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Journal articles on the topic 'Enzalutamide resistance'

Author: Grafiati

Published: 4 June 2021

Last updated: 4 February 2022

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1

Prekovic, S., T. Van den Broeck, S. Linder, et al. "Molecular underpinnings of enzalutamide resistance." Endocrine-Related Cancer 25, no. 11 (2018): R545—R557. http://dx.doi.org/10.1530/erc-17-0136.

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Prostate cancer (PCa) is among the most common adult malignancies, and the second leading cause of cancer-related death in men. As PCa is hormone dependent, blockade of the androgen receptor (AR) signaling is an effective therapeutic strategy for men with advanced metastatic disease. The discovery of enzalutamide, a compound that effectively blocks the AR axis and its clinical application has led to a significant improvement in survival time. However, the effect of enzalutamide is not permanent, and resistance to treatment ultimately leads to development of lethal disease, for which there curr

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2

Thoma, Clemens. "Fitting to overcome enzalutamide resistance." Nature Reviews Urology 13, no. 10 (2016): 564–65. http://dx.doi.org/10.1038/nrurol.2016.160.

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3

Bai, Yunfeng, Zhuangzhuang Zhang, Lijun Cheng, et al. "Inhibition of enhancer of zeste homolog 2 (EZH2) overcomes enzalutamide resistance in castration-resistant prostate cancer." Journal of Biological Chemistry 294, no. 25 (2019): 9911–23. http://dx.doi.org/10.1074/jbc.ra119.008152.

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Enzalutamide, approved by the United States Food and Drug Administration in 2018 for the management of metastatic castration-resistant prostate cancer (CRPC), is an androgen receptor (AR) inhibitor. It blocks androgen binding to the AR, AR nuclear translocation, and AR-mediated DNA binding. Unfortunately, a considerable proportion of tumors eventually develop resistance during the treatment. The molecular mechanisms underlying enzalutamide resistance are not completely understood. Enhancer of zeste homolog 2 (EZH2), the catalytic subunit of polycomb repressor complex 2, has been proposed as a

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Sharifi, Nima, Jianneng Li, Mohammad Alyamani, et al. "Aberrant tumor metabolism to enable glucocorticoid receptor takeover in enzalutamide-resistant prostate cancer." Journal of Clinical Oncology 35, no. 6_suppl (2017): 157. http://dx.doi.org/10.1200/jco.2017.35.6_suppl.157.

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157 Background: Prostate cancer is driven by androgen stimulation of the androgen receptor (AR). The next-generation AR antagonist, enzalutamide, prolongs progression-free and overall survival, but resistance and lethal disease eventually prevail. Emerging data suggest that the glucocorticoid receptor (GR) is upregulated in this context, stimulating expression of approximately 50% of genes normally stimulated by AR, thereby permitting continued growth despite AR blockade. However, countering this mechanism by administration of GR antagonists is problematic because GR is essential for life. Met

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Feng, Tao, Dechao Wei, Jiahui Zhao, et al. "Construction of enzalutamide-resistant cell model of prostate cancer and preliminary screening of potential drug-resistant genes." Experimental Biology and Medicine 246, no. 15 (2021): 1776–87. http://dx.doi.org/10.1177/15353702211012625.

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Among many factors of causing castration-resistant prostate cancer (CRPC) progression, a growing number of evidences have shown androgen receptors play a critical role. Therefore, blocking androgen receptor remains a therapeutic goal of CRPC. However, resistance to androgen receptor inhibitors, for example, enzalutamide, limits therapeutic efficacy for many patients. In this study, to develop an enzalutamide-resistant cell model for molecular mechanism investigation of enzalutamide-resistance, we continuously treated C4-2B cells with multiplied concentrations of enzalutamide. The IC50 of resis

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Chia, KeeMing, Heloisa Milioli, Neil Portman, et al. "Non-canonical AR activity facilitates endocrine resistance in breast cancer." Endocrine-Related Cancer 26, no. 2 (2019): 251–64. http://dx.doi.org/10.1530/erc-18-0333.

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The role of androgen receptor (AR) in endocrine-resistant breast cancer is controversial and clinical trials targeting AR with an AR antagonist (e.g., enzalutamide) have been initiated. Here, we investigated the consequence of AR antagonism using in vitro and in vivo models of endocrine resistance. AR antagonism in MCF7-derived tamoxifen-resistant (TamR) and long-term estrogen-deprived breast cancer cell lines were achieved using siRNA-mediated knockdown or pharmacological inhibition with enzalutamide. The efficacy of enzalutamide was further assessed in vivo in an estrogen-independent endocri

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Chen, Xuedong, Jieyang Lu, Liqun Xia, and Gonghui Li. "Drug Resistance of Enzalutamide in CRPC." Current Drug Targets 19, no. 6 (2018): 613–20. http://dx.doi.org/10.2174/1389450118666170417144250.

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8

Stone, Louise. "Escaping enzalutamide: Malat1 contributes to resistance." Nature Reviews Urology 14, no. 8 (2017): 450. http://dx.doi.org/10.1038/nrurol.2017.91.

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9

Fenner, Annette. "Enzalutamide—differential cross resistance with taxanes." Nature Reviews Urology 12, no. 2 (2014): 64. http://dx.doi.org/10.1038/nrurol.2014.353.

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10

Lee, Hsiu-Chi, Chien-Hui Ou, Yun-Chen Huang, et al. "YAP1 overexpression contributes to the development of enzalutamide resistance by induction of cancer stemness and lipid metabolism in prostate cancer." Oncogene 40, no. 13 (2021): 2407–21. http://dx.doi.org/10.1038/s41388-021-01718-4.

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AbstractMetastatic castration-resistant prostate cancer (mCRPC) is a malignant and lethal disease caused by relapse after androgen-deprivation (ADT) therapy. Since enzalutamide is innovated and approved by US FDA as a new treatment option for mCRPC patients, drug resistance for enzalutamide is a critical issue during clinical usage. Although several underlying mechanisms causing enzalutamide resistance were previously identified, most of them revealed that drug resistant cells are still highly addicted to androgen and AR functions. Due to the numerous physical functions of AR in men, innovated

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11

Kafka, Mona, Fabian Mayr, Veronika Temml, et al. "Dual Inhibitory Action of a Novel AKR1C3 Inhibitor on Both Full-Length AR and the Variant AR-V7 in Enzalutamide Resistant Metastatic Castration Resistant Prostate Cancer." Cancers 12, no. 8 (2020): 2092. http://dx.doi.org/10.3390/cancers12082092.

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The expanded use of second-generation antiandrogens revolutionized the treatment landscape of progressed prostate cancer. However, resistances to these novel drugs are already the next obstacle to be solved. Various previous studies depicted an involvement of the enzyme AKR1C3 in the process of castration resistance as well as in the resistance to 2nd generation antiandrogens like enzalutamide. In our study, we examined the potential of natural AKR1C3 inhibitors in various prostate cancer cell lines and a three-dimensional co-culture spheroid model consisting of cancer cells and cancer-associa

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12

Xu, Huan, Sangsang Li, Yi Sun, et al. "ELOVL5-Mediated Long Chain Fatty Acid Elongation Contributes to Enzalutamide Resistance of Prostate Cancer." Cancers 13, no. 16 (2021): 3957. http://dx.doi.org/10.3390/cancers13163957.

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Prostate cancer (PCa) exhibits an elevated level of de novo lipogenesis that provides both energy and basic metabolites for its malignant development. Long-chain polyunsaturated fatty acids (PUFAs) are elongated and desaturated from palmitate but their effects on PCa progression remain largely unknown. Here, we showed that PUFAs were significantly upregulated by androgen deprivation therapy (ADT) and elevated in neuroendocrine (NE)-like PCa cells. The key enzyme of PUFA elongation, ELOVL5, was overexpressed in NE-like PCa cells as well. Furthermore, we demonstrated that knocking down ELOVL5 in

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13

Linder, Simon, Henk G. van der Poel, Andries M. Bergman, Wilbert Zwart, and Stefan Prekovic. "Enzalutamide therapy for advanced prostate cancer: efficacy, resistance and beyond." Endocrine-Related Cancer 26, no. 1 (2019): R31—R52. http://dx.doi.org/10.1530/erc-18-0289.

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The androgen receptor drives the growth of metastatic castration-resistant prostate cancer. This has led to the development of multiple novel drugs targeting this hormone-regulated transcription factor, such as enzalutamide – a potent androgen receptor antagonist. Despite the plethora of possible treatment options, the absolute survival benefit of each treatment separately is limited to a few months. Therefore, current research efforts are directed to determine the optimal sequence of therapies, discover novel drugs effective in metastatic castration-resistant prostate cancer and define patien

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Li, Jianneng, Michael Berk, Mohammad Alyamani, et al. "Hexose-6-phosphate dehydrogenase blockade reverses prostate cancer drug resistance in xenograft models by glucocorticoid inactivation." Science Translational Medicine 13, no. 595 (2021): eabe8226. http://dx.doi.org/10.1126/scitranslmed.abe8226.

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Prostate cancer resistance to next-generation hormonal treatment with enzalutamide is a major problem and eventuates into disease lethality. Biologically active glucocorticoids that stimulate glucocorticoid receptor (GR) have an 11β-OH moiety, and resistant tumors exhibit loss of 11β-HSD2, the oxidative (11β-OH → 11-keto) enzyme that normally inactivates glucocorticoids, allowing elevated tumor glucocorticoids to drive resistance by stimulating GR. Here, we show that up-regulation of hexose-6-phosphate dehydrogenase (H6PD) protein occurs in prostate cancer tissues of men treated with enzalutam

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15

Simon, Iris, Sonia Perales, Laura Casado-Medina, et al. "Cross-Resistance to Abiraterone and Enzalutamide in Castration Resistance Prostate Cancer Cellular Models Is Mediated by AR Transcriptional Reactivation." Cancers 13, no. 6 (2021): 1483. http://dx.doi.org/10.3390/cancers13061483.

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Androgen deprivation therapy (ADT) and novel hormonal agents (NHAs) (Abiraterone and Enzalutamide) are the goal standard for metastatic prostate cancer (PCa) treatment. Although ADT is initially effective, a subsequent castration resistance status (CRPC) is commonly developed. The expression of androgen receptor (AR) alternative splicing isoforms (AR-V7 and AR-V9) has been associated to CRPC. However, resistance mechanisms to novel NHAs are not yet well understood. Androgen-dependent PCa cell lines were used to generate resistant models to ADT only or in combination with Abiraterone and/or Enz

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16

Fenner, Annette. "Niclosamide jumps the hurdle of enzalutamide resistance." Nature Reviews Urology 11, no. 8 (2014): 424. http://dx.doi.org/10.1038/nrurol.2014.160.

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17

Verma, Shiv, Eswar Shankar, F. Naz Cemre Kalayci, et al. "Androgen Deprivation Induces Transcriptional Reprogramming in Prostate Cancer Cells to Develop Stem Cell-Like Characteristics." International Journal of Molecular Sciences 21, no. 24 (2020): 9568. http://dx.doi.org/10.3390/ijms21249568.

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Enzalutamide, an antiandrogen, is approved for therapy of castration resistant prostate cancer. Clinical applications have shown that approximately 30% of patients acquire resistance after a short period of treatment. However, the molecular mechanisms underlying this resistance is not completely understood. To identify transcriptomic signatures associated with acquisition of drug resistance we profiled gene expression of paired enzalutamide sensitive and resistant human prostate cancer LNCaP (lymph node carcinoma of the prostate) and C4-2B cells. Overlapping genes differentially regulated in t

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18

Han, G. Celine, Justin Hwang, Stephanie A. M. Wankowicz, et al. "Genomic Resistance Patterns to Second-Generation Androgen Blockade in Paired Tumor Biopsies of Metastatic Castration-Resistant Prostate Cancer." JCO Precision Oncology, no. 1 (November 2017): 1–11. http://dx.doi.org/10.1200/po.17.00140.

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Purpose Patients with castration-resistant prostate cancer (CRPC) receive second-generation androgen-deprivation therapy, but frequently experience relapse or do not respond. Understanding the genetic mechanisms of resistance will help to identify strategies and biomarkers that are essential for the next line of therapy. Patients and Methods We analyzed whole exomes of patient-matched pre- and post-treatment tumors from patients with CRPC. These patients had received the secondary androgen-deprivation therapy agent, abiraterone, which suppresses androgens to below castration levels, or enzalut

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19

Yuan, Fuwen, William Hankey, Dayong Wu, et al. "Molecular determinants for enzalutamide-induced transcription in prostate cancer." Nucleic Acids Research 47, no. 19 (2019): 10104–14. http://dx.doi.org/10.1093/nar/gkz790.

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Abstract Enzalutamide, a second-generation androgen receptor (AR) antagonist, has demonstrated clinical benefit in men with prostate cancer. However, it only provides a temporary response and modest increase in survival, indicating a rapid evolution of resistance. Previous studies suggest that enzalutamide may function as a partial transcriptional agonist, but the underlying mechanisms for enzalutamide-induced transcription remain poorly understood. Here, we show that enzalutamide stimulates expression of a novel subset of genes distinct from androgen-responsive genes. Treatment of prostate ca

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20

Li, Chaohao, Nadia A. Lanman, Yifan Kong, et al. "Inhibition of the erythropoietin-producing receptor EPHB4 antagonizes androgen receptor overexpression and reduces enzalutamide resistance." Journal of Biological Chemistry 295, no. 16 (2020): 5470–83. http://dx.doi.org/10.1074/jbc.ra119.011385.

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Prostate cancer (PCa) cells heavily rely on an active androgen receptor (AR) pathway for their survival. Enzalutamide (MDV3100) is a second-generation antiandrogenic drug that was approved by the Food and Drug Administration in 2012 to treat patients with castration-resistant prostate cancer (CRPC). However, emergence of resistance against this drug is inevitable, and it has been a major challenge to develop interventions that help manage enzalutamide-resistant CRPC. Erythropoietin-producing human hepatocellular (Eph) receptors are targeted by ephrin protein ligands and have a broad range of f

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Lounis, Mohamed Amine, Benjamin Péant, Kim Leclerc-Desaulniers, et al. "Modulation of de Novo Lipogenesis Improves Response to Enzalutamide Treatment in Prostate Cancer." Cancers 12, no. 11 (2020): 3339. http://dx.doi.org/10.3390/cancers12113339.

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De novo lipogenesis (DNL) is now considered as a hallmark of cancer. The overexpression of key enzymes of DNL is characteristic of both primary and advanced disease and may play an important role in resistance to therapies. Here, we showed that DNL is highly enhanced in castrate resistant prostate cancer (CRPC) cells compared to hormone sensitive and enzalutamide resistant cells. This observation suggests that this pathway plays an important role in the initiation of aggressive prostate cancer and in the development of enzalutamide resistance. Importantly, here we show that both prostate cance

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22

Chen, William S., Rahul Raj Aggarwal, Li Zhang, et al. "Genomic drivers of poor prognosis and enzalutamide resistance in metastatic castration-resistant prostate cancer." Journal of Clinical Oncology 37, no. 7_suppl (2019): 146. http://dx.doi.org/10.1200/jco.2019.37.7_suppl.146.

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146 Background: Metastatic castration-resistant prostate cancer (mCRPC) is the lethal form of the disease. Several recent efforts have identified genomic alterations in mCRPC, but the clinical implications of these alterations have not been fully elucidated. We conducted a prospective cohort study (n = 101) using whole genome sequencing (WGS) to analyze the association between key driver gene alterations and overall survival. We also performed whole-transcriptome RNA sequencing (RNA-seq) analyses to identify potential mechanisms of enzalutamide resistance in mCRPC. Methods: Metastasis biopsies

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Cui, Yuanyuan, Nagalakshmi Nadiminty, Chengfei Liu, Wei Lou, Chad T. Schwartz та Allen C. Gao. "Upregulation of glucose metabolism by NF-κB2/p52 mediates enzalutamide resistance in castration-resistant prostate cancer cells". Endocrine-Related Cancer 21, № 3 (2014): 435–42. http://dx.doi.org/10.1530/erc-14-0107.

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Cancer cells reprogram their metabolic pathways to facilitate fast proliferation. Previous studies have shown that overexpression of NF-κB2/p52 (p52) in prostate cancer cells promotes cell growth and leads to castration resistance through aberrant activation of androgen receptor (AR). In addition, these cells become resistant to enzalutamide. In this study, we investigated the effects of p52 activation on glucose metabolism and on response to enzalutamide therapy. Data analysis of gene expression arrays showed that genes includingGLUT1(SLC2A1),PKM2,G6PD, andME1involved in the regulation of glu

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Gizzi, Marco, Giulia Baciarello, Aude Flechon, et al. "Previous enzalutamide therapy and response to subsequent taxane therapy in metastatic castration-resistant prostate cancer." Journal of Clinical Oncology 33, no. 7_suppl (2015): 227. http://dx.doi.org/10.1200/jco.2015.33.7_suppl.227.

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227 Background: Cross-resistance between taxanes and androgen receptor axis targeted agents is a matter of debate in metastatic castration-resistant prostate cancer (mCRPC). Preclinical data about response to taxanes after prior enzalutamide suggest some level of cross-resistance (van Soest et al, Eur J Cancer 2013) though this was not confirmed in other models (Al Nakouzi N, Eur Urol 2014). The first objective of this study was to assess the impact of previous enzalutamide therapy on the efficacy of subsequent taxane-based chemotherapy. The second objective was to investigate the prognosis of

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Attard, Gerhardt, and Emmanuel S. Antonarakis. "AR aberrations and resistance to abiraterone or enzalutamide." Nature Reviews Urology 13, no. 12 (2016): 697–98. http://dx.doi.org/10.1038/nrurol.2016.212.

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Gleave, Martin, and Kim Chi. "Toward Predictive Signatures of Enzalutamide Response and Resistance." European Urology 67, no. 1 (2015): 61–63. http://dx.doi.org/10.1016/j.eururo.2014.08.012.

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27

Culig, Zoran. "Molecular Mechanisms of Enzalutamide Resistance in Prostate Cancer." Current Molecular Biology Reports 3, no. 4 (2017): 230–35. http://dx.doi.org/10.1007/s40610-017-0079-1.

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28

Claessens, Frank, Christine Helsen, Stefan Prekovic, et al. "Emerging mechanisms of enzalutamide resistance in prostate cancer." Nature Reviews Urology 11, no. 12 (2014): 712–16. http://dx.doi.org/10.1038/nrurol.2014.243.

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Figg, William Douglas, Elena V. Fernandez, Kelie M. Reece та ін. "Dual targeting of the androgen receptor and hypoxia-inducible factor-1α pathways to synergistically inhibit castrate-resistant prostate cancer." Journal of Clinical Oncology 33, № 7_suppl (2015): 270. http://dx.doi.org/10.1200/jco.2015.33.7_suppl.270.

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270 Background: Enzalutamide is a potent second-generation androgen receptor (AR) antagonist with activity in metastatic castrate-resistant prostate cancer (CRPC). While enzalutamide is initially effective, disease progression inevitably ensues with the emergence of resistance. Intratumoral hypoxia is also associated with CRPC progression and treatment resistance. Given that both AR and HIF-1α are key regulators of these processes, dual targeting of both signaling axis represents an attractive therapeutic approach. Methods: Crosstalk of the AR and HIF-1α signaling pathways were examined in pro

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Roeder, M. Andreas, Frederik Birkebæk Thomsen, Klaus Brasso, Per Rathenborg, Michael Borre, and Peter Iversen. "Biochemical response to enzalutamide therapy in patients with mCRPC following docetaxel and abiraterone treatment." Journal of Clinical Oncology 32, no. 4_suppl (2014): 202. http://dx.doi.org/10.1200/jco.2014.32.4_suppl.202.

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202 Background: Enzalutamide improve overall survival (OS) in patients with metastatic castrate resistant prostate cancer (mCRPC) patients following docetaxel treatment. Optimal sequencing and possible cross-resistance for novel mCRPC therapeutics is less understood. In this study we report biochemical response and OS after enzalutamide treatment in post-chemo mCRPC patients following progression on post-chemo abiraterone treatment. Methods: Twenty-four post-chemotherapy and post-abiraterone mCRPC patients with progressive disease received enzalutamide 160 mg/daily in a Danish compassionate-us

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van Soest, Robert J., Martin E. van Royen, Ellen S. de Morrée, et al. "Effects on androgen receptor nuclear import by docetaxel, cabazitaxel, abiraterone, and enzalutamide: Potential mechanism for cross-resistance in castration-resistant prostate cancer (CRPC)." Journal of Clinical Oncology 31, no. 15_suppl (2013): 5064. http://dx.doi.org/10.1200/jco.2013.31.15_suppl.5064.

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5064 Background: Recent reports have suggested that paclitaxel and docetaxel, which exert their therapeutic activity primarily through inhibition of microtubule function and mitosis, also impair androgen receptor (AR) signaling. AR signaling is the key therapeutic target for the newly available agents abiraterone and enzalutamide. A recent study suggested impaired efficacy of docetaxel when given after progression on abiraterone in patients with CRPC. To identify potential mechanisms of cross-resistance, we investigated whether and to what extent AR nuclear translocation is affected by docetax

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Nadal, Rosa, Zhe Zhang, Hitesh Raheja, Mario A. Eisenberger, and Emmanuel S. Antonarakis. "Clinical activity of enzalutamide pre- and post-docetaxel in patients with metastatic castration-resistant prostate cancer (mCRPC)." Journal of Clinical Oncology 32, no. 4_suppl (2014): 216. http://dx.doi.org/10.1200/jco.2014.32.4_suppl.216.

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216 Background: Enzalutamide is an androgen receptor signaling inhibitor that is FDA-approved for post-docetaxel mCRPC patients. Overlapping mechanisms of action and clinical evidence for an interaction between taxanes and androgen-targeted therapies complicates optimal sequencing of taxanes and enzalutamide. We retrospectively evaluated the efficacy of enzalutamide pre- (preD) and post-docetaxel (postD) therapy. Methods: Men with mCRPC who received enzalutamide preD or postD were identified from a single institution database. We investigated factors influencing enzalutamide activity by using

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Popov, S. V. "Modern antiandrogenic therapy of patients with castration-resistant prostate cancer without metastases." Meditsinskiy sovet = Medical Council, no. 20 (December 21, 2020): 84–88. http://dx.doi.org/10.21518/2079-701x-2020-20-84-88.

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The prevalence of prostate cancer continues to increase worldwide. The effectiveness of androgen deprivation therapy for advanced prostate cancer has a time limit, after which castration resistance and disease progression are formed. A part of patients with castrate-resistant prostate cancer has no metastases (according to standard imaging methods). The main goal of treatment of these patients is to prolong the time before metastasis formation. This article presents a review of the current understanding of the molecular mechanisms underlying the inhibition of androgen-receptor signaling with e

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Thoma, Clemens. "Breaking AKR1C3-mediated enzalutamide resistance by inhibiting androgen synthesis." Nature Reviews Urology 12, no. 3 (2015): 124. http://dx.doi.org/10.1038/nrurol.2015.31.

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Buonerba, Carlo, and Giuseppe Di Lorenzo. "Isin vitro-acquired resistance to enzalutamide a useful model?" Future Oncology 10, no. 16 (2014): 2551–53. http://dx.doi.org/10.2217/fon.14.212.

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Watson, R. William, Haleema Azam, Claudia Aura, et al. "Inhibition of Serum Response Factor Improves Response to Enzalutamide in Prostate Cancer." Cancers 12, no. 12 (2020): 3540. http://dx.doi.org/10.3390/cancers12123540.

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Castrate-resistant prostate cancer (CRPC) is challenging to treat with the androgen receptor (AR), the main target and key focus of resistance. Understanding the mechanisms of AR interaction with co-regulators will identify new therapeutic targets to overcome AR resistance mechanisms. We previously identified the serum response factor (SRF) as a lead target in an in vitro model of CRPC and showed that SRF expression in tissues of CRPC patients was associated with shorter survival. Here, we tested SRF inhibition in vitro and in vivo to assess SRF as a potential target in CRPC. Inhibition of SRF

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Shiota, Masaki, Akira Yokomizo, Ario Takeuchi та ін. "Protein kinase C regulates Twist1 expression via NF-κB in prostate cancer". Endocrine-Related Cancer 24, № 4 (2017): 171–80. http://dx.doi.org/10.1530/erc-16-0384.

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The progression of prostate cancer to metastatic and castration-resistant disease represents a critical step. We previously showed that protein kinase C (PKC) activation followed by Twist1 and androgen receptor (AR) induction played a critical role in castration resistance, but the precise molecular mechanism remains unknown. This study aimed to elucidate the relevant molecular mechanism, focusing on NF-κB transcription factor. We examined the activity of NF-κB after PKC inhibition, and the expression of Twist1 and AR after inhibition of NF-κB in human prostate cancer cells. We also investigat

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Armstrong, Andrew J., Russell Z. Szmulewitz, Daniel P. Petrylak, et al. "ARCHES: A Randomized, Phase III Study of Androgen Deprivation Therapy With Enzalutamide or Placebo in Men With Metastatic Hormone-Sensitive Prostate Cancer." Journal of Clinical Oncology 37, no. 32 (2019): 2974–86. http://dx.doi.org/10.1200/jco.19.00799.

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PURPOSE Enzalutamide, a potent androgen-receptor inhibitor, has demonstrated significant benefits in metastatic and nonmetastatic castration-resistant prostate cancer. We evaluated the efficacy and safety of enzalutamide in metastatic hormone-sensitive prostate cancer (mHSPC). METHODS ARCHES (ClinicalTrials.gov identifier: NCT02677896 ) is a multinational, double-blind, phase III trial, wherein 1,150 men with mHSPC were randomly assigned 1:1 to enzalutamide (160 mg/day) or placebo, plus androgen deprivation therapy (ADT), stratified by disease volume and prior docetaxel chemotherapy. The prima

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Boudadi, Karim, and Emmanuel S. Antonarakis. "Resistance to Novel Antiandrogen Therapies in Metastatic Castration-Resistant Prostate Cancer." Clinical Medicine Insights: Oncology 10s1 (January 2016): CMO.Ss34534. http://dx.doi.org/10.4137/cmo.ss34534.

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Despite the introduction of novel therapies that maximally decrease androgen-receptor (AR) signaling activity, metastatic castration-resistant prostate cancer (mCRPC) remains a lethal disease. Even though abiraterone and enzalutamide represent breakthroughs in the treatment of mCRPC and have demonstrated significant survival benefits, a significant proportion of patients have primary resistance to these agents and virtually all patients develop secondary resistance. While the mechanisms of resistance to these agents are not fully understood, many hypotheses of AR-dependent and AR-independent m

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Denmeade, Samuel R., Hao Wang, Neeraj Agarwal, et al. "TRANSFORMER: A Randomized Phase II Study Comparing Bipolar Androgen Therapy Versus Enzalutamide in Asymptomatic Men With Castration-Resistant Metastatic Prostate Cancer." Journal of Clinical Oncology 39, no. 12 (2021): 1371–82. http://dx.doi.org/10.1200/jco.20.02759.

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PURPOSE Prostate cancer (PCa) becomes resistant to androgen ablation through adaptive upregulation of the androgen receptor in response to the low-testosterone microenvironment. Bipolar androgen therapy (BAT), defined as rapid cycling between high and low serum testosterone, disrupts this adaptive regulation in castration-resistant PCa (CRPC). METHODS The TRANSFORMER (Testosterone Revival Abolishes Negative Symptoms, Fosters Objective Response and Modulates Enzalutamide Resistance) study is a randomized study comparing monthly BAT (n = 94) with enzalutamide (n = 101). The primary end point was

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Verma, Shiv, Eswar Shankar, E. Ricky Chan, and Sanjay Gupta. "Metabolic Reprogramming and Predominance of Solute Carrier Genes during Acquired Enzalutamide Resistance in Prostate Cancer." Cells 9, no. 12 (2020): 2535. http://dx.doi.org/10.3390/cells9122535.

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Androgen deprivation therapy (ADT) is standard-of-care for advanced-stage prostate cancer, and enzalutamide (Xtandi®, Astellas, Northbrook, IL, USA), a second generation antiandrogen, is prescribed in this clinical setting. The response to this medication is usually temporary with the rapid emergence of drug resistance. A better understanding of gene expression changes associated with enzalutamide resistance will facilitate circumventing this problem. We compared the transcriptomic profile of paired enzalutamide-sensitive and resistant LNCaP and C4-2B prostate cancer cells for identification o

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He, Meng Xiao, Michael S. Cuoco, Jett Crowdis, et al. "Transcriptional mediators of treatment resistance in lethal prostate cancer." Nature Medicine 27, no. 3 (2021): 426–33. http://dx.doi.org/10.1038/s41591-021-01244-6.

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AbstractMetastatic castration-resistant prostate cancer is typically lethal, exhibiting intrinsic or acquired resistance to second-generation androgen-targeting therapies and minimal response to immune checkpoint inhibitors1. Cellular programs driving resistance in both cancer and immune cells remain poorly understood. We present single-cell transcriptomes from 14 patients with advanced prostate cancer, spanning all common metastatic sites. Irrespective of treatment exposure, adenocarcinoma cells pervasively coexpressed multiple androgen receptor isoforms, including truncated isoforms hypothes

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Torquato, Samantha, Aparna Pallavajjala, Alexa Goldstein, et al. "Genetic Alterations Detected in Cell-Free DNA Are Associated With Enzalutamide and Abiraterone Resistance in Castration-Resistant Prostate Cancer." JCO Precision Oncology, no. 3 (December 2019): 1–14. http://dx.doi.org/10.1200/po.18.00227.

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PURPOSE Androgen receptor ( AR) gene alterations, including ligand-binding domain mutations and copy number (CN) gain, have yet to be fully established as predictive markers of resistance to enzalutamide and abiraterone in men with metastatic castration-resistant prostate cancer (mCRPC). The goal of this study was to validate AR gene alterations detected in cell-free DNA (cfDNA) as markers of enzalutamide and abiraterone resistance in patients with mCRPC. METHODS Patients with mCRPC (N = 62) were prospectively enrolled between 2014 and 2018. Blood was collected before therapies—enzalutamide (n

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Cristóbal, Ion, Blanca Torrejón, Manuel Pedregal, Federico Rojo, and Jesús García-Foncillas. "Targeting PP2A to overcome enzalutamide resistance in AR+ breast tumors." Endocrine-Related Cancer 24, no. 1 (2017): L5—L6. http://dx.doi.org/10.1530/erc-16-0444.

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Lee, Geun Taek, Jeffrey A. Rosenfeld, Won Tae Kim, et al. "TCF4 induces enzalutamide resistance via neuroendocrine differentiation in prostate cancer." PLOS ONE 14, no. 9 (2019): e0213488. http://dx.doi.org/10.1371/journal.pone.0213488.

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Shore, Neal D., Eleni Efstathiou, Rupal Patel, et al. "An open-label phase Ib study of ORIC-101 in combination with enzalutamide in patients with metastatic prostate cancer progressing on enzalutamide." Journal of Clinical Oncology 38, no. 6_suppl (2020): TPS253. http://dx.doi.org/10.1200/jco.2020.38.6_suppl.tps253.

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TPS253 Background: The glucocorticoid receptor (GR) has been identified as a potential antiandrogen bypass mechanism of resistance to enzalutamide treatment in prostate cancer. In an in vivo enzalutamide resistant prostate cancer model, GR activates a transcriptional program that is similar but distinguishable from AR and maintains the resistant phenotype (Arora et al 2013). In human prostate cancer cells, GR expression increases upon exposure to AR antagonists, and higher GR expression is associated with treatment resistance. These findings suggest that combined inhibition of both GR and AR m

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Reig, Òscar, Mercedes Marin, Maria Mila, et al. "The influence of treatment sequence in the prognostic value of TMPRSS2-ERG as a biomarker of taxane resistance in castration-resistant prostate cancer." Journal of Clinical Oncology 37, no. 7_suppl (2019): 235. http://dx.doi.org/10.1200/jco.2019.37.7_suppl.235.

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235 Background: TMPRSS2-ERG expression at peripheral blood has been correlated with lower docetaxel benefit. This multicenter study prospectively assessed the role of TMPRSS2-ERG mRNA as a taxane-resistance biomarker in blood and retrospectively in tumors, and explored the impact of prior abiraterone/enzalutamide (A/E) in castration-resistant prostate cancer (CRPC) patients and in vitro. Methods: TMPRSS2-ERG was tested by quantitative reverse-transcription PCR. We included 204 patients (137 blood and 124 tumor samples) treated with taxanes. TMPRSS2-ERG expression was correlated with PSA-progre

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Komura, Kazumasa, Yuya Fujiwara, Taizo Uchimoto, et al. "Comparison of Radiographic Progression-Free Survival and PSA Response on Sequential Treatment Using Abiraterone and Enzalutamide for Newly Diagnosed Castration-Resistant Prostate Cancer: A Propensity Score Matched Analysis from Multicenter Cohort." Journal of Clinical Medicine 8, no. 8 (2019): 1251. http://dx.doi.org/10.3390/jcm8081251.

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Background: There is emerging evidence that radiographic progression-free survival (rPFS) is highly correlated with overall survival (OS), potentially serving as an indicator of treatment outcome for castration-resistant prostate cancer (CRPC). The objective of this study is to assess rPFS and prostate specific antigen (PSA) response in sequential treatment using androgen signaling inhibitors (ASIs) including abiraterone and enzalutamide in newly diagnosed CRPC. Methods: Propensity score matching was performed to reduce bias by confounding factors between first-line ASIs. The primary endpoints

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Rajaram, Pravien, Alyssa Rivera, Kevin Muthima, Nicholas Olveda, Hubert Muchalski, and Qiao-Hong Chen. "Second-Generation Androgen Receptor Antagonists as Hormonal Therapeutics for Three Forms of Prostate Cancer." Molecules 25, no. 10 (2020): 2448. http://dx.doi.org/10.3390/molecules25102448.

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Enzalutamide is the first second-generation nonsteroidal androgen receptor (AR) antagonist with a strong binding affinity to AR. Most significantly, enzalutamide can prolong not only overall survival time and metastatic free survival time for patients with lethal castration-resistant prostate cancer (CRPC), but also castration-resistant free survival time for patients with castration-sensitive prostate cancer (CSPC). Enzalutamide has thus been approved by the US Food and Drug Administration (FDA) for the treatment of both metastatic (in 2012) and non-metastatic (in 2018) CRPC, as well as CSPC

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Xiang, Zhendong, Chengdang Xu, Gang Wu, Bo Liu, and Denglong Wu. "CircRNA-UCK2 increased TET1 inhibits proliferation and invasion of prostate cancer cells via sponge miRNA-767-5p." Open Medicine 14, no. 1 (2019): 833–42. http://dx.doi.org/10.1515/med-2019-0097.

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AbstractA majority of the patients with advanced prostate cancer initially respond to androgen deprivation therapy and enzalutamide therapy, but eventually enter the castration-resistant prostate cancer (CRPC) phase. Some studies have shown that the activation of other signalling pathways in CRPC cells replaces the function of the androgen receptor, as well as promotes cell metastasis and progression. However, the mechanisms underlying this side effect remain unclear. The present study aims to explore the continued progression of cells after enzalutamide resistance. Low expression of circRNA-U

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