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Journal articles on the topic 'Androgen deprivation'

Author: Grafiati
Published: 4 June 2021
Last updated: 9 March 2023

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1

Hoon Lee, Jung, Haibiao Gong, Shaheen Khadem, Yi Lu, Xiang Gao, Song Li, Jian Zhang, and Wen Xie. "Androgen Deprivation by Activating the Liver X Receptor." Endocrinology 149, no. 8 (May 1, 2008): 3778–88. http://dx.doi.org/10.1210/en.2007-1605.

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Prostate cancer is the most commonly diagnosed and the second leading cause of cancer death in men. The androgens-androgen receptor signaling plays an important role in normal prostate development, as well as in prostatic diseases, such as benign hyperplasia and prostate cancer. Accordingly, androgen ablation has been the most effective endocrine therapy for hormone-dependent prostate cancer. Here, we report a novel nuclear receptor-mediated mechanism of androgen deprivation. Genetic or pharmacological activation of the liver X receptor (LXR) in vivo lowered androgenic activity by inducing the hydroxysteroid sulfotransferase 2A1, an enzyme essential for the metabolic deactivation of androgens. Activation of LXR also inhibited the expression of steroid sulfatase in the prostate, which may have helped to prevent the local conversion of sulfonated androgens back to active metabolites. Interestingly, LXR also induced the expression of selected testicular androgen synthesizing enzymes. At the physiological level, activation of LXR in mice inhibited androgen-dependent prostate regeneration in castrated mice. Treatment with LXR agonists inhibited androgen-dependent proliferation of prostate cancer cells in a LXR- and sulfotransferase 2A1-dependent manner. In summary, we have revealed a novel function of LXR in androgen homeostasis, an endocrine role distinct to the previously known sterol sensor function of this receptor. LXR may represent a novel therapeutic target for androgen deprivation, and may aid in the treatment and prevention of hormone-dependent prostate cancer.
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2

Rozhivanov, Roman V., Elena N. Andreeva, Galina A. Melnichenko, and Natalya G. Mokrysheva. "Androgens and Antiandrogens influence on COVID-19 disease in men." Problems of Endocrinology 66, no. 4 (December 7, 2020): 77–81. http://dx.doi.org/10.14341/probl12500.

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The WHO has declared a SARS-CoV-2 pandemic. During a pandemic, the researches aimed at finding the new treatments for SARS-CoV-2 become relevant. The review focuses on studies of androgens and antiandrogens in this disease. Since the beginning of the COVID-19 epidemic, it has been noted that men have more severe forms of infection and higher mortality. The main cause of both the severity of the disease and the high mortality of men from COVID-19 are associated with androgens. It was found that patients receiving androgen deprivation are less likely to become infected and easily tolerate COVID-19. The researchers explain the effect of the therapy by the effect on the TMPRSS2 protein. It was found that both TMPRSS2 expression and a more severe course of coronavirus infection are observed in men with hyperandrogenism – androgenic alopecia, acne, excessive facial hair growth and increased skin oiliness. In this regard, some researchers suggest to use androgen deprivation for men at high risk of developing COVID-19. Steroid and non-steroidal antiandrogens are used for androgen deprivation. At the same time, obtaned scientific data on the relationship of severe forms and mortality of COVID-19 with low testosterone levels leads to a hypothesis about the possibility of a positive effect not of androgen devrivation therapy but of androgen replacement therapy in case of hypogonadism have diagnosed. These studies have not been completed recently, and data on the effectiveness and safety of antiandrogens and androgens in the treatment of a new coronavirus infection require clarification.
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3

Gamat, Melissa, and Douglas G. McNeel. "Androgen deprivation and immunotherapy for the treatment of prostate cancer." Endocrine-Related Cancer 24, no. 12 (December 2017): T297—T310. http://dx.doi.org/10.1530/erc-17-0145.

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Prostate cancer is the most common newly diagnosed malignancy in men, and the second most common cause of cancer-related death in the United States. The primary treatment for recurrent prostate cancer is androgen deprivation, and this therapy is typically continued lifelong for patients with metastatic prostate cancer. Androgens and androgen deprivation have profound effects on the immune system, a finding that has become more appreciated in an era where immune-based treatments for cancer are being increasingly explored. Preclinical studies suggest that androgen deprivation could potentially positively or negatively affect the use of approved immunotherapies, or those that are being developed for the treatment of prostate cancer. In this review, we provide a brief overview of the different types of androgen deprivation treatments used in the management of prostate cancer, discuss their effects on prostate tumors and the immune system and how they are being explored in combination with immunotherapy. Finally, we address some of the critical questions in the field that must be answered to identify the best approaches to combine androgen deprivation with immunotherapy for the treatment of prostate cancer.
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4

Kamalov, A. A., D. A. Ohobotov, O. Yu Nesterova, A. A. Strigunov, and A. S. Tivtikyan. "Androgen deprivation therapy and hormonal status in men with COVID-19." Urology Herald 10, no. 4 (December 26, 2022): 141–54. http://dx.doi.org/10.21886/2308-6424-2022-10-4-141-154.

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Severe course of COVID-19 among men compared to the female led to a detailed study of the hormonal status of men with COVID-19. The earliest works about this focused on the incidence and severity of COVID-19 depending on the intake of androgen deprivation therapy. At the same time, different classes of androgen deprivation therapy have different effects on androgen concentration that was not always considered in the analysis. In this regard, we conducted a review of the available literature data with a targeted study of works that included androgen deprivation therapy with a unidirectional effect on the concentration of male sex hormones. In addition, we conducted a review of studies focused on the relationship between COVID-19 and androgens (testosterone and dihydrotestosterone).
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5

McCarty, Mark F., Jalal Hejazi, and Reza Rastmanesh. "Beyond Androgen Deprivation." Integrative Cancer Therapies 13, no. 5 (May 26, 2014): 386–95. http://dx.doi.org/10.1177/1534735414534728.

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6

Mendiratta, Prateek, and Jorge Garcia. "Androgen Deprivation Fortified." International Journal of Radiation Oncology*Biology*Physics 100, no. 5 (April 2018): 1098. http://dx.doi.org/10.1016/j.ijrobp.2018.01.103.

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7

Dawson, Nancy A. "Intermittent androgen deprivation." Current Oncology Reports 2, no. 5 (October 2000): 409–16. http://dx.doi.org/10.1007/s11912-000-0060-6.

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8

Hussain, Maha, and Mario Eisenberger. "Intermittent Androgen Deprivation." JAMA Oncology 2, no. 12 (December 1, 2016): 1533. http://dx.doi.org/10.1001/jamaoncol.2016.2650.

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9

Chen, Jia-Feng, Pei-Wen Lin, Yi-Ru Tsai, Yi-Chien Yang, and Hong-Yo Kang. "Androgens and Androgen Receptor Actions on Bone Health and Disease: From Androgen Deficiency to Androgen Therapy." Cells 8, no. 11 (October 25, 2019): 1318. http://dx.doi.org/10.3390/cells8111318.

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Androgens are not only essential for bone development but for the maintenance of bone mass. Therefore, conditions with androgen deficiency, such as male hypogonadism, androgen-insensitive syndromes, and prostate cancer with androgen deprivation therapy are strongly associated with bone loss and increased fracture risk. Here we summarize the skeletal effects of androgens—androgen receptors (AR) actions based on in vitro and in vivo studies from animals and humans, and discuss bone loss due to androgens/AR deficiency to clarify the molecular basis for the anabolic action of androgens and AR in bone homeostasis and unravel the functions of androgen/AR signaling in healthy and disease states. Moreover, we provide evidence for the skeletal benefits of androgen therapy and elucidate why androgens are more beneficial than male sexual hormones, highlighting their therapeutic potential as osteoanabolic steroids in improving bone fracture repair. Finally, the application of selective androgen receptor modulators may provide new approaches for the treatment of osteoporosis and fractures as well as building stronger bones in diseases dependent on androgens/AR status.
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10

Sountoulides, Petros, and Thomas Rountos. "Adverse Effects of Androgen Deprivation Therapy for Prostate Cancer: Prevention and Management." ISRN Urology 2013 (July 25, 2013): 1–8. http://dx.doi.org/10.1155/2013/240108.

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The prostate is an androgen-dependent organ. The increase, growth, homeostasis, and function of the prostate largely depend upon the intraprostatic and serum concentrations of androgens. Therefore, androgens are essential for the physiologic growth of prostatic epithelium. Prostate cancer, the second leading cause of death for men, is also androgen dependent, and androgen suppression is the mainstay of treatment for advanced and metastatic disease. In the state of metastatic disease, androgen suppression is a palliative treatment leading to a median progression-free survival of 18–20 months and an overall survival of 24–36 months. Theoretically, the majority of patients will develop hormone-refractory disease provided that they will not die from other causes. Although androgen suppression therapy may be associated with significant and sometimes durable responses, it is not considered a cure, and its potential efficacy is further limited by an array of significant and bothersome adverse effects caused by the suppression of androgens. These effects have potentially significant consequences on a variety of parameters of everyday living and may further decrease health-related quality of life. This review focuses on the aetiology of these adverse effects and provides information on their prevention and management.
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11

Zhang, Bin, Qiuqiong Cheng, Zhimin Ou, Jung Hoon Lee, Meishu Xu, Upasana Kochhar, Songrong Ren, Min Huang, Beth R. Pflug, and Wen Xie. "Pregnane X Receptor as a Therapeutic Target to Inhibit Androgen Activity." Endocrinology 151, no. 12 (October 20, 2010): 5721–29. http://dx.doi.org/10.1210/en.2010-0708.

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The androgen-androgen receptor signaling pathway plays an important role in the pathogenesis of prostate cancer. Accordingly, androgen deprivation has been the most effective endocrine therapy for hormone-dependent prostate cancer. Here, we report a novel pregnane X receptor (PXR)-mediated and metabolism-based mechanism to reduce androgenic tone. PXR is a nuclear receptor previously known as a xenobiotic receptor regulating the expression of drug metabolizing enzymes and transporters. We showed that genetic (using a PXR transgene) or pharmacological (using a PXR agonist) activation of PXR lowered androgenic activity and inhibited androgen-dependent prostate regeneration in castrated male mice that received daily injections of testosterone propionate by inducing the expression of cytochrome P450 (CYP)3As and hydroxysteroid sulfotransferase (SULT)2A1, which are enzymes important for the metabolic deactivation of androgens. In human prostate cancer cells, treatment with the PXR agonist rifampicin (RIF) inhibited androgen-dependent proliferation of LAPC-4 cells but had little effect on the growth of the androgen-independent isogenic LA99 cells. Down-regulation of PXR or SULT2A1 in LAPC-4 cells by short hairpin RNA or small interfering RNA abolished the RIF effect, indicating that the inhibitory effect of RIF on androgens was PXR and SULT2A1 dependent. In summary, we have uncovered a novel function of PXR in androgen homeostasis. PXR may represent a novel therapeutic target to lower androgen activity and may aid in the treatment and prevention of hormone-dependent prostate cancer.
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12

Wasano, Koichiro, Kouhei Sakurai, Taiji Kawasaki, Kimihide Kusafuka, Masao Kasahara, Naoki Kondo, Ken-ichi Inada, and Kaoru Ogawa. "Acquisition of resistance to androgen deprivation therapy in salivary duct carcinoma: A case report." Rare Tumors 10 (January 2018): 203636131879886. http://dx.doi.org/10.1177/2036361318798867.

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Salivary duct carcinoma is a relatively rare salivary cancer, and most cases are androgen receptor -positive. Salivary duct carcinoma growth is suggested to be androgen dependent, which can reportedly be controlled by androgen deprivation therapy. However, the effectiveness and underlying molecular mechanisms of androgen deprivation therapy for salivary duct carcinoma remain unknown. We report a salivary duct carcinoma case (65-year-old man) arising from the parotid gland with metastasis to the neck lymph nodes and lungs. Androgen deprivation therapy was performed according to the same protocol for prostate cancer treatment. Expression levels of androgen receptor and FOXA1 (forkhead box A1) were immunohistochemically analyzed before and after androgen deprivation therapy. Although the tumor volume was partially diminished during the first 3 months, acquired resistance to androgen deprivation therapy occurred. FOXA1 was not detected in parotid gland after androgen deprivation therapy, whereas androgen receptor expression was positive. FOXA1 expression might be related to acquired androgen deprivation therapy resistance in salivary duct carcinoma.
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13

Russell, Nicholas, Ada Cheung, and Mathis Grossmann. "Estradiol for the mitigation of adverse effects of androgen deprivation therapy." Endocrine-Related Cancer 24, no. 8 (August 2017): R297—R313. http://dx.doi.org/10.1530/erc-17-0153.

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Prostate cancer (PCa) is the second most commonly diagnosed cancer in men. Conventional endocrine treatment for PCa leads to global sex steroid deprivation. The ensuing severe hypogonadism is associated with well-documented adverse effects. Recently, it has become apparent that many of the biological actions attributed to androgens in men are in fact not direct, but mediated by estradiol. Available evidence supports a primary role for estradiol in vasomotor stability, skeletal maturation and maintenance, and prevention of fat accumulation. Hence there has been interest in revisiting estradiol as a treatment for PCa. Potential roles for estradiol could be in lieu of conventional androgen deprivation therapy or as low-dose add-back treatment while continuing androgen deprivation therapy. These strategies may limit some of the side effects associated with conventional androgen deprivation therapy. However, although available data are reassuring, the potential for cardiovascular risk and pro-carcinogenic effects on PCa via estrogen receptor signalling must be considered.
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14

Terrisse, Safae, Laurence Zitvogel, and Guido Kroemer. "Effects of the intestinal microbiota on prostate cancer treatment by androgen deprivation therapy." microbial Cell 9, no. 12 (December 5, 2022): 202–6. http://dx.doi.org/10.15698/mic2022.12.787.

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Prostate cancer (PC) can be kept in check by androgen deprivation therapy (ADT, usually with the androgen synthesis inhibitor abiraterone acetate or the androgen receptor antagonist such as enzalutamide) until the tumor evolves to castration-resistant prostate cancer (CRPC). The transition of hormone-sensitive PC (HSPC) to CPRC has been explained by cancer cell-intrinsic resistance mechanisms. Recent data indicate that this transition is also marked by cancer cell-extrinsic mechanisms such as the failure of ADT-induced PC immunosurveillance, which depends on the presence of immunostimulatory bacteria in the gut. Moreover, intestinal bacteria that degrade drugs used for ADT, as well as bacteria that produce androgens, can interfere with the efficacy of ADT. Thus, specific bacteria in the gut serve as a source of testosterone, which accelerates prostate cancer progression, and men with CRPC exhibit an increased abundance of such bacteria with androgenic functions. In conclusion, the response of PC to ADT is profoundly influenced by the composition of the microbiota with its immunostimulatory, immunosuppressive and directly ADT-subversive elements.
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15

Bonfill-Cosp, Xavier, Ariadna Auladell-Rispau, Ignasi Gich, Javier Zamora, Luis Carlos Saiz, Jose Ignacio Pijoan, Iratxe Urreta, and José Antonio Cordero. "Prevalence study of intermittent hormonal therapy of Prostate Cancer patients in Spain." F1000Research 10 (October 21, 2021): 1069. http://dx.doi.org/10.12688/f1000research.53875.1.

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Background: Although intermittent androgen deprivation therapy was introduced many years ago to improve patients’ quality of life with the same carcinologic efficiency as continuous hormonal therapy, recent data suggest that those patients could be overtreated. This study aims to estimate the prevalence of prostate cancer patients receiving intermittent androgen deprivation therapy in Spain. Methods: A retrospective, longitudinal study was conducted using electronic drug dispensation data from four Spanish autonomous communities, which encompass 17.23 million inhabitants (36.22% of the total population in Spain). We estimated intermittent androgen therapy use (%IAD) and the prevalence of patients under intermittent androgen therapy (PIAD) overall and stratified by region. Other outcome variables included the pharmaceutical forms dispensed and the total direct annual expenditure on androgen deprivation therapy‐associated medications. Results: A total of 863,005 dispensations corresponding to a total of 65,752 men were identified, treated with either luteinizing hormone-releasing hormone (LHRH) analogues (353,162) administered alone or in combination with anti‐androgens (509,843). Overall, the mean (±SD) age of the patients was 76.9 (±10.4) years. Results revealed that the mean annual PIAD along the study was 6.6% in the total population studied, and the overall %IAD during the five‐year study period was 5.6%. The mean cost of hormonal therapy per year was 25 million euros for LHRH analogues and 6.3 million euros for anti-androgens. Conclusions: An important proportion of prostate cancer patients in Spain could benefit from intermittent androgen therapy during the study period while avoiding overtreatment harms associated with continuous hormonal therapy.
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16

Sabharwal, Navin, and Nima Sharifi. "HSD3B1 Genotypes Conferring Adrenal-Restrictive and Adrenal-Permissive Phenotypes in Prostate Cancer and Beyond." Endocrinology 160, no. 9 (July 4, 2019): 2180–88. http://dx.doi.org/10.1210/en.2019-00366.

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Abstract Castration-resistant prostate cancer (PCa) almost invariably occurs after androgen deprivation therapy for metastatic disease and is driven in part by androgen synthesis within the tumor. 3β-hydroxysteroid dehydrogenase isoenzyme-1 catalyzes the conversion of adrenal precursor steroids into potent androgens essential for PCa progression. A common 1245 A→C missense-encoding single nucleotide polymorphism in HSD3B1 (rs1047303), the gene that encodes this enzyme, leads to a more stable protein that is resistant to degradation and thus increased production of potent androgens from adrenal precursors, facilitating castration-resistant PCa development. Consistent with this mechanism, this adrenal-permissive HSD3B1(1245C) genotype is associated with inferior outcomes after androgen deprivation therapy for advanced PCa, and increased sensitivity to pharmacologic blockade of adrenal precursors in metastatic disease. Herein, we review current knowledge of the mechanisms conferred by HSD3B1 genotype to alter androgen physiology and accelerate development of castration-resistant disease and its associations with clinical PCa outcomes. In light of its effect on steroid physiology, we also discuss its potential associations with non-PCa phenotypes.
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17

Allan, Carolyn A., Veronica R. Collins, Mark Frydenberg, Robert I. McLachlan, and Kati L. Matthiesson. "Androgen deprivation therapy complications." Endocrine-Related Cancer 21, no. 4 (May 28, 2014): T119—T129. http://dx.doi.org/10.1530/erc-13-0467.

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Androgen deprivation therapy (ADT) is increasingly used to treat advanced prostate cancer and is also utilised as adjuvant or neo-adjuvant treatment for high-risk disease. The resulting suppression of endogenous testosterone production has deleterious effects on quality of life, including hot flushes, reduced mood and cognition and diminished sexual function. Cross-sectional and longitudinal studies show that ADT has adverse bone and cardio-metabolic effects. The rate of bone loss is accelerated, increasing the risk of osteoporosis and subsequent fracture. Fat mass is increased and lean mass reduced, and adverse effects on lipid levels and insulin resistance are observed, the latter increasing the risk of developing type 2 diabetes. ADT also appears to increase the risk of incident cardiovascular events, although whether it increases cardiovascular mortality is not certain from the observational evidence published to date. Until high-quality evidence is available to guide management, it is reasonable to consider men undergoing ADT to be at a higher risk of psychosexual dysfunction, osteoporotic fracture, diabetes and cardiovascular disease, especially when treated for extended periods of time and therefore subjected to profound and prolonged hypoandrogenism. Health professionals caring for men undergoing treatment for prostate cancer should be aware of the potential risks of ADT and ensure appropriate monitoring and clinical management.
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18

Smith, Matthew R. "Androgen Deprivation and Osteoporosis." Prostate Journal 1, no. 4 (July 1999): 161–65. http://dx.doi.org/10.1046/j.1525-1411.1999.14002.x.

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19

Lattouf, Jean-Baptiste, Hicham Fadlallah, and Fred Saad. "Androgen Deprivation and Bone." Current Osteoporosis Reports 9, no. 1 (December 16, 2010): 20–24. http://dx.doi.org/10.1007/s11914-010-0045-9.

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20

Greco, Federico, Alessandro Tafuri, Andrea Panunzio, Bruno Beomonte Zobel, and Carlo Augusto Mallio. "Relationship between Androgen Deprivation Therapy and Abdominal Adipose Tissue." Uro 2, no. 4 (December 2, 2022): 270–76. http://dx.doi.org/10.3390/uro2040030.

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The role of androgens in body composition is well known. Androgen deprivation therapy (ADT) has shown beneficial effects in the treatment of advanced prostate cancer (PCa). Given that androgens are important for the homeostasis of different organs, the effects of ADT can affect body composition and therefore adipose tissue. Computed tomography (CT) and magnetic resonance imaging (MRI) are non-invasive methods that allow for quantification of the different fat compartments. In this review we describe the effects of ADT on abdominal adipose tissue in PCa patients.
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21

Jennbacken, Karin, Tajana Tešan, Wanzhong Wang, Heléne Gustavsson, Jan-Erik Damber, and Karin Welén. "N-cadherin increases after androgen deprivation and is associated with metastasis in prostate cancer." Endocrine-Related Cancer 17, no. 2 (June 2010): 469–79. http://dx.doi.org/10.1677/erc-10-0015.

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Androgen-deprivation therapy (ADT) is the standard treatment for metastatic prostate cancer. One factor that has been implicated in the metastatic process is the cell adhesion molecule N-cadherin. In this study, we investigated if the expression of N-cadherin was influenced by androgen deprivation and was associated with metastasis in prostate cancer. The effect of androgen deprivation on N-cadherin expression was initially studied in androgen-dependent (AD) LNCaP and androgen-independent (AI) LNCaP-19 and PC-3 prostate cancer cell lines. Expression of N-cadherin increased in the absence of androgens in AI LNCaP-19 primary tumors and metastases and also in vitro, but not in AI PC-3 tumors, indicating a possible involvement of the androgen receptor in the regulation of N-cadherin. N-cadherin was absent in AD LNCaP tumors. No clear associations between N-cadherin and factors related with epithelial–mesenchymal transition or neuroendocrine differentiation could be established. In addition, N-cadherin was evaluated by immunohistochemistry in human prostate tumors. Expression of N-cadherin was more frequently found in tumors from patients treated with ADT than in tumors from patients with no prior hormonal treatment. N-cadherin expression was also associated with metastasis and Gleason score. Furthermore, increased N-cadherin was detected in prostate cancer biopsies already 3 months after initiation of ADT when tumors were in a regressed state. In summary the results indicate that androgen deprivation induces N-cadherin in prostate tumors. Moreover, N-cadherin was increased in castration-resistant tumors in patients with established metastases. This might indicate that castration induces molecular alterations in the tumor cells, resulting in a more invasive and metastatic phenotype.
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22

Auchus, Richard J., and Nima Sharifi. "Sex Hormones and Prostate Cancer." Annual Review of Medicine 71, no. 1 (January 27, 2020): 33–45. http://dx.doi.org/10.1146/annurev-med-051418-060357.

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The prostate is an androgen-dependent organ that develops only in male mammals. Prostate cancer is the most common nonskin malignancy in men and the second leading cause of cancer deaths. Metastatic prostate cancer initially retains its androgen dependence, and androgen-deprivation therapy often leads to disease control; however, the cancer inevitably progresses despite treatment as castration-resistant prostate cancer, the lethal form of the disease. Although it was assumed that the cancer became androgen independent during this transition, studies over the last two decades have shown that these tumors evade treatment via mechanisms that augment acquisition of androgens from circulating precursors, increase sensitivity to androgens and androgen precursors, bypass the androgen receptor, or a combination of these mechanisms. This review summarizes the history of prostate cancer research leading to the contemporary view of androgen dependence for prostate cancers and the current treatment approaches based on this modern paradigm.
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23

Desai, Kunal, Jeffrey M. McManus, and Nima Sharifi. "Hormonal Therapy for Prostate Cancer." Endocrine Reviews 42, no. 3 (January 22, 2021): 354–73. http://dx.doi.org/10.1210/endrev/bnab002.

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Abstract Huggins and Hodges demonstrated the therapeutic effect of gonadal testosterone deprivation in the 1940s and therefore firmly established the concept that prostate cancer is a highly androgen-dependent disease. Since that time, hormonal therapy has undergone iterative advancement, from the types of gonadal testosterone deprivation to modalities that block the generation of adrenal and other extragonadal androgens, to those that directly bind and inhibit the androgen receptor (AR). The clinical states of prostate cancer are the product of a superimposition of these therapies with nonmetastatic advanced prostate cancer, as well as frankly metastatic disease. Today’s standard of care for advanced prostate cancer includes gonadotropin-releasing hormone agonists (e.g., leuprolide), second-generation nonsteroidal AR antagonists (enzalutamide, apalutamide, and darolutamide) and the androgen biosynthesis inhibitor abiraterone. The purpose of this review is to provide an assessment of hormonal therapies for the various clinical states of prostate cancer. The advancement of today’s standard of care will require an accounting of an individual’s androgen physiology that also has recently recognized germline determinants of peripheral androgen metabolism, which include HSD3B1 inheritance.
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Johnson, Matthew E., and Mark K. Buyyounouski. "Androgen Deprivation Therapy Toxicity and Management for Men Receiving Radiation Therapy." Prostate Cancer 2012 (2012): 1–8. http://dx.doi.org/10.1155/2012/580306.

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Androgen deprivation therapy is commonly used in combination with radiotherapy as part of the definitive treatment for men with clinically localized and locally advanced prostate cancer. Androgen deprivation has been associated with a wide range of iatrogenic effects impacting a variety of body systems including metabolic, musculoskeletal, cardiovascular, neurocognitive, and sexual. This review aims to provide the radiation oncology community with the knowledge to monitor and manage androgen deprivation therapy toxicity in an effort to provide the highest level of care for patients and to minimize the iatrogenic effects of androgen deprivation as much as possible.
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25

Muresanu, Horia. "Benefits of intermittent/continuous androgen deprivation in patients with advanced prostate cancer." Medicine and Pharmacy Reports 89, no. 3 (July 31, 2016): 419–22. http://dx.doi.org/10.15386/cjmed-594.

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Background and aims: Huggins described in 1941 the effect of castration on prostate cancer. Gonadotropin-releasing hormone (GNRH) analogue were introduced in 1985. Complete androgen blocade (association of GNRH analogue with antiandrogen) was introduced by Fernand Labrie to achieve supression of suprarenalian testosterone. Long time androgen deprivation lead to androgen independence of prostate cancer cell.Our principal aim was to demonstrate longer survival rates on prostate cancer patients with intermittent androgen deprivation.Methods: 82 patients were enrolled at the Urology Deparment of West University „Vasile Goldiș” Arad in two groups with continous and intermittent androgen deprivation.Treatment efficiency was assesed by the level of testosterone and PSA.Adverse events (AE) and serious adverse events were reported according to Common Terminology Cryteria of Adverse Events (CTCAE) of the National Cancer Institute (NCI).Results:Evolution towards castrate resistant prostate cancer: 12.5% from the intermittent androgen deprivation group and 23.8% from the continues androgen deprivation groupMortality rate: 15% of patients from the intermittent androgen deprivation group; 19% of patients from the continue androgen deprivation group Conclusions:1. Better quality of life (Qo)l in periods without treatment due to testosteron recovery; 2. Less AE’s and methabolic syndrom (MS) related complications; 3. Better survival and longer time of disease control and 4. Cost reduction
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26

Mizushima, Taichi, and Hiroshi Miyamoto. "The Role of Androgen Receptor Signaling in Ovarian Cancer." Cells 8, no. 2 (February 19, 2019): 176. http://dx.doi.org/10.3390/cells8020176.

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Emerging evidence has suggested that androgen receptor signaling plays an important role in ovarian cancer outgrowth. Specifically, androgen receptor activation appears to be associated with increased risks of developing ovarian cancer and inducing tumor progression. However, conflicting findings have also been reported. This review summarizes and discusses the available data indicating the involvement of androgens as well as androgen receptor and related signals in ovarian carcinogenesis and cancer growth. Although the underlying molecular mechanisms for androgen receptor functions in ovarian cancer remain far from being fully understood, current observations may offer effective chemopreventive and therapeutic approaches, via modulation of androgen receptor activity, against ovarian cancer. Indeed, several clinical trials have been conducted to determine the efficacy of androgen deprivation therapy in patients with ovarian cancer.
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27

Zhu, Ziqi, Yoon-Mi Chung, Olga Sergeeva, Vladimir Kepe, Michael Berk, Jianneng Li, Hyun-Kyung Ko, et al. "Loss of dihydrotestosterone-inactivation activity promotes prostate cancer castration resistance detectable by functional imaging." Journal of Biological Chemistry 293, no. 46 (September 27, 2018): 17829–37. http://dx.doi.org/10.1074/jbc.ra118.004846.

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Androgens such as testosterone and dihydrotestosterone are a critical driver of prostate cancer progression. Cancer resistance to androgen deprivation therapies ensues when tumors engage metabolic processes that produce sustained androgen levels in the tissue. However, the molecular mechanisms involved in this resistance process are unclear, and functional imaging modalities that predict impending resistance are lacking. Here, using the human LNCaP and C4-2 cell line models of prostate cancer, we show that castration treatment–sensitive prostate cancer cells that normally have an intact glucuronidation pathway that rapidly conjugates and inactivates dihydrotestosterone and thereby limits androgen signaling, become glucuronidation deficient and resistant to androgen deprivation. Mechanistically, using CRISPR/Cas9-mediated gene ablation, we found that loss of UDP glucuronosyltransferase family 2 member B15 (UGT2B15) and UGT2B17 is sufficient to restore free dihydrotestosterone, sustained androgen signaling, and development of castration resistance. Furthermore, loss of glucuronidation enzymatic activity was also detectable with a nonsteroid glucuronidation substrate. Of note, glucuronidation-incompetent cells and the resultant loss of intracellular conjugated dihydrotestosterone were detectable in vivo by 18F-dihydrotestosterone PET. Together, these findings couple a mechanism with a functional imaging modality to identify impending castration resistance in prostate cancers.
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Skolarus, Ted A., Megan V. Caram, and Vahakn B. Shahinian. "Androgen-deprivation-associated bone disease." Current Opinion in Urology 24, no. 6 (November 2014): 601–7. http://dx.doi.org/10.1097/mou.0000000000000101.

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29

McKenzie, Michael R. "Androgen deprivation and radiation therapy." Urology 47, no. 2 (February 1996): 286. http://dx.doi.org/10.1016/s0090-4295(99)80439-7.

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30

Keizman, Daniel, and Michael A. Carducci. "Intermittent androgen deprivation—questions remain." Nature Reviews Urology 6, no. 8 (August 2009): 412–14. http://dx.doi.org/10.1038/nrurol.2009.145.

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31

Basaria, Shehzad. "Cardiovascular mortality and androgen deprivation." Nature Reviews Urology 6, no. 5 (May 2009): 252–53. http://dx.doi.org/10.1038/nrurol.2009.75.

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32

Shahinian, Vahakn B. "Androgen deprivation for prostate cancer." Cancer 118, no. 13 (November 9, 2011): 3232–35. http://dx.doi.org/10.1002/cncr.26624.

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33

Iwamoto, Hiroaki, Kouji Izumi, Tomoyuki Makino, and Atsushi Mizokami. "Androgen Deprivation Therapy in High-Risk Localized and Locally Advanced Prostate Cancer." Cancers 14, no. 7 (April 1, 2022): 1803. http://dx.doi.org/10.3390/cancers14071803.

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The recommended treatment for high-risk localized or locally advanced prostate cancer is radical prostatectomy plus extended pelvic lymph node dissection or radiation therapy plus long-term androgen deprivation therapy. However, some patients are treated with androgen deprivation therapy alone for various reasons. In this review, we will discuss the position, indications, complications, and future prospects of androgen deprivation therapy for high-risk localized and locally advanced prostate cancer.
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34

Shahabi Raberi, Venus, Akram Shariati, Mohsen Abbasnezhad, Naser Aslanabadi, Amirreza Abbasnezhad, and Amir Bahmani. "Drug Resistance and Cardiovascular Safety of Second-Generation Anti-Androgens in Patients with Advanced Prostate Cancer." Galen Medical Journal 11 (December 31, 2022): e2727. http://dx.doi.org/10.31661/gmj.v11i.2727.

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Prostate cancer is recognized as one of the most common cancers affecting the male population. The prostate is revealed to be a hormone-dependent tissue as testosterone and dihydrotestosterone could bind to the androgen receptor, activate it, and initiate the nuclear translocation of this receptor which is followed by subsequent signaling cascades. Regarding this androgen dependency of the prostate, it is believed that androgen deprivation therapies are able to confront aggressive prostate cancer as first-line treatment. However, prostate cancer could overcome hormone deprivation strategies through a number of cellular mechanisms, such as intratumoral androgen production and the production of ligand-independent androgen receptor splice variants, which are known clinically as castration-resistant prostate cancer. Due to the limited efficacy of first-generation antiandrogens in complete blockage of androgen receptor activity, recently, four second-generation anti-androgens, including abiraterone acetate, enzalutamide, apalutamide, and darolutamide approved by the Food and Drug Administration, and considered standard of care for patients with advanced prostate cancer. Nevertheless, prostate cancer cells may acquire drug-resistance mechanisms to overcome these novel chemotherapeutics. Furthermore, potential adverse effects on nontargeted organs such as the cardiovascular system, are possible. Hence, the current study aimed to review the efficacy and cardio-safety of these novel therapeutical strategies.
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35

Wall, Bradley A., Daniel A. Galvão, Naeem Fatehee, Dennis R. Taaffe, Nigel Spry, David Joseph, and Robert U. Newton. "Reduced Cardiovascular Capacity and Resting Metabolic Rate in Men with Prostate Cancer Undergoing Androgen Deprivation: A Comprehensive Cross-Sectional Investigation." Advances in Urology 2015 (2015): 1–7. http://dx.doi.org/10.1155/2015/976235.

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Objectives. To investigate if androgen deprivation therapy exposure is associated with additional risk factors for cardiovascular disease and metabolic treatment-related toxicities.Methods. One hundred and seven men (42–89 years) with prostate cancer undergoing androgen deprivation therapy completed a maximal graded objective exercise test to determine maximal oxygen uptake, assessments for resting metabolic rate, body composition, blood pressure and arterial stiffness, and blood biomarker analysis. A cross-sectional analysis was undertaken to investigate the potential impact of therapy exposure with participants stratified into two groups according to duration of androgen deprivation therapy (<3 months and ≥3 months).Results. Maximal oxygen uptake (26.1 ± 6.0 mL/kg/min versus 23.2 ± 5.8 mL/kg/min,p=0.020) and resting metabolic rate (1795 ± 256 kcal/d versus 1647 ± 236 kcal/d,p=0.005) were significantly higher in those with shorter exposure to androgen deprivation. There were no differences between groups for peripheral and central blood pressure, arterial stiffness, or metabolic profile.Conclusion. Three months or longer exposure to androgen deprivation therapy was associated with reduced cardiorespiratory capacity and resting metabolic rate, but not in a range of blood biomarkers. These findings suggest that prolonged exposure to androgen deprivation therapy is associated with negative alterations in cardiovascular outcomes. Trial registry is:ACTRN12609000200280.
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Sun, Yuting, Bu-Er Wang, Kevin G. Leong, Peng Yue, Li Li, Suchit Jhunjhunwala, Darrell Chen, et al. "Androgen Deprivation Causes Epithelial–Mesenchymal Transition in the Prostate: Implications for Androgen-Deprivation Therapy." Cancer Research 72, no. 2 (November 22, 2011): 527–36. http://dx.doi.org/10.1158/0008-5472.can-11-3004.

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Shahinian, V. B. "Risk of the "Androgen Deprivation Syndrome" in Men Receiving Androgen Deprivation for Prostate Cancer." Archives of Internal Medicine 166, no. 4 (February 27, 2006): 465–71. http://dx.doi.org/10.1001/.465.

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Shahinian, Vahakn B., Yong-Fang Kuo, Jean L. Freeman, and James S. Goodwin. "Risk of the “Androgen Deprivation Syndrome” in Men Receiving Androgen Deprivation for Prostate Cancer." Archives of Internal Medicine 166, no. 4 (February 27, 2006): 465. http://dx.doi.org/10.1001/archinte.166.4.465.

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Liu, June, Laura E. Pascal, Sudhir Isharwal, Daniel Metzger, Raquel Ramos Garcia, Jan Pilch, Susan Kasper, et al. "Regenerated Luminal Epithelial Cells Are Derived from Preexisting Luminal Epithelial Cells in Adult Mouse Prostate." Molecular Endocrinology 25, no. 11 (November 1, 2011): 1849–57. http://dx.doi.org/10.1210/me.2011-1081.

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Abstract Determining the source of regenerated luminal epithelial cells in the adult prostate during androgen deprivation and replacement will provide insights into the origin of prostate cancer cells and their fate during androgen deprivation therapy. Prostate stem cells in the epithelial layer have been suggested to give rise to luminal epithelium. However, the extent of stem cell participation to prostate regrowth is not clear. In this report, using prostate-specific antigen-CreERT2-based genetic lineage marking/tracing in mice, preexisting luminal epithelial cells were shown to be a source of regenerated luminal epithelial cells in the adult prostate. Prostatic luminal epithelial cells could survive androgen deprivation and were capable of proliferating upon androgen replacement. Prostate cancer cells, typically exhibiting a luminal epithelial phenotype, may retain this intrinsic capability to survive and regenerate in response to changes in androgen signaling, providing part of the mechanism for the ultimate failure of androgen deprivation therapy in prostate cancer.
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Pernigoni, Nicolò, Elena Zagato, Arianna Calcinotto, Martina Troiani, Ricardo Pereira Mestre, Bianca Calì, Giuseppe Attanasio, et al. "Commensal bacteria promote endocrine resistance in prostate cancer through androgen biosynthesis." Science 374, no. 6564 (October 8, 2021): 216–24. http://dx.doi.org/10.1126/science.abf8403.

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Microbes hijack prostate cancer therapy Androgens such as testosterone and dihydrotestosterone are essential for male reproduction and sexual function. Androgens can also influence the growth of prostate tumor cells, and androgen deprivation therapy (ADT) either by surgical means (castration) or pharmacological approaches (hormone suppression), is the cornerstone of current prostate cancer treatments. Pernigoni et al . found that when the body was deprived of androgens during ADT, the gut microbiome could produce androgens from androgen precursors (see the Perspective by McCulloch and Trinchieri). Gut commensal microbiota in ADT-treated patients or castrated mice produced androgens that were absorbed into the systemic circulation. These microbe-derived androgens appeared to favor the growth of prostate cancer and helped to facilitate development into a castration- or endocrine therapy–resistant state. —PNK
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Ge, Raoling, Xi Xu, Pengfei Xu, Lei Li, Zhiyu Li, and Jinlei Bian. "Degradation of Androgen Receptor through Small Molecules for Prostate Cancer." Current Cancer Drug Targets 18, no. 7 (July 31, 2018): 652–67. http://dx.doi.org/10.2174/1568009617666171107103936.

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Prostate cancer is the most common carcinoma among aged males in western countries and more aggressive and lethal castration resistant prostate cancer often occurs after androgen deprivation therapy. The high expression of androgens and androgen receptor is closely related to prostate cancer. Efficient androgen receptor antagonists, such as enzalutamide and ARN-509, could be employed as potent anti-prostate cancer agents. Nevertheless, recent studies have revealed that F876L mutation in androgen receptor converts the action of enzalutamide and ARN-509 from an antagonist to agonist, so that novel strategies are urgent to address this resistance mechanism. In this review, we focus on the discussion about some novel strategies, which targets androgen receptor mainly through the degrading pathway as potential treatments for prostate cancer.
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42

Gedeborg, Rolf, Johan Styrke, Stacy Loeb, Hans Garmo, and Pär Stattin. "Androgen deprivation therapy and excess mortality in men with prostate cancer during the initial phase of the COVID-19 pandemic." PLOS ONE 16, no. 10 (October 7, 2021): e0255966. http://dx.doi.org/10.1371/journal.pone.0255966.

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Background Men have a higher risk of death from COVID-19 than women and androgens facilitate entrance of the SARS-CoV-2 virus into respiratory epithelial cells. Thus, androgen deprivation therapy may reduce infection rates and improve outcomes for COVID-19. In the spring of 2020, Sweden was highly affected by COVID-19. The aim was to estimate the impact of androgen deprivation therapy on mortality from COVID-19 in men with prevalent prostate cancer by comparing all-cause mortality in the spring of 2020 to that in previous years. Patients and methods Using the Prostate Cancer data Base Sweden all men with prostate cancer on March 1 each year in 2015–2020 were followed until June 30 the same year. Exposure to androgen deprivation therapy was ascertained from filled prescriptions for bicalutamide monotherapy, gonadotropin-releasing hormone agonists (GnRH), or bilateral orchidectomy. Results A total of 9,822 men died in March-June in the years 2015–2020, of whom 5,034 men were on androgen deprivation therapy. There was an excess mortality in 2020 vs previous years in all men. The crude relative mortality rate ratio for 2020 vs 2015–2019 was 0.93 (95% confidence interval (CI) 0.83 to 1.04) in men on GnRH, and 0.90 (95% CI 0.78 to 1.05) in men on bicalutamide monotherapy. After multivariable adjustment these ratios were attenuated to 1.00 (95% CI 0.89 to 1.12) and 0.97 (95% CI 0.84 to 1.12), respectively. When restricting the analysis to the regions with the highest incidence of COVID-19 or to the time period between 2 April to 10 June when mortality in 2020 was increased >30% compared to previous years, the results were similar to the main analysis. Conclusions In this large national population-based cohort of men with prevalent prostate cancer, there was no clear evidence in support for an effect of androgen deprivation therapy on COVID-19 mortality.
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43

Shahinian, Vahakn B., Yong-fang Kuo, Jean L. Freeman, Eduardo Orihuela, and James S. Goodwin. "Characteristics of Urologists Predict the Use of Androgen Deprivation Therapy for Prostate Cancer." Journal of Clinical Oncology 25, no. 34 (December 1, 2007): 5359–65. http://dx.doi.org/10.1200/jco.2006.09.9580.

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Purpose We previously have reported wide variations among urologists in the use of androgen deprivation for prostate cancer. Using the Surveillance, Epidemiology, and End Results–Medicare linked database, we examined how individual urologist characteristics influenced the use of androgen deprivation therapy. Methods Participants included 82,375 men with prostate cancer who were diagnosed from January 1, 1992, through December 31, 2002, and the 2,080 urologists who provided care to them. Multilevel analyses were used to estimate the likelihood of androgen deprivation use within 6 months of diagnosis in the overall cohort, in a subgroup in which use would be of uncertain benefit (primary therapy for localized prostate cancer), and in a subgroup in which use would be evidence-based (adjuvant therapy with radiation for locally advanced disease). Results In the overall cohort of patients, a multilevel model adjusted for patient characteristics, tumor characteristics, and urologist characteristics (eg, board certification, academic affiliation, patient panel size, years since medical school graduation) showed that the likelihood of androgen deprivation use was significantly greater for patients who saw urologists without an academic affiliation. This pattern also was noted when the analysis was limited to settings in which androgen deprivation would have been of uncertain benefit. Odds ratios for use in that context were 1.66 (95% CI, 1.27 to 2.16) for urologists with no academic affiliation and 1.45 (95% CI, 1.13 to 1.85) for urologists with minor versus major academic affiliations. Conclusion Use of androgen deprivation for prostate cancer varies by the characteristics of the urologist. Patients of non–academically affiliated urologists were significantly more likely to receive primary androgen deprivation therapy for localized prostate cancer, a setting in which the benefits are uncertain.
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44

Carroll, Peter. "IL4 Androgen Deprivation Therapy for Prostate Cancer : A US Perspective." Japanese Journal of Urology 101, no. 2 (2010): 53. http://dx.doi.org/10.5980/jpnjurol.101.53.

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45

Bayraktar, Soley. "The Mechanism of Androgen Deprivation and the Androgen Receptor." Open Prostate Cancer Journal 3, no. 1 (May 30, 2010): 47–56. http://dx.doi.org/10.2174/1876822901003010047.

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46

Wang, Yongqing, Yan Wang, Jialong Liang, Wanshi Cai, Zhongsheng Sun, Yan Wang, and Huajing Teng. "Androgen deprivation drives variation of androgen receptor trinucleotide repeats." Acta Biochimica et Biophysica Sinica 51, no. 9 (August 8, 2019): 972–75. http://dx.doi.org/10.1093/abbs/gmz086.

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47

Shastri, Bhavin R., and Subhashini Yaturu. "Metabolic Complications and Increased Cardiovascular Risks as a Result of Androgen Deprivation Therapy in Men with Prostate Cancer." Prostate Cancer 2011 (2011): 1–9. http://dx.doi.org/10.1155/2011/391576.

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Prostate cancer is one of the most common malignancies in men. Charles Huggins and Clarence V. Hodges reported the androgen dependence of prostate cancer in 1941. That led to the utilization of androgen deprivation therapy as an important therapeutic modality to treat prostate cancer. Androgen deprivation therapy has additional systemic effects that include sexual dysfunction, psychological changes and more important are the metabolic changes. Metabolic changes in particular include insulin resistance, increase fat mass and low-density lipoprotein cholesterol, and induce type 2 diabetes. In this review we will focus on the cardiovascular risk associated with androgen deprivation therapy that includes the mechanisms involved.
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Gooren, LJ, and MC Bunck. "Transsexuals and competitive sports." European Journal of Endocrinology 151, no. 4 (October 1, 2004): 425–29. http://dx.doi.org/10.1530/eje.0.1510425.

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Men generally have an inherent performance advantage over women due to their average greater height and muscle mass and power, as the result of correspondingly different exposures to androgens. Therefore, it is considered fair that in sports men and women compete in separate categories. The question now emerging is whether reassigned transsexuals can compete in fairness with others of their new sex. The pertinent question is how far the previous effects of testosterone in male-to-female transsexuals (M-F) are reversible upon androgen deprivation so that M-F have no advantage over women, and, vice versa, what the effects are of androgen exposure in female-to-male transsexuals (F-M) on variables relevant to competition in sports. Before puberty, boys and girls do not differ in height, muscle and bone mass. Recent information shows convincingly that actual levels of circulating testosterone determine largely muscle mass and strength, though with considerable interindividual diversity. This study analyzed the effects of androgen deprivation in 19 M-F and of androgen administration to 17 F-M on muscle mass, hemoglobin (Hb) and insulin-like growth factor-1 (IGF-1). Before cross-sex hormone administration, there was a considerable overlap in muscle mass between M-F and F-M. In both M-F and F-M, height was a strong predictor of muscle mass. Androgen deprivation of M-F decreased muscle mass, increasing the overlap with untreated F-M, but mean muscle mass remained significantly higher in M-F than in F-M. Androgen administration to F-M increased muscle mass without inducing an advantage over nontreated M-F. The conclusion is that androgen deprivation in M-F increases the overlap in muscle mass with women but does not reverse it, statistically. The question of whether reassigned M-F can fairly compete with women depends on what degree of arbitrariness one wishes to accept, keeping in mind, for instance, that similar blood testosterone levels in men have profoundly different biologic effects on muscle properties, rendering competition in sports intrinsically a matter of how nature endows individuals for this competition.
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Kumari, Sangeeta, Dhirodatta Senapati, and Hannelore V. Heemers. "Rationale for the development of alternative forms of androgen deprivation therapy." Endocrine-Related Cancer 24, no. 8 (August 2017): R275—R295. http://dx.doi.org/10.1530/erc-17-0121.

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With few exceptions, the almost 30,000 prostate cancer deaths annually in the United States are due to failure of androgen deprivation therapy. Androgen deprivation therapy prevents ligand-activation of the androgen receptor. Despite initial remission after androgen deprivation therapy, prostate cancer almost invariably progresses while continuing to rely on androgen receptor action. Androgen receptor’s transcriptional output, which ultimately controls prostate cancer behavior, is an alternative therapeutic target, but its molecular regulation is poorly understood. Recent insights in the molecular mechanisms by which the androgen receptor controls transcription of its target genes are uncovering gene specificity as well as context-dependency. Heterogeneity in the androgen receptor’s transcriptional output is reflected both in its recruitment to diverse cognate DNA binding motifs and in its preferential interaction with associated pioneering factors, other secondary transcription factors and coregulators at those sites. This variability suggests that multiple, distinct modes of androgen receptor action that regulate diverse aspects of prostate cancer biology and contribute differentially to prostate cancer’s clinical progression are active simultaneously in prostate cancer cells. Recent progress in the development of peptidomimetics and small molecules, and application of Chem-Seq approaches indicate the feasibility for selective disruption of critical protein–protein and protein–DNA interactions in transcriptional complexes. Here, we review the recent literature on the different molecular mechanisms by which the androgen receptor transcriptionally controls prostate cancer progression, and we explore the potential to translate these insights into novel, more selective forms of therapies that may bypass prostate cancer’s resistance to conventional androgen deprivation therapy.
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Zamagni, Alice, Michele Zanoni, Michela Cortesi, Chiara Arienti, Sara Pignatta, Antonella Naldini, Anna Sarnelli, Antonino Romeo, and Anna Tesei. "Investigating the Benefit of Combined Androgen Modulation and Hypofractionation in Prostate Cancer." International Journal of Molecular Sciences 21, no. 22 (November 10, 2020): 8447. http://dx.doi.org/10.3390/ijms21228447.

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Hypofractionation is currently considered a valid alternative to conventional radiotherapy for the treatment of patients with organ-confined prostate cancer. Recent data have demonstrated that extreme hypofractionation, which involves the use of a high radiation dose per delivered fraction and concomitant reduction of sessions, is a safe and effective treatment, even though its radiobiological rationale is still lacking. The present work aims to investigate the biological basis sustaining this approach and to evaluate the potential of a hypofractionated regimen in combination with androgen deprivation therapy, one of the major standards of care for prostate cancer. Findings show that androgen receptor (AR) modulation, by use of androgens and antiandrogens, has a significant impact on cell survival, especially in hypoxic conditions (4% O2). Subsequent experiments have revealed that AR activity as a transcription factor is involved in the onset of malignant senescence-associated secretory phenotype (SASP) and activation of DNA repair cascade. In particular, we found that AR stimulation in hypoxic conditions promotes the enhanced transcription of ATM gene, the cornerstone kinase of the DNA damage repair genes. Together, these data provide new potential insights to justify the use of androgen deprivation therapy, in particular with second-generation anti-androgens such as enzalutamide, in combination with radiotherapy.
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