Submitted Successfully!
To reward your contribution, here is a gift for you: A free trial for our video production service.
Thank you for your contribution! You can also upload a video entry or images related to this topic.
Version Summary Created by Modification Content Size Created at Operation
1
Bo-Ren Wang
 -- 1422 2022-08-23 17:54:44 |
2 format corrected.
Beatrix Zheng
 Meta information modification 1422 2022-08-24 03:24:11 | |
3 format corrected.
Beatrix Zheng
 + 6 word(s) 1428 2022-08-24 03:28:46 | |
4 format corrected.
Beatrix Zheng
 + 3 word(s) 1431 2022-08-24 03:30:39 |

Video Upload Options

Do you have a full video?
Send video materials Upload full video

Confirm

Are you sure to Delete?
Yes No
Cite
If you have any further questions, please contact Encyclopedia Editorial Office.
Wang, B.;  Chen, Y.;  Kao, W.;  Lai, C.;  Lin, H.;  Hsieh, J. Hormone Therapy for Castration-Resistant Prostate Cancer. Encyclopedia. Available online: https://encyclopedia.pub/entry/26409 (accessed on 27 July 2024).
Wang B,  Chen Y,  Kao W,  Lai C,  Lin H,  Hsieh J. Hormone Therapy for Castration-Resistant Prostate Cancer. Encyclopedia. Available at: https://encyclopedia.pub/entry/26409. Accessed July 27, 2024.
Wang, Bo-Ren, Yu-An Chen, Wei-Hsiang Kao, Chih-Ho Lai, Ho Lin, Jer-Tsong Hsieh. "Hormone Therapy for Castration-Resistant Prostate Cancer" Encyclopedia, https://encyclopedia.pub/entry/26409 (accessed July 27, 2024).
Wang, B.,  Chen, Y.,  Kao, W.,  Lai, C.,  Lin, H., & Hsieh, J. (2022, August 23). Hormone Therapy for Castration-Resistant Prostate Cancer. In Encyclopedia. https://encyclopedia.pub/entry/26409
Wang, Bo-Ren, et al. "Hormone Therapy for Castration-Resistant Prostate Cancer." Encyclopedia. Web. 23 August, 2022.
Hormone Therapy for Castration-Resistant Prostate Cancer
Edit
This entry is adapted from the peer-reviewed paper 10.3390/biomedicines10081872

Prostate cancer (PCa) is the most common cancer and the second deadliest cancer among men in the United States, which is mainly due to metastatic disease. In general, surgery or radiation is potentially a curative treatment for localized disease. Since PCa is characterized as a typical androgen-dependent disease, hormone therapy (i.e., androgen deprivation therapy (ADT)) is the most effective therapy to control metastatic disease. However, almost all patients eventually develop castration-resistant PCa (CRPC) within 12 to 18 months, with a median survival of 14 to 26 months. Nowadays, new anti-androgens (Enzalutamide or Abiraterone), radiotherapy (Radium-223) or immunotherapy (sipuleucel-T) have been approved for metastatic CRPC (mCRPC) patients to prolong the overall survival. Inevitably, mCRPC further acquires resistance and becomes therapy- and castration-resistant PCa (t-CRPC), which is considered as an end-stage disease without effective therapy, and on which new therapeutic strategies have been actively explored.

castration-resistant prostate cancer recurrent therapy and castration-resistant prostate cancer precision medicine

1. Enzalutamide

In Prostate cancer (PCa), androgen receptor (AR) activated by androgens still represents a critical oncogenic pathway. Enzalutamide is a novel antiandrogen agent that can block AR with high affinity compared to traditional antiandrogens such as bicalutamide or flutamide [1]. Besides direct binding to AR, it can reduce AR translocation into the nucleus and prevent its transcription by binding to DNA [2] (Figure 1).
/media/item_content/202208/63057ccd1c58fbiomedicines-10-01872-g001.png
Figure 1. Molecular mechanism of the therapies for prostate cancer.
Enzalutamide was approved by the Food and Drug Administration (FDA) in 2012 for use on metastatic castration-resistant PCa (CRPC) based on the randomized, phase III trial study (AFFIRM) [3][4] (Table 1). The study demonstrated that patients who received enzalutamide after chemotherapy improved median survival from 13.6 to 18.4 months (HR: 0.63 p < 0.001). Another phase III, double-blind, randomized study (PREVAIL) (Table 1) compared patients receiving enzalutamide before chemotherapy and showed that radiographic progression-free survival (rPFS) and overall survival (OS) benefit from 31.3 to 35.3 months [5][6]. It also can delay the initiation of chemotherapy in patients with metastatic PCa. In the phase III randomized trial (PROSPER), enzalutamide demonstrated the benefit of metastasis-free survival rate compared to placebo (36.6 months vs. 14.7 months, p < 0.001) in patients with non-metastatic CRPC (nmCRPC) [7] (Table 1). Therefore, the FDA expand the use of enzalutamide in patients with nmCRPC since 2018.
Table 1. FDA-approved therapies for prostate cancer.
Drug Class Therapy Indication Clinical
Trial		 Efficacy
(Mon.)		 Impact on PCa Treatment Reference
2nd-generation antiandrogen Enzalutamide mCRPC AFFIRM OS 18.4 vs. 13.6 ENZ improves OS
after chemotherapy		 [4]
PREVAIL OS 35.3 vs. 31.3 ENZ improves OS in
chemotherapy naïve		 [5][6]
nmCRPC PROSPER MFS 36.6 vs. 14.7 ENZ decreases the risk of metastasis [7]
mCSPC ENZEMET 80% vs. 72%
(3-year OS)		 ENZ improves OS and decreases disease progression [8]
ARCHES rPFS
NR vs. 19.0		 ENZ decreases the risk of metastatic progression [9]
Apalutamide nmCRPC SPARTAN MFS 40.5 vs. 16.2 APA decreasse the risk of metastasis [10]
mCSPC TITAN 2-year OS
82.4 vs. 73.5		 APA improves OS and PFS [11]
Darolutamide nmCRPC ARAMIS MFS 40.4 vs. 18.4 DA decreases the risk of metastasis [12]
Abiraterone mCRPC COA-301 OS 15.8 vs. 11.2 AB improves OS
after chemotherapy		 [13]
COA-302 OS 34.7 vs. 30.3 AB improves OS in
chemotherapy naïve		 [14]
High-volume CSPC LATITUDE OS 53.3 vs. 36.5 AB improves OS in
high-risk CSPC		 [15][16]
Radiotherapy Radium 223 CRPC with symptomatic bone metastasis, no visceral metastasis ALSYMPCA OS 14.9 vs. 11.3 RA-223 improves OS in symptomatic bony metastatic mCRPC [17]
177Lu-PSMA 617 PSMA-positive mCRPC and already treated with ARB and chemotherapy VISION OS 15.3 vs. 11.3
rPFS 8.7 vs. 3.4		 177Lu-PSMA 617 improves OS and rPFS in PSMA-positive mCRPC [18]
Immunotherapy Sipuleucel-T mCRPC IMPACT OS 25.8 vs. 21.7 Sipuleucel-T improves OS in mCRPC [19]
PARP-I Olaparib mCRPC with HRR genes mutation after ENZ or AB PROfound OS 18.5 vs.15.1
rPFS 7.4 vs. 3.6		 Olaparib improves OS and rPFS in mCRPC with HRR gene mutation [20]
Rubraca mCRPC with BRCA genes after ARB or chemotherapy TRITON2
(phase2)
TRITON3
(phase3)		 ORR 43.5% (IRR)
PSA response rate 54.8%		 Rubraca has the antitumor activity in mCRPC with BRCA gene mutation [21][22]
PCa = prostate cancer; nmCRPC = non-metastatic castration-resistant prostate cancer; mCSPC = metastatic castration-sensitive prostate cancer; mCRPC = metastatic castration-resistant prostate cancer; OS = overall survival; rPFS = Radiographic progression-free survival; FDA = Food and Drug Administration; ENZ = Enzalutamide; APA = Apalutamide; DA = Darolutamide; AB = Abiraterone; MFS = metastatic-free survival; NR = non-reached; RA-223 = Radium 223; ARB = androgen receptor blocker; HRR = homologous recombination repair; ORR = objective response rate; IRR = independent radiology review; PARP-I = Polyadenosine diphosphate ribose polymerase inhibitors.
In patients with metastatic, hormone-sensitive PCa (mHSPC), enzalutamide improved the overall survival rate and progression-free survival over standard care in the phase III, randomized trial (ENZAMET) [8] (Table 1). In another double-blind, randomized trial (ARCHES), enzalutamide also revealed the benefit of rPFS (not-reached vs. 19 months, p < 0.001) in mHSPC patients [9] (Table 1). Regarding the safety and adverse effects of the drug, enzalutamide had the adverse effect to the central nervous system via entering the blood–brain barrier. Therefore, seizure and even posterior encephalopathy syndrome were reported in rare cases [2][7].

2. Apalutamide

Apalutamide is a second-generation androgen inhibitor and is already approved for use in nmCRPC and mHSPC. A double-blind, placebo-controlled, phase III trial (SPARTAN) demonstrated that apalutamide improved median metastasis-free survival compared with placebo (40.5 vs. 16.2 months. p < 0.001) in patients with non-mCRPC [10] (Table 1). Time to symptomatic progression was significantly longer with apalutamide than with placebo [10]. Another randomized phase III trial (TITAN), in the patients with mHSPC, apalutamide plus androgen deprivation therapy (ADT), significantly improved OS and rPFS compared with ADT plus placebo [11] (Table 1).
The adverse effects of interest include fracture, dizziness, and hypothyroidism. Compared with other androgen inhibitors with enzalutamide and darolutamide, skin rash was mostly found in apalutamide [2][10][11].

3. Darolutamide

Like other second-generation androgen inhibitors, darolutamide can inhibit AR translocation, DNA binding, and AR-mediated transcription (Figure 1). From the phase I/II study, darolutamide inhibited cell proliferation more efficiently than enzalutamide in a castration animal model [23]. Besides, it also blocks the activity of the mutant ARs like the F876L mutation caused by enzalutamide or apalutamide [23].
In a randomized, double-blind, placebo-controlled, phase III trial (ARAMIS), darolutamide improved metastasis-free survival (40.4 months vs. 18.4 months, p < 0.001) compared with placebo in patients with nmCRPC [12] (Table 1). Additionally, it also demonstrated benefit in OS, time to pain progression, time to cytotoxic chemotherapy, and time to a symptomatic skeletal event [12]. Another randomized, phase III trial (ARASENS), combination therapy with darolutamide, ADT, and docetaxel improve OS over placebo plus ADT and docetaxel in patients with mHSPC [24].
Generally, darolutamide causes less toxic effect because of low blood–brain barrier penetration and low binding affinity for γ-aminobutyric acid type A receptors due to its unique structure, which is different from enzalutamide and apalutamide. Therefore, it causes less central nervous system effect like a seizure [2][12]. The most reported adverse effects were fatigue and asthenic conditions [12].

4. Abiraterone

Abiraterone acetate is a selective CYP17 enzyme inhibitor that can decrease the synthesis of androgen of the testis, adrenal gland and prostate gland [25][26][27][28] (Figure 1). In the double-blind, placebo-controlled phase 3 study (CO-AA-301 clinical trial), it demonstrated that abiraterone combined with prednisolone improved OS compared to the placebo plus prednisolone group (15.8 vs. 11.2 months. p < 0.0001) in patients with metastatic CRPC (mCRPC) who progressed after chemotherapy [13] (Table 1). Another phase III study (CO-AA-302) further confirmed the benefit of abiraterone used in patients with mCPRC before chemotherapy. It improved rPFS and OS (34.7 months vs. 30.3 months) compared with placebo [14] (Table 1). The FDA approved the use of abiraterone in patients with mCRPC post-chemotherapy in 2011, subsequently, pre-chemotherapy based on these two phases III clinical trials in 2012. Furthermore, the FDA further approved the use of abiraterone in patients with high-risk mHSPC based on the phase III clinical trial (LATITUDE study) in 2018 [15][16] (Table 1). Abiraterone plus ADT and prednisolone improved OS and rPFS in patients with mHSPC compared with placebo plus ADT, because the use of abiraterone may cause the miner alocorticoid increase, which will cause fluid edema, liver function impairment, low potassium level, and high blood pressure [13][14][15]. Therefore, abiraterone must be used in combination with steroid, and regular follow-up of liver function and potassium level is necessary [13][14][15]. Previous study indicated that the E3 ubiquitin ligase adaptor speckle-type pox virus and zinc finger (POZ) protein (SPOP) are involved in controlling protein stability of AR by interacting with steroid receptor coactivator 3 (SRC-3) protein and some of the transcriptional coactivators [29]. Wild-type SPOP can promote the SRC-3 protein and then suppress AR transcriptional activity, thus functioning as a potential tumor suppressor [29]. However, some studies identified mutant SPOP in 6–15% of PCa and it can alleviate the tumor suppressive effect [30][31]. Surprisingly, PCa patients with mutant SPOP appear to delay the onset of ADT resistance to 42.0 (95% CI: 25.7–60.8) months. Also, the better outcomes in patients with mutant SPOP treated with abiraterone and enzalutamide were observed [32][33]. Therefore, it implies that SPOP mutation could enhance ADT effect by maintaining AR dependency. Inflammatory response is related to patients treated with ADT. It can cause a IL-6 increase through testosterone suppression [34] and disease progression to CRPC through the activation STAT3 pathway in PCa [35], because IL-6 is known to induce epithelial–mesenchymal transition (EMT) leading to PCa invasion [36]. It is warranted that inflammation factors can be of prognostic value in PCa progression [35].

References

  1. Tran, C.; Ouk, S.; Clegg, N.J.; Chen, Y.; Watson, P.A.; Arora, V.; Wongvipat, J.; Smith-Jones, P.M.; Yoo, D.; Kwon, A.; et al. Development of a second-generation antiandrogen for treatment of advanced prostate cancer. Science 2009, 324, 787–790.
  2. Heidegger, I.; Brandt, M.P.; Heck, M.M. Treatment of non-metastatic castration resistant prostate cancer in 2020: What is the best? Urol. Oncol. 2020, 38, 129–136.
  3. Fizazi, K.; Scher, H.I.; Miller, K.; Basch, E.; Sternberg, C.N.; Cella, D.; Forer, D.; Hirmand, M.; de Bono, J.S. Effect of enzalutamide on time to first skeletal-related event, pain, and quality of life in men with castration-resistant prostate cancer: Results from the randomised, phase 3 AFFIRM trial. Lancet Oncol. 2014, 15, 1147–1156.
  4. Scher, H.I.; Fizazi, K.; Saad, F.; Taplin, M.E.; Sternberg, C.N.; Miller, K.; de Wit, R.; Mulders, P.; Chi, K.N.; Shore, N.D.; et al. Increased survival with enzalutamide in prostate cancer after chemotherapy. N. Engl. J. Med. 2012, 367, 1187–1197.
  5. Beer, T.M.; Armstrong, A.J.; Rathkopf, D.; Loriot, Y.; Sternberg, C.N.; Higano, C.S.; Iversen, P.; Evans, C.P.; Kim, C.S.; Kimura, G.; et al. Enzalutamide in Men with Chemotherapy-naïve Metastatic Castration-resistant Prostate Cancer: Extended Analysis of the Phase 3 PREVAIL Study. Eur. Urol. 2017, 71, 151–154.
  6. Beer, T.M.; Armstrong, A.J.; Rathkopf, D.E.; Loriot, Y.; Sternberg, C.N.; Higano, C.S.; Iversen, P.; Bhattacharya, S.; Carles, J.; Chowdhury, S.; et al. Enzalutamide in metastatic prostate cancer before chemotherapy. N. Engl. J. Med. 2014, 371, 424–433.
  7. Hussain, M.; Fizazi, K.; Saad, F.; Rathenborg, P.; Shore, N.; Ferreira, U.; Ivashchenko, P.; Demirhan, E.; Modelska, K.; Phung, D.; et al. Enzalutamide in Men with Nonmetastatic, Castration-Resistant Prostate Cancer. N. Engl. J. Med. 2018, 378, 2465–2474.
  8. Davis, I.D.; Martin, A.J.; Stockler, M.R.; Begbie, S.; Chi, K.N.; Chowdhury, S.; Coskinas, X.; Frydenberg, M.; Hague, W.E.; Horvath, L.G.; et al. Enzalutamide with Standard First-Line Therapy in Metastatic Prostate Cancer. N. Engl. J. Med. 2019, 381, 121–131.
  9. Armstrong, A.J.; Szmulewitz, R.Z.; Petrylak, D.P.; Holzbeierlein, J.; Villers, A.; Azad, A.; Alcaraz, A.; Alekseev, B.; Iguchi, T.; Shore, N.D.; et al. ARCHES: A Randomized, Phase III Study of Androgen Deprivation Therapy with Enzalutamide or Placebo in Men With Metastatic Hormone-Sensitive Prostate Cancer. J. Clin. Oncol. 2019, 37, 2974–2986.
  10. Smith, M.R.; Saad, F.; Chowdhury, S.; Oudard, S.; Hadaschik, B.A.; Graff, J.N.; Olmos, D.; Mainwaring, P.N.; Lee, J.Y.; Uemura, H.; et al. Apalutamide Treatment and Metastasis-free Survival in Prostate Cancer. N. Engl. J. Med. 2018, 378, 1408–1418.
  11. Chi, K.N.; Agarwal, N.; Bjartell, A.; Chung, B.H.; Pereira de Santana Gomes, A.J.; Given, R.; Juárez Soto, Á.; Merseburger, A.S.; Özgüroğlu, M.; Uemura, H.; et al. Apalutamide for Metastatic, Castration-Sensitive Prostate Cancer. N. Engl. J. Med. 2019, 381, 13–24.
  12. Fizazi, K.; Shore, N.; Tammela, T.L.; Ulys, A.; Vjaters, E.; Polyakov, S.; Jievaltas, M.; Luz, M.; Alekseev, B.; Kuss, I.; et al. Darolutamide in Nonmetastatic, Castration-Resistant Prostate Cancer. N. Engl. J. Med. 2019, 380, 1235–1246.
  13. Fizazi, K.; Scher, H.I.; Molina, A.; Logothetis, C.J.; Chi, K.N.; Jones, R.J.; Staffurth, J.N.; North, S.; Vogelzang, N.J.; Saad, F.; et al. Abiraterone acetate for treatment of metastatic castration-resistant prostate cancer: Final overall survival analysis of the COU-AA-301 randomised, double-blind, placebo-controlled phase 3 study. Lancet Oncol. 2012, 13, 983–992.
  14. Ryan, C.J.; Smith, M.R.; Fizazi, K.; Saad, F.; Mulders, P.F.; Sternberg, C.N.; Miller, K.; Logothetis, C.J.; Shore, N.D.; Small, E.J.; et al. Abiraterone acetate plus prednisone versus placebo plus prednisone in chemotherapy-naive men with metastatic castration-resistant prostate cancer (COU-AA-302): Final overall survival analysis of a randomised, double-blind, placebo-controlled phase 3 study. Lancet Oncol. 2015, 16, 152–160.
  15. Fizazi, K.; Tran, N.; Fein, L.; Matsubara, N.; Rodriguez-Antolin, A.; Alekseev, B.Y.; Özgüroğlu, M.; Ye, D.; Feyerabend, S.; Protheroe, A.; et al. Abiraterone plus Prednisone in Metastatic, Castration-Sensitive Prostate Cancer. N. Engl. J. Med. 2017, 377, 352–360.
  16. Fizazi, K.; Tran, N.; Fein, L.; Matsubara, N.; Rodriguez-Antolin, A.; Alekseev, B.Y.; Özgüroğlu, M.; Ye, D.; Feyerabend, S.; Protheroe, A.; et al. Abiraterone acetate plus prednisone in patients with newly diagnosed high-risk metastatic castration-sensitive prostate cancer (LATITUDE): Final overall survival analysis of a randomised, double-blind, phase 3 trial. Lancet Oncol. 2019, 20, 686–700.
  17. Parker, C.; Nilsson, S.; Heinrich, D.; Helle, S.I.; O’Sullivan, J.M.; Fosså, S.D.; Chodacki, A.; Wiechno, P.; Logue, J.; Seke, M.; et al. Alpha emitter radium-223 and survival in metastatic prostate cancer. N. Engl. J. Med. 2013, 369, 213–223.
  18. Sartor, O.; de Bono, J.; Chi, K.N.; Fizazi, K.; Herrmann, K.; Rahbar, K.; Tagawa, S.T.; Nordquist, L.T.; Vaishampayan, N.; El-Haddad, G.; et al. Lutetium-177-PSMA-617 for Metastatic Castration-Resistant Prostate Cancer. N. Engl. J. Med. 2021, 385, 1091–1103.
  19. Kantoff, P.W.; Higano, C.S.; Shore, N.D.; Berger, E.R.; Small, E.J.; Penson, D.F.; Redfern, C.H.; Ferrari, A.C.; Dreicer, R.; Sims, R.B.; et al. Sipuleucel-T immunotherapy for castration-resistant prostate cancer. N. Engl. J. Med. 2010, 363, 411–422.
  20. de Bono, J.; Mateo, J.; Fizazi, K.; Saad, F.; Shore, N.; Sandhu, S.; Chi, K.N.; Sartor, O.; Agarwal, N.; Olmos, D.; et al. Olaparib for Metastatic Castration-Resistant Prostate Cancer. N. Engl. J. Med. 2020, 382, 2091–2102.
  21. Abida, W.; Patnaik, A.; Campbell, D.; Shapiro, J.; Bryce, A.H.; McDermott, R.; Sautois, B.; Vogelzang, N.J.; Bambury, R.M.; Voog, E.; et al. Rucaparib in Men with Metastatic Castration-Resistant Prostate Cancer Harboring a BRCA1 or BRCA2 Gene Alteration. J. Clin. Oncol. 2020, 38, 3763–3772.
  22. A Study of Rucaparib Versus Physician’s Choice of Therapy in Patients with Metastatic Castration-Resistant Prostate Cancer and Homologous Recombination Gene Deficiency (TRITON3). Available online: https://clinicaltrials.gov/ct2/show/NCT02975934?term=TRITON3&draw=2&rank=1 (accessed on 15 July 2022).
  23. Moilanen, A.M.; Riikonen, R.; Oksala, R.; Ravanti, L.; Aho, E.; Wohlfahrt, G.; Nykänen, P.S.; Törmäkangas, O.P.; Palvimo, J.J.; Kallio, P.J. Discovery of ODM-201, a new-generation androgen receptor inhibitor targeting resistance mechanisms to androgen signaling-directed prostate cancer therapies. Sci. Rep. 2015, 5, 12007.
  24. Smith, M.R.; Hussain, M.; Saad, F.; Fizazi, K.; Sternberg, C.N.; Crawford, E.D.; Kopyltsov, E.; Park, C.H.; Alekseev, B.; Montesa-Pino, Á.; et al. Darolutamide and Survival in Metastatic, Hormone-Sensitive Prostate Cancer. N. Engl. J. Med. 2022, 386, 1132–1142.
  25. Barrie, S.E.; Haynes, B.P.; Potter, G.A.; Chan, F.C.; Goddard, P.M.; Dowsett, M.; Jarman, M. Biochemistry and pharmacokinetics of potent non-steroidal cytochrome P450(17alpha) inhibitors. J. Steroid. Biochem. Mol. Biol. 1997, 60, 347–351.
  26. Ryan, C.J.; Smith, M.R.; de Bono, J.S.; Molina, A.; Logothetis, C.J.; de Souza, P.; Fizazi, K.; Mainwaring, P.; Piulats, J.M.; Ng, S.; et al. Abiraterone in metastatic prostate cancer without previous chemotherapy. N. Engl. J. Med. 2013, 368, 138–148.
  27. Molina, A.; Belldegrun, A. Novel therapeutic strategies for castration resistant prostate cancer: Inhibition of persistent androgen production and androgen receptor mediated signaling. J. Urol. 2011, 185, 787–794.
  28. Naseer, F.; Ahmad, T.; Kousar, K.; Anjum, S. Advanced Therapeutic Options for Treatment of Metastatic Castration Resistant Prostatic Adenocarcinoma. Front. Pharmacol. 2021, 12, 728054.
  29. Geng, C.; He, B.; Xu, L.; Barbieri, C.E.; Eedunuri, V.K.; Chew, S.A.; Zimmermann, M.; Bond, R.; Shou, J.; Li, C.; et al. Prostate cancer-associated mutations in speckle-type POZ protein (SPOP) regulate steroid receptor coactivator 3 protein turnover. Proc. Natl. Acad. Sci. USA 2013, 110, 6997–7002.
  30. Barbieri, C.E.; Baca, S.C.; Lawrence, M.S.; Demichelis, F.; Blattner, M.; Theurillat, J.P.; White, T.A.; Stojanov, P.; Van Allen, E.; Stransky, N.; et al. Exome sequencing identifies recurrent SPOP, FOXA1 and MED12 mutations in prostate cancer. Nat. Genet. 2012, 44, 685–689.
  31. Blattner, M.; Lee, D.J.; O’Reilly, C.; Park, K.; MacDonald, T.Y.; Khani, F.; Turner, K.R.; Chiu, Y.L.; Wild, P.J.; Dolgalev, I.; et al. SPOP mutations in prostate cancer across demographically diverse patient cohorts. Neoplasia 2014, 16, 14–20.
  32. Karantanos, T.; Corn, P.G.; Thompson, T.C. Prostate cancer progression after androgen deprivation therapy: Mechanisms of castrate resistance and novel therapeutic approaches. Oncogene 2013, 32, 5501–5511.
  33. Nakazawa, M.; Fang, M.; Marshall, C.H.; Lotan, T.L.; Isaacsson Velho, P.; Antonarakis, E.S. Clinical and genomic features of SPOP-mutant prostate cancer. Prostate 2022, 82, 260–268.
  34. Hoogland, A.I.; Jim, H.S.L.; Gonzalez, B.D.; Small, B.J.; Gilvary, D.; Breen, E.C.; Bower, J.E.; Fishman, M.; Zachariah, B.; Jacobsen, P.B. Systemic inflammation and symptomatology in patients with prostate cancer treated with androgen deprivation therapy: Preliminary findings. Cancer 2021, 127, 1476–1482.
  35. Sciarra, A.; Gentilucci, A.; Salciccia, S.; Pierella, F.; Del Bianco, F.; Gentile, V.; Silvestri, I.; Cattarino, S. Prognostic value of inflammation in prostate cancer progression and response to therapeutic: A critical review. J. Inflamm. 2016, 13, 35.
  36. Nguyen, D.P.; Li, J.; Tewari, A.K. Inflammation and prostate cancer: The role of interleukin 6 (IL-6). BJU Int. 2014, 113, 986–992.
More
© Text is available under the terms and conditions of the Creative Commons Attribution (CC BY) license; additional terms may apply. By using this site, you agree to the Terms and Conditions and Privacy Policy.
Upload a video for this entry
Information
Subjects: Oncology
Contributors MDPI registered users' name will be linked to their SciProfiles pages. To register with us, please refer to https://encyclopedia.pub/register :
Bo-Ren Wang
,
Yu-An Chen
,
Wei-Hsiang Kao
,
Chih-Ho Lai
,
Ho Lin
,
Jer-Tsong Hsieh
View Times: 745
Entry Collection: Biopharmaceuticals Technology
Revisions: 4 times (View History)
Update Date: 24 Aug 2022
Table of Contents
    1000/1000
    Hot Most Recent
    Video Production Service
    Feedback