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Comment
. 2017 Sep 17;16(18):1639-1640.
doi: 10.1080/15384101.2017.1360645. Epub 2017 Aug 18.

Rationale for bipolar androgen therapy (BAT) for metastatic prostate cancer

John T Isaacs  1 , W Nathaniel Brennen  1 , Samuel R Denmeade  1
Affiliations
Comment

Rationale for bipolar androgen therapy (BAT) for metastatic prostate cancer

John T Isaacs et al. Cell Cycle. .
No abstract available

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Figures

Figure 1.
Figure 1.
Overview of role and timing of Androgen Receptor (AR) in licensing DNA Replication in metastatic Castration Resistant Prostate Cancer Cells. For full details see reference 4. When androgen is low during androgen ablation, AR is degraded appropriately during late mitosis such that mitotic figures (denoted by arrows in upper right panel) do not contain detectable AR protein as determined via immunohistochemical staining. When androgen is too high one day following injection with a high pharmacological level of testosterone, AR is now detectable in mitotic figures (denoted by arrows in lower right panel) and in the next cell cycle, this cell will die due to its inability to relicense its DNA for S-phase replication.
See this image and copyright information in PMC

Comment on

References

    1. Schweizer MT, Antonarakis ES, Wang H, Ajiboye AS, Spitz A, Cao H, Luo J, Haffner MC, Yegnasubramanian S, Carducci MA, Eisenberger MA, Isaacs JT, Denmeade SR.. Effect of bipolar androgen therapy for asymptomatic men with castration-resistant prostate cancer: results from a pilot clinical study. Sci Transl Med. 2015;7:269ra2. doi: 10.1126/scitranslmed. PMID:25568070 - DOI - PMC - PubMed
    1. Litvinov IV, Vander Griend DJ, Antony L, Dalrymple S, De Marzo AM, Drake CG, Isaacs JT. Androgen receptor as a licensing factor for DNA replication in androgen-sensitive prostate cancer cells. Proc Natl Acad Sci. USA. 2006;103:15085−90. doi: 10.1073/pnas.0603057103. PMID:17015840 - DOI - PMC - PubMed
    1. Vander Griend DJ, Litvinov IV, Isaacs JT. Stabilizing androgen receptor in mitosis inhibits prostate cancer proliferation. Cell Cycle. 2007;6:647−51. doi: 10.4161/cc.6.6.4028. PMID: 17387277 - DOI - PubMed
    1. D'Antonio JM, Vander Griend DJ, Isaacs JT. DNA licensing as a novel androgen receptor mediated therapeutic target for prostate cancer. Endocr Relat Cancer. 2009;16:325−32. doi: 10.1677/ERC-08-0205. PMID:19240183 - DOI - PMC - PubMed
    1. Isaacs JT, D'Antonio JM, Chen S, Antony L, Dalrymple SP, Ndikuyeze GH, Luo J, Denmeade SR. Adaptive auto-regulation of androgen receptor provides a paradigm shifting rationale for bipolar androgen therapy (BAT) for castrate resistant human prostate cancer. Prostate. 2012;72:1491−505. doi: 10.1002/pros.22504. PMID:22396319 - DOI - PMC - PubMed

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