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Christos C Zouboulis – One of the best experts on this subject based on the ideXlab platform.

  • Is There a Role for Antiandrogen Therapy for Hidradenitis Suppurativa? A Systematic Review of Published Data
    American Journal of Clinical Dermatology, 2019
    Co-Authors: Georgios Nikolakis, Athanassios Kyrgidis, Christos C Zouboulis

    Abstract:

    Background Hidradenitis suppurativa/acne inversa is a disease with deep-seated chronic painful nodules, abscesses, and draining sinus tracts, which manifests on the apocrine gland-rich skin areas of the body. Observational findings demonstrate that the disease usually appears after puberty, exhibits pre-menstrual flares in women, improves in pregnancy, and worsens post-partum, which indicates a role of hormones and particularly of androgens in its pathophysiology. Because increased androgen levels in serum have not been widely reported, an end-organ androgen hypersensitivity has been postulated. Objective The aim of this systematic review was to identify and present evidence for Antiandrogen therapeutic options for the treatment of hidradenitis suppurativa/acne inversa. Methods A literature search was conducted in different medical electronic databases using the keywords “hidradenitis”, “suppurativa”, “acne inversa”, and “Antiandrogen” on 1 December, 2018. The main therapeutic options were subsequently used as separate keywords with the disease terms in a separate search. Results The main therapeutic options yielded were cyproterone acetate, spironolactone, finasteride, and metformin. One randomized controlled crossover trial and seven case series were identified following use of a standard extraction form for eligibility. Conclusion The existing studies do not allow a robust evidence-based recommendation for the use of Antiandrogens in the treatment of hidradenitis suppurativa/acne inversa. Further randomized controlled trials are needed to define the role of hormonal treatment as an alternative or concomitant therapy together with antibiotics or biologics.

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  • is there a role for Antiandrogen therapy for hidradenitis suppurativa a systematic review of published data
    American Journal of Clinical Dermatology, 2019
    Co-Authors: Georgios Nikolakis, Athanassios Kyrgidis, Christos C Zouboulis

    Abstract:

    Hidradenitis suppurativa/acne inversa is a disease with deep-seated chronic painful nodules, abscesses, and draining sinus tracts, which manifests on the apocrine gland-rich skin areas of the body. Observational findings demonstrate that the disease usually appears after puberty, exhibits pre-menstrual flares in women, improves in pregnancy, and worsens post-partum, which indicates a role of hormones and particularly of androgens in its pathophysiology. Because increased androgen levels in serum have not been widely reported, an end-organ androgen hypersensitivity has been postulated. The aim of this systematic review was to identify and present evidence for Antiandrogen therapeutic options for the treatment of hidradenitis suppurativa/acne inversa. A literature search was conducted in different medical electronic databases using the keywords “hidradenitis”, “suppurativa”, “acne inversa”, and “Antiandrogen” on 1 December, 2018. The main therapeutic options were subsequently used as separate keywords with the disease terms in a separate search. The main therapeutic options yielded were cyproterone acetate, spironolactone, finasteride, and metformin. One randomized controlled crossover trial and seven case series were identified following use of a standard extraction form for eligibility. The existing studies do not allow a robust evidence-based recommendation for the use of Antiandrogens in the treatment of hidradenitis suppurativa/acne inversa. Further randomized controlled trials are needed to define the role of hormonal treatment as an alternative or concomitant therapy together with antibiotics or biologics.

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  • Hormonal Antiandrogens in acne treatment
    Journal der Deutschen Dermatologischen Gesellschaft = Journal of the German Society of Dermatology : JDDG, 2010
    Co-Authors: Christos C Zouboulis, Thomas Rabe

    Abstract:

    An enhanced sebaceous gland activity with production of proinflammtory sebaceous lipids belongs to the major pathogenetic factors of acne. Hormonal Antiandrogen treatment targets the androgen-metabolizing cells of the pilosebaceous unit, i. e. follicular kertinocytes and sebocytes, and leads to sebostasis, with a reduction of the sebum secretion rate of 12.5 to 65 %. Concerning their mechanism of action, hormonal Antiandrogens are classified in androgen receptor blockers, inhibitors of circulating androgens by affecting the ovarial function (oral contraceptives), inhibitors of circulating androgens by affecting the pituitary (gonadotrophin-releasing hormone agonists and dopamin agonists in hyperprolactinemia), inhibitors of the adrenal function, and inhibitors of peripheral androgen metabolism (5-reductase inhibitors, inhibitors of other enzymes).
    In this study, all original and review publications on hormonal Antiandrogen treatment of acne as monotherapy or in combination included in MEDLINE, EMBASE and COCHRANE libraries were extracted by using the terms “acne”, “seborrhea”, “polycystic ovary syndrome”, “hyperandrog*” and “treatment” and classified according to their level of evidence.
    Antiandrogen treatment is overall active on acne lesions. The combinations of ethinyl estradiol with cyproterone acetate chlormadinone acetate, dienogest desogestrel and drospirenone have shown the strongest antiacne activity. Gestagens or estrogens as monotherapy, spironolactone, flutamide, gonadotrophin-releasing hormone agonists and inhibitors of peripheral androgen metabolism are not recommended according to the current stand of knowledge. Low dose prednisolone is to only be administered at late onset congenital adrenal hyperplasia and dopamine agonists at hyperprolactinemia. Treatment with hormonal Antiandrogens requires missing of any contraindications.
    Hormonal Antiandrogen treatment is limited to female patients who present additional signs of peripheral hyperandrogenism or hyperandrogenemia. In addition, females with acne tarda, persistent acne recalcitrant to treatment, with parallel wish of contraception, and as a requirement for a systemic isotretinoin treatment can be treated with hormonal Antiandrogens. Hormonal Antiandrogen treatment is not a primary monotherapy for uncomplicated acne.

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Heather L. Montie – One of the best experts on this subject based on the ideXlab platform.

  • inhibition of stat5a b enhances proteasomal degradation of androgen receptor liganded by Antiandrogens in prostate cancer
    Molecular Cancer Therapeutics, 2015
    Co-Authors: David T. Hoang, Lei Gu, Zhiyong Liao, Feng Shen, Pooja Talati, Mateusz Koptyra, Elyse Ellsworth, Shilpa Gupta, Heather L. Montie

    Abstract:

    Although poorly understood, androgen receptor (AR) signaling is sustained despite treatment of prostate cancer with Antiandrogens and potentially underlies development of incurable castrate-resistant prostate cancer. However, therapies targeting the AR signaling axis eventually fail when prostate cancer progresses to the castrate-resistant stage. Stat5a/b, a candidate therapeutic target protein in prostate cancer, synergizes with AR to reciprocally enhance signaling of both proteins. In this work, we demonstrate that Stat5a/b sequesters Antiandrogen-liganded (MDV3100, Bicalutamide, Flutamide) AR in prostate cancer cells and protects it against proteasomal degradation in prostate cancer. Active Stat5a/b increased nuclear levels of both unliganded and Antiandrogen-liganded AR, as demonstrated in prostate cancer cell lines, xenograft tumors and clinical patient-derived prostate cancer samples. Physical interaction between Stat5a/b and AR in prostate cancer cells was mediated by the DNA-binding domain of Stat5a/b and the N-terminal domain of AR. Moreover, active Stat5a/b increased AR occupancy of the Prostate Specific Antigen promoter and AR-regulated gene expression in prostate cancer cells. Mechanistically, both Stat5a/b genetic knockdown and Antiandrogen treatment induced proteasomal degradation of AR in prostate cancer cells, with combined inhibition of Stat5a/b and AR leading to maximal loss of AR protein and prostate cancer cell viability. Our results indicate that therapeutic targeting of AR in prostate cancer using Antiandrogens may be substantially improved by targeting of Stat5a/b.

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  • Inhibition of Stat5a/b enhances proteasomal degradation of androgen receptor liganded by Antiandrogens in prostate cancer
    Molecular Cancer Therapeutics, 2014
    Co-Authors: David T. Hoang, Lei Gu, Zhiyong Liao, Feng Shen, Pooja Talati, Mateusz Koptyra, Elyse Ellsworth, Shilpa Gupta, Heather L. Montie

    Abstract:

    Although poorly understood, androgen receptor (AR) signaling is sustained despite treatment of prostate cancer with Antiandrogens and potentially underlies development of incurable castrate-resistant prostate cancer. However, therapies targeting the AR signaling axis eventually fail when prostate cancer progresses to the castrate-resistant stage. Stat5a/b, a candidate therapeutic target protein in prostate cancer, synergizes with AR to reciprocally enhance signaling of both proteins. In this work, we demonstrate that Stat5a/b sequesters Antiandrogen-liganded (MDV3100, Bicalutamide, Flutamide) AR in prostate cancer cells and protects it against proteasomal degradation in prostate cancer. Active Stat5a/b increased nuclear levels of both unliganded and Antiandrogen-liganded AR, as demonstrated in prostate cancer cell lines, xenograft tumors and clinical patient-derived prostate cancer samples. Physical interaction between Stat5a/b and AR in prostate cancer cells was mediated by the DNA-binding domain of Stat5a/b and the N-terminal domain of AR. Moreover, active Stat5a/b increased AR occupancy of the Prostate Specific Antigen promoter and AR-regulated gene expression in prostate cancer cells. Mechanistically, both Stat5a/b genetic knockdown and Antiandrogen treatment induced proteasomal degradation of AR in prostate cancer cells, with combined inhibition of Stat5a/b and AR leading to maximal loss of AR protein and prostate cancer cell viability. Our results indicate that therapeutic targeting of AR in prostate cancer using Antiandrogens may be substantially improved by targeting of Stat5a/b.

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Shilpa Gupta – One of the best experts on this subject based on the ideXlab platform.

  • inhibition of stat5a b enhances proteasomal degradation of androgen receptor liganded by Antiandrogens in prostate cancer
    Molecular Cancer Therapeutics, 2015
    Co-Authors: David T. Hoang, Lei Gu, Zhiyong Liao, Feng Shen, Pooja Talati, Mateusz Koptyra, Elyse Ellsworth, Shilpa Gupta, Heather L. Montie

    Abstract:

    Although poorly understood, androgen receptor (AR) signaling is sustained despite treatment of prostate cancer with Antiandrogens and potentially underlies development of incurable castrate-resistant prostate cancer. However, therapies targeting the AR signaling axis eventually fail when prostate cancer progresses to the castrate-resistant stage. Stat5a/b, a candidate therapeutic target protein in prostate cancer, synergizes with AR to reciprocally enhance signaling of both proteins. In this work, we demonstrate that Stat5a/b sequesters Antiandrogen-liganded (MDV3100, Bicalutamide, Flutamide) AR in prostate cancer cells and protects it against proteasomal degradation in prostate cancer. Active Stat5a/b increased nuclear levels of both unliganded and Antiandrogen-liganded AR, as demonstrated in prostate cancer cell lines, xenograft tumors and clinical patient-derived prostate cancer samples. Physical interaction between Stat5a/b and AR in prostate cancer cells was mediated by the DNA-binding domain of Stat5a/b and the N-terminal domain of AR. Moreover, active Stat5a/b increased AR occupancy of the Prostate Specific Antigen promoter and AR-regulated gene expression in prostate cancer cells. Mechanistically, both Stat5a/b genetic knockdown and Antiandrogen treatment induced proteasomal degradation of AR in prostate cancer cells, with combined inhibition of Stat5a/b and AR leading to maximal loss of AR protein and prostate cancer cell viability. Our results indicate that therapeutic targeting of AR in prostate cancer using Antiandrogens may be substantially improved by targeting of Stat5a/b.

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  • Inhibition of Stat5a/b enhances proteasomal degradation of androgen receptor liganded by Antiandrogens in prostate cancer
    Molecular Cancer Therapeutics, 2014
    Co-Authors: David T. Hoang, Lei Gu, Zhiyong Liao, Feng Shen, Pooja Talati, Mateusz Koptyra, Elyse Ellsworth, Shilpa Gupta, Heather L. Montie

    Abstract:

    Although poorly understood, androgen receptor (AR) signaling is sustained despite treatment of prostate cancer with Antiandrogens and potentially underlies development of incurable castrate-resistant prostate cancer. However, therapies targeting the AR signaling axis eventually fail when prostate cancer progresses to the castrate-resistant stage. Stat5a/b, a candidate therapeutic target protein in prostate cancer, synergizes with AR to reciprocally enhance signaling of both proteins. In this work, we demonstrate that Stat5a/b sequesters Antiandrogen-liganded (MDV3100, Bicalutamide, Flutamide) AR in prostate cancer cells and protects it against proteasomal degradation in prostate cancer. Active Stat5a/b increased nuclear levels of both unliganded and Antiandrogen-liganded AR, as demonstrated in prostate cancer cell lines, xenograft tumors and clinical patient-derived prostate cancer samples. Physical interaction between Stat5a/b and AR in prostate cancer cells was mediated by the DNA-binding domain of Stat5a/b and the N-terminal domain of AR. Moreover, active Stat5a/b increased AR occupancy of the Prostate Specific Antigen promoter and AR-regulated gene expression in prostate cancer cells. Mechanistically, both Stat5a/b genetic knockdown and Antiandrogen treatment induced proteasomal degradation of AR in prostate cancer cells, with combined inhibition of Stat5a/b and AR leading to maximal loss of AR protein and prostate cancer cell viability. Our results indicate that therapeutic targeting of AR in prostate cancer using Antiandrogens may be substantially improved by targeting of Stat5a/b.

    Free Register to Access Article