate gland; which is essential to address the implications in the oncogenic development and progression of hormone-dependent malignancy. The oncogenic factor along with testosterone-dependent and prolactin-dependent relationships leads to the plausible concept that androgen ablation for the treatment of testosteronedependent malignancy results in the development of prolactindependent malignancy; which is testosterone-independent malignancy. Consequently, both testosterone ablation and prolactin ablation are required to prevent and/or abort terminal hormonedependent prostate cancer. � Copyright L.C. Costello and R.B. Franklin., 2018.
    Sponsors
    Funding: the studies of LCC and RBF presented in this review were supported in part by NIH grants CA79903, DK076783 and DK42839 and AR064808.
    Keyword
    Citrate-producing acinar cells. n-
    Hormone-dependent malignancy
    Prolactin and testosterone
    Prostate cancer
    Identifier to cite or link to this item
    https://www.scopus.com/inward/record.uri?eid=2-s2.0-85052022438&doi=10.4081%2foncol.2018.356&partnerID=40&md5=7d8e41e7fa9441b9de30895bd1569abf; http://hdl.handle.net/10713/8783
    ae974a485f413a2113503eed53cd6c53
    10.4081/oncol.2018.356
    Scopus Count
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