J Urol Oncol > Volume 21(3); 2023 > Article
Cho, Suh, You, Jeong, Hong, Ahn, and Lim: Predictive Factors of Abiraterone Response in Patients With High-Risk Metastatic Hormone-Sensitive Prostate Cancer

Abstract

Purpose

This study aimed to identify predictive factors for the response to abiraterone in patients with high-risk metastatic hormone-sensitive prostate cancer (mHSPC).

Materials and Methods

This study analyzed the clinical characteristics of 167 patients with high-risk mHSPC who received abiraterone. Univariate and multivariable Cox proportional hazard regression analyses were conducted to identify predictive factors for castration-resistant prostate cancer (CRPC)-free survival and cancer-specific survival.

Results

The mean age at presentation was 71.62±8.12 years. The prostate-specific antigen level was 218 ng/mL (interquartile range, 70-654 ng/mL). Of the 167 patients, 118 (72%) had a biopsy Gleason grade of 5, 43 patients (28.7%) had CRPC, and 30 patients (18.0%) died after a mean follow-up period of 13.5 months. In the multivariable Cox proportional hazard regression analyses for CRPC-free survival, a Gleason grade of 5 (hazard ratio [HR], 2.888; 95% confidence interval [CI], 1.133-7.361; p=0.026) and bone lesions ≥10 (HR, 4.194; 95% CI, 1.760-9.997; p=0.001) were significantly associated with CRPC-free survival. In the multivariable Cox proportional hazard regression analyses for cancer-specific survival, bone lesions ≥10 (HR, 3.185; 95% CI, 1.215-8.348; p=0.001) was significantly associated with cancer-specific survival.

Conclusions

Patients with bone lesions ≥10 and Gleason grade of 5 are at higher risk of developing CRPC, and bone lesions ≥10 is at higher risk of cancer-specific survival in high-risk mHSPC treated with abiraterone.

INTRODUCTION

Prostate cancer is a major health concern for men, and it is the second most common cancer and the fifth leading cause of cancer-related deaths worldwide [1]. In addition, there is a steady increase in prostate cancer in Korea, and according to statistics released by the National Cancer Information Center in 2022, it ranked third in age-standardized prevalence rate [2]. At the time of initial diagnosis, approximately 6% of men with prostate cancer are diagnosed with metastatic prostate cancer [3]. Historically, the first-line treatment for metastatic prostate cancer has been androgen-deprivation therapy (ADT), which was introduced by Dr. Charles Huggins in the 1940s and earned him the Nobel Prize in Physiology or Medicine in 1966 [4]. Despite the initial response to ADT, the cancer can progress to a more aggressive form known as metastatic castration-resistant prostate cancer (mCRPC) within a mean time of 2-3 years [5]. mCPRC is associated with a poor prognosis, and the survival time of patients is only 16-18 months [6,7]. Several therapies have emerged to treat mCRPC, including chemotherapy, hormonal therapy, immunotherapy, and targeted therapy. Chemotherapy agents such as docetaxel and cabazitaxel have demonstrated efficacy in extending the survival of patients with mCRPC. Second-generation antiandrogens, such as abiraterone and enzalutamide, have shown promising results by targeting the androgen receptor signaling pathway.
These drugs have also exhibited effectiveness in treating metastatic hormone-sensitive prostate cancer (mHSPC) when used in combination with ADT, leading to improvements in the overall survival. The chemohormonal therapy versus androgen ablation randomized trial for extensive disease in prostate cancer (CHAARTED) study provided evidence for the benefit of early chemotherapy by revealing that the addition of docetaxel to ADT significantly improved the overall survival in patients with mHSPC [8]. Similarly, the STAMPEDE (systemic therapy in advancing or metastatic prostate cancer: evaluation of drug efficacy) trial demonstrated that the addition of docetaxel chemotherapy or abiraterone acetate, a second-generation anti-androgen, to standard ADT resulted in substantial improvements in the overall survival of patients with advanced prostate cancer, including mHSPC [9]. The ARCHES trial further supported the efficacy of enzalutamide in combination with ADT, showing superior outcomes in radiographic progression-free survival, time to prostate-specific antigen (PSA) progression, and overall survival to placebo plus ADT in patients with mHSPC [10].
In addition, a triplet therapy that uses ADT + androgen receptor signaling inhibitor (ARSI) + docetaxel was found to have a therapeutic effect on mHSPC. In the PEACE-1 trial, the addition of abiraterone to ADT and docetaxel significantly improved the overall survival (hazard ratio [HR], 0.75; 95.1% confidence interval [CI], 0.59-0.95; p=0.017)) and radiographic progression-free survival (HR, 0.50; 99.9% CI, 0.34-0.71; p<0.001). In the ARASENS trial, the combination of darolutamide, ADT, and docetaxel demonstrated significantly longer overall survival than placebo plus ADT and docetaxel (HR, 0.68; 95% CI, 0.57-0.80; p<0.001) [11,12]. These treatments are now listed in the guidelines for mHSPC treatment.
Although triplet therapy can increase survival, no evidence shows that it is better than abiraterone alone, and compared with abiraterone therapy, triplet therapy in all patients with mHSPC is associated with higher costs and unexpected side effects. Therefore, this study aimed to identify the predictive factors of response to abiraterone therapy in patients with high-risk mHSPC.

MATERIALS AND METHODS

1. Patient Population

This study was approved by the Institutional Review Board (IRB) of Asan Medical Center (IRB No. 2022-1516). The study retrospectively screened medical records of patients diagnosed with high-risk mHSPC between 2018 and 2021. A total of 167 patients who were diagnosed with de novo high-risk mHSPC and initiated ADT and abiraterone were enrolled. However, patients were excluded if their pretreatment stage examinations (including PSA, computed tomography [CT], magnetic resonance imaging [MRI], bone scan, and biopsy results) were unclear or if they had inadequate regular follow-up at the hospital.
Metastatic prostate cancer is defined when a histologically confirmed prostate cancer has at least one metastatic lesion identified through thoracic abdominal pelvic CT and bone scan.
The study referred to the LATITUDE studies and CHAARTED trial for the definition of high-risk and high volume, respectively. A high-volume disease was defined as the presence of visceral metastasis, or ≥4 bone lesions with at least one lesion located beyond the vertebral bodies and pelvis. A high-risk disease was defined as meeting at least 2 of the following 3 criteria: (1) Gleason score of ≥8, (2) presence of 3 or more lesions on a bone scan, and (3) presence of measurable visceral lesions [8,13,14].
CRPC is defined as a castration level of serum testosterone plus one of the following: (1) 3 consecutive rises (over the nadir) in PSA levels at least 1 week apart and a PSA >2 ng/mL (biochemical progression) and (2) development of 2 or more new lesions in bones or progressive disease according to Response Evaluation Criteria in Solid Tumors version 1.1 criteria (radiographic progression) [15-18].
Data on metastatic burden and site were collected from bone, CT, or MRI scans conducted within 3 months before ADT initiation. Patients underwent clinical examination, imaging examination, and serum PSA analysis every 3-6 months for evaluation.

2. Statistical Analysis

Regarding patient characteristics, quantitative data were reported as either mean with standard deviation or median with interquartile range, whereas categorical variables were presented as absolute values with percentages. Univariate and multivariate logistic regression analyses were performed to examine the response to ADT and abiraterone. The associations between outcomes and evaluated variables were expressed as HRs with their corresponding 95% CIs. CRPC-free survival based on risk factors was assessed using Kaplan-Meier survival analysis. All statistical analyses were performed using IBM SPSS Statistics ver. 25.0 (IBM Co., Armonk, NY, USA).

RESULTS

The study included 167 patients with mHSPC. The clinical characteristics of patients are listed in Table 1. The mean patient age, height, and weight were 71.62±8.12 years, 166.06±5.71 cm, and 68.46±10.34 kg, respectively, resulting in an average body mass index of 24.82±3.51 kg/m2. The initial PSA levels varied widely, with a median of 218 ng/mL (interquartile range, 70-654 ng/mL). The follow-up period ranged from 0.9 to 56.7 months, with a median of 13.5 months. In addition, the biopsy results showed varying International Society of Urological Pathology (ISUP) grade, with the majority of patients having a ISUP grade of 5 (71.4%) or 4 (27.4%). Metastasis was predominantly observed in the bone (98.8%) and lymph nodes (80.8%), and a subset of patients was experiencing visceral metastasis (29.9%), lung metastasis (28.7%), and liver metastasis (3.0%). Other evaluated factors were the presence of high-volume disease (86.2%), high-risk disease (100%), development of CRPC (25.7%), and mortality (18.0%)
Univariate and multivariate Cox proportional hazards regression analyses were performed to evaluate the association between the characteristics of patients and CRPC-free survival (Table 2). In the univariate Cox regression analysis, age, BMI, and initial PSA levels were not significantly associated with CRPC-free survival. Similarly, the presence of bone metastasis, visceral metastasis, lung metastasis, liver metastasis, lymph node metastasis, and high volume did not demonstrate significant predictive value. However, a Gleason grade of 5 and the presence of bone lesions ≥10 was found to be significant predictors of CRPC-free survival in the univariate analysis. In the multivariable Cox regression analysis, which was adjusted for multiple factors simultaneously, both the Gleason grade of 5 and the presence of bone lesions ≥10 remained significant predictors of CRPC-free survival. The adjusted HR for a Gleason grade of 5 was 2.888 (95% CI, 1.133-7.361), and the adjusted HR for bone lesions ≥10 was 4.194 (95% CI, 1.760-9.997). This indicates that patients with a Gleason grade of 5 and those with bone lesions ≥10 have a higher risk of experiencing CRPC progression.
Univariate and multivariate Cox proportional hazards regression analyses were also performed to determine predictors of cancer-specific survival by assessing the association between patient characteristics and cancer-specific survival (Table 3). In the univariate Cox regression analysis, age, BMI, and initial PSA levels were not significantly associated with cancer-specific survival. Similarly, the presence of bone metastasis, visceral metastasis, lung metastasis, liver metastasis, lymph node metastasis, and high volume did not show a significant predictive value. However, the presence of bone lesions ≥10 and a Gleason grade of 5 were found to be significant predictors of cancer-specific survival. In the multivariable Cox regression analysis, the presence of bone lesions ≥10 remained a significant predictor of cancer-specific survival. The adjusted HR for bone lesions ≥10 was 3.185 (95% CI 1.215-8.348). This suggests that patients with bone lesions ≥10 have a higher risk of cancer-related mortality.

DISCUSSION

Prostate cancer shows a 5-year survival of >99% in the case of localized lesions but a 5-year survival of 32% in the case of metastatic lesions, and treatment for this has been steadily studied [19]. The introduction of ADT as the first-line treatment has been a significant advancement in disease management. However, the development of mCRPC remains a challenge, and alternative treatments have emerged to address this issue. Chemotherapy agents such as docetaxel and cabazitaxel have shown effectiveness in extending the survival of patients with mCRPC [20-22]. Furthermore, second-generation antiandrogens such as abiraterone and enzalutamide have demonstrated promising results by targeting the androgen receptor signaling pathway [23,24]. The CHAARTED and STAMPEDE trials have provided evidence supporting the addition of docetaxel to ADT, resulting in improved overall survival for patients with mHSPC [8,9]. The ARCHES trial also showed the efficacy of enzalutamide in combination with ADT for patients with mHSPC [10].
Recently, the PEACE-1 study and ARASENS trial have shown therapeutic benefits for mHSPC through triplet therapy involving ADT, anti-ARSIs, and docetaxel [11,12]. Although adding ARSIs to docetaxel is said to be beneficial, no evidence suggests its superiority over abiraterone alone. Moreover, triplet therapy in all patients with mHSPC has been associated with higher costs and unexpected side effects than abiraterone alone. In the CHAARTED trial, the rate of adverse events of grade ≥3 among patients who received the docetaxel-containing regimen was 29.6%. The rate of grade 3 or 4 febrile neutropenia was 6.2%; grade 3 or 4 infection with neutropenia, 2.3%; and grade 3 sensory neuropathy and grade 3 motor neuropathy, 0.5% [8].
Consequently, identifying the predictors of the decision to treat using ADT plus abiraterone plus docetaxel as a triplet therapy in patients with mHSPC is important. Therefore, in this study, we aimed to identify predictors of response to abiraterone therapy in patients with mHSPC to determine the patients for whom triplet therapy with docetaxel would be more effective than ADT plus abiraterone therapy.
The study included 167 patients with mHSPC and evaluated various clinical characteristics. The results showed that age, BMI, and initial PSA levels were not significant predictors of CRPC-free survival or cancer-specific survival. However, the presence of bone lesions ≥10 and a Gleason grade of 5 were found to be significant predictors in both univariate and multivariate Cox regression analyses.
In the multivariable Cox regression analysis, adjusting for multiple factors simultaneously, a Gleason grade of 5 (HR, 2.888; p=0.026) and the presence of bone lesions ≥10 (HR, 4.194; p=0.001) remained significant predictors of CRPC-free survival. This suggests that patients with a Gleason grade of 5 and those with bone lesions ≥10 are at a higher risk of experiencing CRPC progression. Similarly, in the analysis of cancer-specific survival, the presence of bone lesions ≥10 (HR, 3.185; p=0.001) remained a significant predictor. This indicates that patients with bone lesions ≥10 have a higher risk of cancer-related mortality.
The findings of this study highlight the importance of considering a Gleason grade of 5 and the presence of bone lesions ≥10 when determining the response to abiraterone therapy in patients with mHSPC. In other words, if a patient has a Gleason grade 5 or bone lesion ≥10, docetaxel as part of the triplet therapy can be added instead of using ADT plus abiraterone therapy.
Several studies have reported predictive or prognostic factors for prostate cancer treatment; however, this study has the following advantages. First, unlike other studies that has evaluated prognostic factors based on response to drug use or treatment results, the present study focuses on identifying prognostic factors at the beginning of treatment. In a retrospective study of patients with mCRPC treated with abiraterone, a PSA response was observed as a prognostic factor [25]; however, this is a factor that can determine the patient’s prognosis after treatment begins. On the contrary, this study has the advantage of examining clinical characteristics before the initiation of abiraterone therapy in patients with mHSPC, which provides early predictive factors for treatment response and assists in treatment selection.
Although studies have investigated prognostic factors in patients with mHSPC, the present study focused on identifying predictive factors for response to abiraterone therapy. It narrows down the analysis to the effects of abiraterone alone, providing insights into the factors that can influence the effectiveness of this treatment modality. In addition, with a sample size of 167 patients, which is relatively large in these conditions, the results of this study are meaningful. In a multicenter, retrospective study of a similar study, a Gleason pattern of 5, performance status, and hemoglobin could be potential predictors of progression-free survival in 112 patients with high-risk mHSPC treated with abiraterone [26].
Finally, this study assessed CRPC-free survival. Usually, many studies have focused solely on overall survival or cancer-specific survival as the primary outcome measure. However, the present study expands the scope by assessing CRPC-free survival as a separate endpoint. By analyzing this distinct survival outcome, the study provides a more comprehensive understanding of the effect of prognostic factors on disease progression and cancer-related mortality.
This study has several limitations. First, it is a retrospective study. Second, although the study includes a relatively large number of patients within a particular patient group, the absolute sample size is still relatively small. This limited sample size may affect the generalizability and statistical power of the findings, warranting caution in extrapolating the results to a larger population. Third, the study lacks a comprehensive exploration of the underlying mechanisms that drive the observed results, leaving gaps in understanding the biological and physiological explanations. Fourth, the follow-up period of patients who received abiraterone therapy was short; this may restrict the assessment of long-term treatment outcomes and the durability of the observed effects. Therefore, prospective studies with larger and more diverse patient populations are needed to validate and expand upon the findings of this study.

CONCLUSIONS

The study identified significant predictors of response to abiraterone therapy in patients with high-risk mHSPC. The presence of bone lesions ≥10 and a Gleason grade of 5 emerged as important prognostic factors for CRPC-free survival. Patients with bone lesions ≥10 demonstrated a higher risk of cancer-specific survival. Therefore, adding docetaxel as part of the triplet therapy may be more effective than using ADT plus abiraterone therapy in patients with mHSPC who have these high-risk features.

NOTES

Conflicts of Interest

HJA, a member of the Editorial Board of Journal of Urologic Oncology, is the co-author of this article. However, he played no role whatsoever in the editorial evaluation of this article or the decision to publish it. The other authors have nothing to disclose.

Funding/Support

This study received no specific grant from any funding agency in the public, commercial, or not-for-profit sectors.

Author Contribution

Conceptualization: JYC, BJL, HJA; Data curation: JYC; Formal analysis: IGJ; Methodology: DSY, JHH; Project administration: BJL; Visualization: JGS; Writing - original draft: JYC, BJL; Writing - review & editing: BJL, HJA, JHH.

Table 1.
Clinical characteristics of the study patients (n=167)
Characteristic Value
Age (yr) 71.62±8.12
Height (cm) 166.06±5.71
Weight (kg) 68.46±10.34
Body mass index (kg/m2) 24.82±3.51
Initial PSA (ng/mL), median (IQR) 218 (70-654)
Follow-up period (mo), median (range) 13.5 (0.9-56.7)
ISUP grade
 2 1 (0.6)
 3 1 (0.6)
 4 45 (27.4)
 5 117 (71.4)
Gleason grade of 5 118 (72)
Metastasis site
 Bone 165 (98.8)
  Bone lesion ≥10 106 (63.5)
 Lymph node* 135 (80.8)
 Visceral metastasis 50 (29.9)
  Lung metastasis 48 (28.7))
  Liver metastasis 5 (3.0)
High volume 144 (86.2)
High-risk 167 (100)
CRPC 43 (25.7)
Death 30 (18.0)

Values are presented as mean±standard deviation or number (%) unless otherwise indicated.

PSA, prostate-specific antigen; IQR, interquartile range; ISUP, International Society of Urological Pathology; CRPC, castration-resistant prostate cancer.

* Lymph node (LN) meta was analyzed in all cases, including extrapelvic LN meta and N1.

Table 2.
Univariate and multivariable Cox proportional hazard regression analyses for CRPC-free survival
Variable Univariate
p-value Multivariable
p-value
HR 95% CI HR 95% CI
Age 0.996 0.958-1.035 0.828 - - -
BMI 0.977 0.867-1.100 0.697 - - -
Initial PSA 1.000 0.999-1.000 0.092 - - -
Bone metastasis 21.698 0.007-66,195.317 0.452 - - -
Visceral metastasis 0.550 0.243-1.245 0.151 - - -
Lung metastasis 0.468 0.196-1.116 0.087 - - -
Liver metastasis 0.835 0.114-6.103 0.859 - - -
LN metastasis 0.907 0.434-1.893 0.794 - - -
High volume 3.840 0.924-15.952 0.064 - - -
Gleason grade of 5 3.284 1.291-8.352 0.013 2.888 1.133-7.361 0.026
Bone lesion ≥10 4.338 1.825-10.313 0.001 4.194 1.760-9.997 0.001

CRPC, castration-resistant prostate cancer; HR, hazard ratio; CI, confidence interval; BMI, body mass index; PSA, prostate-specific antigen; LN, lymph node.

Table 3.
Univariate and multivariable Cox proportional hazard regression analyses for cancer-specific survival
Variable Univariate
p-value Multivariable
p-value
HR 95% CI HR 95% CI
Age 1.016 0.968-1.066 0.520
BMI 0.874 0.756-1.010 0.069
Initial PSA 1.000 1.000-1.000 0.558
Bone metastasis 21.550 0.002-22,6517.3 0.516
Visceral metastasis 0.705 0.265-1.873 0.483
Lung metastasis 0.563 0194-1.636 0.291
Liver metastasis 1.271 0.170-9.480 0.815
LN metastasis 0.676 0.300-1.520 0.343
High volume 5.167 0.702-38.028 0.107
Gleason grade of 5 3.563 1.080-11.746 0.037 3.228 0.977-10.663 0.055
Bone lesion ≥10 3.314 1.266-8.678 0.015 3.185 1.215-8.348 0.018

HR, hazard ratio; CI, confidence interval; BMI, body mass index; PSA, prostate-specific antigen; LN, lymph node.

REFERENCES

1. Sung H, Ferlay J, Siegel RL, Laversanne M, Soerjomataram I, Jemal A, et al. Global cancer statistics 2020: GLOBOCAN estimates of incidence and mortality worldwide for 36 cancers in 185 countries. CA Cancer J Clin 2021;71:209-49.
crossref pmid pdf
2. Ha YS, Kim KT, Nam W, Park H, Yoo S, Lee CH, et al. A survey on the quality of life of prostate cancer patients in Korean Prostate Cancer Patients Association. Korean J Urol Oncol 2022;20:265-72.
crossref pdf
3. Gartrell BA, Coleman R, Efstathiou E, Fizazi K, Logothetis CJ, Smith MR, et al. Metastatic prostate cancer and the bone: significance and therapeutic options. Eur Urol 2015;68:850-8.
crossref pmid
4. Huggins C, Hodges CV. Studies on prostatic cancer. I. The effect of castration, of estrogen and androgen injection on serum phosphatases in metastatic carcinoma of the prostate. CA Cancer J Clin 1972;22:232-40.
pmid
5. Harris WP, Mostaghel EA, Nelson PS, Montgomery B. Androgen deprivation therapy: progress in understanding mechanisms of resistance and optimizing androgen depletion. Nat Clin Pract Urol 2009;6:76-85.
crossref pmid pmc pdf
6. Karantanos T, Corn PG, Thompson TC. Prostate cancer progression after androgen deprivation therapy: mechanisms of castrate resistance and novel therapeutic approaches. Oncogene 2013;32:5501-11.
crossref pmid pmc pdf
7. Marques RB, Dits NF, Erkens-Schulze S, van Weerden WM, Jenster G. Bypass mechanisms of the androgen receptor pathway in therapy-resistant prostate cancer cell models. PLoS One 2010;5:e13500.
crossref pmid pmc
8. Sweeney CJ, Chen YH, Carducci M, Liu G, Jarrard DF, Eisenberger M, et al. Chemohormonal therapy in metastatic hormone-sensitive prostate cancer. N Engl J Med 2015;373:737-46.
crossref pmid pmc
9. James ND, de Bono JS, Spears MR, Clarke NW, Mason MD, Dearnaley DP, et al. Abiraterone for prostate cancer not previously treated with hormone therapy. N Engl J Med 2017;377:338-51.
pmid pmc
10. Armstrong AJ, Szmulewitz RZ, Petrylak DP, Holzbeierlein J, Villers A, Azad A, 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;37:2974-86.
crossref pmid pmc
11. Fizazi K, Foulon S, Carles J, Roubaud G, McDermott R, Fléchon A, et al. Abiraterone plus prednisone added to androgen deprivation therapy and docetaxel in de novo metastatic castration-sensitive prostate cancer (PEACE-1): a multicentre, open-label, randomised, phase 3 study with a 2×2 factorial design. Lancet 2022;399:1695-707.
crossref pmid
12. Smith MR, Hussain M, Saad F, Fizazi K, Sternberg CN, Crawford ED, et al. Darolutamide and survival in metastatic, hormone-sensitive prostate cancer. N Engl J Med 2022;386:1132-42.
pmid pmc
13. Kawahara T, Yoneyama S, Ohno Y, Iizuka J, Hashimoto Y, Tsumura H, et al. Prognostic value of the LATITUDE and CHAARTED risk criteria for predicting the survival of men with bone metastatic hormone-naïve prostate cancer treated with combined androgen blockade therapy: real-world data from a Japanese Multi-Institutional Study. Biomed Res Int 2020;2020:7804932.
crossref pmid pmc pdf
14. Fizazi K, Tran N, Fein L, Matsubara N, Rodriguez-Antolin A, Alekseev BY, et al. Abiraterone plus prednisone in metastatic, castration-sensitive prostate cancer. N Engl J Med 2017;377:352-60.
crossref pmid
15. Kim IH, Shin SJ, Kang BW, Kang J, Kim D, Kim M, et al. 2020 Korean guidelines for the management of metastatic prostate cancer. Korean J Intern Med 2021;36:491-514.
crossref pmid pmc pdf
16. Cornford P, Bellmunt J, Bolla M, Briers E, De Santis M, Gross T, et al. EAU-ESTRO-SIOG guidelines on prostate cancer. Part II: treatment of relapsing, metastatic, and castration-resistant prostate cancer. Eur Urol 2017;71:630-42.
crossref pmid
17. Scher HI, Halabi S, Tannock I, Morris M, Sternberg CN, Carducci MA, et al. Design and end points of clinical trials for patients with progressive prostate cancer and castrate levels of testosterone: recommendations of the Prostate Cancer Clinical Trials Working Group. J Clin Oncol 2008;26:1148-59.
crossref pmid pmc
18. Schwartz LH, Seymour L, Litière S, Ford R, Gwyther S, Mandrekar S, et al. RECIST 1.1 - Standardisation and disease-specific adaptations: perspectives from the RECIST Working Group. Eur J Cancer 2016;62:138-45.
crossref pmid pmc
19. Siegel RL, Miller KD, Wagle NS, Jemal A. Cancer statistics, 2023. CA Cancer J Clin 2023;73:17-48.
crossref pmid pdf
20. de Bono JS, Oudard S, Ozguroglu M, Hansen S, Machiels JP, Kocak I, et al. Prednisone plus cabazitaxel or mitoxantrone for metastatic castration-resistant prostate cancer progressing after docetaxel treatment: a randomised open-label trial. Lancet 2010;376:1147-54.
crossref pmid
21. Petrylak DP, Tangen CM, Hussain MH, Lara PN Jr, Jones JA, Taplin ME, et al. Docetaxel and estramustine compared with mitoxantrone and prednisone for advanced refractory prostate cancer. N Engl J Med 2004;351:1513-20.
crossref pmid
22. Tannock IF, de Wit R, Berry WR, Horti J, Pluzanska A, Chi KN, et al. Docetaxel plus prednisone or mitoxantrone plus prednisone for advanced prostate cancer. N Engl J Med 2004;351:1502-12.
crossref pmid
23. Beer TM, Armstrong AJ, Rathkopf DE, Loriot Y, Sternberg CN, Higano CS, et al. Enzalutamide in metastatic prostate cancer before chemotherapy. N Engl J Med 2014;371:424-33.
pmid pmc
24. de Bono JS, Logothetis CJ, Molina A, Fizazi K, North S, Chu L, et al. Abiraterone and increased survival in metastatic prostate cancer. N Engl J Med 2011;364:1995-2005.
pmid pmc
25. Alvim CM, Mansinho A, Paiva RS, Brás R, Semedo PM, Lobo-Martins S, et al. Prognostic factors for patients treated with abiraterone. Future Sci OA 2019;6:FSO436.
crossref pmid pmc
26. Takahara K, Naiki T, Ito T, Nakane K, Koie T, Yasui T, et al. Useful predictors of progression-free survival for Japanese patients with LATITUDE-high-risk metastatic castration-sensitive prostate cancer who received upfront abiraterone acetate. Int J Urol 2022;29:229-34.
crossref pmid pmc pdf


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