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Pathologic response as an early endpoint for survival following neoadjuvant androgen deprivation therapy plus abiraterone acetate for metastatic prostate cancer

European Journal of Medical Research volume 30, Article number: 238 (2025) Cite this article

Abstract

Purpose

This study aimed to explore the factors affecting pathologic complete response (pCR) and prognosis of locally advanced prostate cancer (LAPCa) or metastatic prostate cancer (mPCa) treated with neoadjuvant androgen deprivation therapy (ADT) with abiraterone acetate (AA).

Methods

This retrospective study enrolled patients diagnosed with LAPCa or mPCa who were divided into three groups based on prostate-specific antigen (PSA) nadir following ADT with AA: group 1 (PSA ≤ 0.2 ng/ml), group 2 (PSA 0.2–4.0 ng/ml), and group 3 (PSA > 4.0 ng/ml). Univariate and multivariate logistic regression models were utilized to investigate the relationship between the variables and pCR, and risk factors of castration-resistant prostate cancer (CRPC).

Results

Among 79 enrolled patients, 33 (41.8%) patients presented with tumor downstaging and 12 (15.2%) patients presented with pCR. PSA nadir was an independent risk factor for tumor downstaging and pCR. Total 71 (89.87%) patients developed CRPC. The median progression time to CRPC in group 1, 2, and 3 was 28, 26, and 24.5 months, respectively. Compared to control group, patients with tumor downstaging, pCR, or PSA nadir < 0.2 ng/ml had better progression-free survival. Tumor downstaging, pCR, and PSA nadir were independent risk factors for progression to CRPC in LAPCa or mPCa.

Conclusion

For patients with LAPCa or mPCa after neoadjuvant AA plus ADT, PSA nadir help predict tumor downstaging or pCR. The patients with tumor downstaging, pCR, or PSA nadir < 0.2 ng/ml have a longer progression time to CRPC.

Introduction

Prostate cancer (PCa) is one of the most frequent malignancies in males globally. According to worldwide cancer statistics 2020, PCa is the second most prevalent malignancy and the fifth largest cause of cancer-related death in men [1]. Therefore, early detection of PCa is urgent [2]. Although the widespread availability of prostate-specific antigen (PSA) screening has increased the rate of PCa early diagnosis, many patents have either locally advanced or metastases at the initial diagnosis.

Radical prostatectomy (RP) is standard treatment for localized prostate cancer. However, the role of RP in the treatment of LAPCa or mPCa is still controversial. Cytoreductive surgery plays an important role in comprehensive treatment of metastatic ovarian cancer, colorectal cancer, renal cancer, and other malignant tumors [3,4,5,6]. Therefore, researchers have begun exploring clinical application and safety of RP for LAPCa or mPCa. A retrospective study showed that patients with mPCa had 5-year overall survival (OS) and disease-specific survival (DSS) rates of 67.4% and 75.8%, respectively, after cytoreductive surgery. In comparison, 5-year OS and DSS rates for patients who did not undergo surgery were 22.5% and 48.7%, respectively [7].

Neoadjuvant hormonal therapy (NHT) has been widely employed for treating LAPCa or mPCa. The patients treated with NHT had a reduction in tumor volume, a decrease in pathological stage, and a lower incidence of positive surgical margins [8]. Abiraterone acetate (AA) is a prodrug of abiraterone, a CYP450 cytochrome P450 c17 (CYP17) inhibitor that allows for intensive androgen deprivation therapy (ADT). AA inhibits androgens from all sources, including testicular, adrenal, prostate, and possibly tumor androgens [9]. Compared with ADT alone, tumor volume was significantly lower in the abiraterone acetate plus prednisone (AAP) plus ADT group (P ≤ 0.001) [10]. Taplin et al. conducted a neoadjuvant randomized phase II trial of luteinizing hormone-releasing hormone Agonist (LHRHa) with AA in patients with LAPCa or mPCa. The results showed that LHRHa plus AA treatment suppressed tissue androgens more effectively compared with LHRHa alone [11]. The combination of two androgen-receptor signaling inhibitors (ARSIs) and an LHRHa in the neoadjuvant setting was explored in recent years. These results showed that maximal blocking of AR signaling with dual ARSI therapy plus an LHRHa did not result in any pathological benefit [12,13,14]. However, few studies have evaluated the treatment effects of neoadjuvant ADT plus AA in LAPCa or mPCa.

Therefore, in this study we aimed to investigate the factors affecting tumor downstaging, pathological pCR, and prognosis after neoadjuvant ADT plus AA therapy for LAPCa or mPCa.

Patients and methods

This single-center retrospective study enrolled patients with LAPCa or mPCa who underwent RP after neoadjuvant ADT plus AA between March 2016 and October 2019. The inclusion criteria were: (1) Patients were diagnosed with prostate acinar adenocarcinoma by ultrasound-guided prostate biopsy without neuroendocrine or small cell features. (2) All patients underwent adequate preoperative imaging including magnetic resonance imaging and whole-body bone imaging. The exclusion criteria were: (1) Patients who have previously received any anti-prostate cancer therapy, including chemotherapy, immunotherapy, targeted therapy, or interventional clinical trial drugs. (2) Patients who have previously received new androgen receptor inhibitors such as enheterulamine and apatamide. These patients received neoadjuvant ADT plus AA for 2 to 6 months before surgery and then underwent RP. Postoperative PSA and testosterone follow-up was performed monthly, CT and whole-body bone imaging were performed every 6 months. The included patients were divided into three groups based on PSA nadir following ADT with AA: group 1 (PSA ≤ 0.2 ng/ml), group 2 (PSA 0.2–4.0 ng/ml), and group 3 (PSA > 4.0 ng/ml).

All clinicopathological data were extracted from the medical records, including age, body mass index (BMI), initial PSA level, Eastern Cooperative Oncology Group performance status (ECOG PS), radiological data, and postoperative pathology.

Castration-resistant prostate cancer (CRPC) was defined as post-castration serum testosterone < 50 ng/dl or 1.7 nmol/l, in addition to either biochemical progression (3 consecutive increases in PSA at least one week apart, resulting in 50% increases over the nadir, with PSA > 2 ng/ml), or radiological progression, based on the 2020 European Association of Urology (EAU) guidelines.

To confirm the original diagnosis, experienced urological pathologist rechecked all pathological specimens. In addition, experienced urological radiologist reexamined the patient's preoperative imaging to identify the clinical stage. Clinical stage and pathological stage were compared to determine whether the tumor downstaging. The tumor stage was determined utilizing the TNM staging system for prostate cancer developed by the American Joint Committee on Cancer (AJCC) (eighth edition, 2017). All procedures involving human participants in this study were carried out in line with the institutional and/or national research committee's ethical standards and compliance with Helsinki Declaration. The institutional review board authorized this study (approval No. XYFY2021-KL325-01). All of the patients provided informed consent.

Statistical analysis

Continuous variables were evaluated using the median (interquartile range [IQR]). Categorical variables include frequencies and proportions. One-way ANOVA test and Kruskal–Wallis test were used to compare continuous variables. Univariate and multivariate logistic regression models were utilized to investigate the relationship between the variables and tumor downstaging or pCR. The Kaplan–Meier survival curve method was used to calculate progression-free survival (PFS). The time frame between the initial diagnosis and CRPC, death from any cause, or the final follow-up was used to determine PFS. In addition, univariate and multivariate Cox regression analyses were used to examine the risk factors contributing to the progression of castration-resistant prostate cancer (CRPC). All reported P values were two-sided. Statistical significance was set at P < 0.05. The SPSS 26.0 software (IBM Corporation, Armonk, NY, USA) was used for all statistical analyses.

Results

Seventy-nine patients diagnosed with LAPCa or mPCa were enrolled in this study. Patients were given neoadjuvant ADT plus AA for several months prior to RP. Using the PSA nadir following neoadjuvant ADT plus AA, 28 patients were categorized into Group 1 (35.4%), 29 patients into group 2 (36.7%), and 22 patients into group 3 (27.9%). The clinicopathological features of the patients are shown in Table 1. The patient median age was 69 years (IQR 64–74 years). The median initial PSA of groups 1, 2, and 3 were 111.84 (IQR 75.64–193.46), 99.07 (IQR 66.73–139.99), and 144.00 (IQR 95.69–247.72) ng/ml, respectively. In group 1, 20 patients were classified as having LAPCa, and 8 had mPCa. In group 2, 21 patients with lLAPCa and 8 patients with mPCa were identified. In group 3, 17 patients were diagnosed with LAPCa or mPCa, while 5 patients had mPCa. There were no significant differences in age, ECOG PS, Gleason score, BMI, or metastasis among the three groups.

Table 1 Clinical features of patients in the three groups
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With neoadjuvant ADT plus AA, 33 (41.8%) patients showed tumor downstaging and 12 (15.2%) presented with pCR. In group 1, there were 18 (64.29%) patients with tumor downstaging and 8 (28.57%) patients with pCR. In group 2, there were 11(37.93%) patients with tumor downstaging and 3 (10.34%) patients with pCR. In group 3, there were 4(18.18%) patients with tumor downstaging and 1 (4.55%) patient with pCR. The three groups showed significant differences in the tumor downstaging rate (P = 0.004) and pCR rate (P = 0.043). Multivariate logistic regression analyses demonstrated that the PSA nadir was an independent risk factor for tumor downstaging and pCR after adjustment for clinical parameters such as age, BMI, ECOG PS, and initial PSA (Table 2).

Table 2 Multivariate logistic regression analysis of the influencing factors of tumor downstaging and PCR
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The median follow-up time was 27 (IQR25-29) months. A total of 71(89.87%) patients developed CRPC. The median progression times to CRPC in groups 1, 2, and 3 were 28, 26, and 24.5 months, respectively. As shown in Fig. 1, there was a significant difference in PFS between patients with and without tumor downstaging (P < 0.001). As shown in Fig. 2, PFS differed significantly between patients with pCR and non-pCR (P < 0.001). Compared to patients with PSA nadir > 0.2 ng/ml, patients with PSA nadir < 0.2 ng/ml presented with longer PFS (Fig. 3, P < 0.001). Multivariate Cox regression analyses revealed that tumor downstaging, PCR, and PSA nadir were independent risk factors for progression to CRPC in LAPCa or mPCa after adjusting for age, BMI, ECOG PS and Gleason score (Table 3).

Fig. 1
figure 1

Kaplan–Meier analysis for progression-free survival in patients between tumor downstaging and non-downstaging

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Fig. 2
figure 2

Kaplan–Meier analysis for progression-free survival in patients between pCR and non-pCR

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Fig. 3
figure 3

Kaplan–Meier analysis for progression-free survival in patients with different PSA nadir

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Table 3 Multivariate COX analysis for progression to castration-resistant prostate cancer
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Discussion

LAPCa or mPCa accounts for about approximately two-thirds of the newly diagnosed PCa cases in China [15]. For patients with LAPCa, EAU and other clinical guidelines mainly recommend external radiation therapy combined with ADT for 2 to 3 years [16, 17]. The safety and efficacy of RP in the treatment of LAPCa or mPCa have been reported [18,19,20]. Heidenreich et al. conducted a case–control study to evaluate the feasibility of cytoreductive radical prostatectomy (CRP) for mPCa. Compared with ADT alone, the patients who underwent CRP after NHT had a longer median time to progress to CPRC (40 months vs29 months, P = 0.040) and a longer asymptomatic survival (38.6 months vs. 26.5 months, P = 0.032). However, the results showed no significant difference in OS between two groups [21]. Based on the meta-analysis results, RP for mPCa was associated with improved OS and decreased cancer-specific mortality (CSM) in selected cases. According to the strata of treatments, compared to no local therapy or radiation therapy, RP reduced CSM and improved OS [22]. Patients with LAPCa or mPCa can benefit from RP, which is both safe and reliable. However, the treatment for LAPCa or mPCa should be comprehensive and include radical surgery, neoadjuvant therapy, adjuvant therapy, and systematic therapy.

In recent years, more attention has been paid to pathological response, including tumor downstaging and pCR. In several studies, pCR has been shown to predict survival in patients with breast cancer after neoadjuvant chemotherapy. It has been approved by the FDA and EMA as a surrogate endpoint for survival in neoadjuvant studies for breast cancer [23]. The CA209-8Y9 trial used pathological response as an early endpoint of neoadjuvant therapy for non-small cell lung cancer (NSCLC). The results showed that patients who achieved pCR had a 50% lower risk of death than those who did not, indicating a strong correlation between pathological response and survival end points [24]. Similarly, patients with tumor downstaging or pCR had a longer progression time to CRPC, as shown in our study.

PSA is a widely used serological index for PCa diagnosis, evaluation of treatment effects and prognosis prediction [25,26,27]. The present study found that the initial PSA level was not associated with the progression to CRPC. Similarly, a systematic review found that the initial PSA level before ADT was not linked to the rate of development or survival in mPCa [28]. In this study, we found that patients with PSA nadir ≤ 0.2 ng/ml had a higher rate of tumor downstaging or pCR and presented with a longer progression time to CRPC. According to a systematic review, the PSA nadir was highly associated with survival benefits in metastatic hormone-sensitive prostate cancer (mHSPC). The majority of prostate cancer cells respond to androgen, and androgen-independent cells are rarely present before ADT. The decline in serum PSA levels depends on ADT and ADT-induced apoptosis. When there are many androgen-independent cells and their proportion is high before ADT, it cannot significantly reduce serum PSA levels. The PSA nadir is high because serum PSA levels are controlled by androgen-independent prostate cancer cells [29]. This may explain why PSA nadir affects the prognosis in patients with PCa.

The limitations of this study should be taken into account when interpreting the findings. First, during the data-gathering phase of this retrospective investigation, inevitable data losses occurred. Second, this was an individual-center retrospective investigation. Therefore, this study lacked randomization and selection bias was inevitable. Lastly, there were 8, 8, and 5 patients with mPCa in each of the three groups, respectively. Owing to the small sample size, we could not perform a separate statistical analysis. We will continue to expand the sample size and follow-up period.

Conclusion

For patients with LAPCa or mPCa after neoadjuvant ADT plus AA, the PSA nadir helps predict the rate of tumor downstaging or PCR. Furthermore, compared with the control group, patients with tumor downstaging, PCR, or PSA nadir < 0.2 ng/ml after neoadjuvant AA plus ADT had a longer progression time to CRPC.

Availability of data and materials

All data are available from the corresponding authors upon reasonable request.

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Acknowledgements

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Funding

This study was funded by Xuzhou Science and Technology project..

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Author notes

  1. Kaichen Zhou, Haosen Lu and Fukun Wei have contributed equally to this work and share first authorship.

Authors and Affiliations

  1. Department of Urology, The Affiliated Hospital of Xuzhou Medical University, No. 99 Huaihai West Road, Quanshan District, Xuzhou, 221100, People’s Republic of China

    Kaichen Zhou, Haosen Lu, Fukun Wei, Jie Wang, Zhen Song & Lijun Mao

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Contributions

LM and ZS designed the study, KZ, HL, FW and JW collected and analyzed data. All authors read and approved the manuscript.

Corresponding authors

Correspondence to Zhen Song or Lijun Mao.

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The institutional review board authorized this study (approval No. XYFY2021-KL325-01). All of the patients provided informed consent.

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Zhou, K., Lu, H., Wei, F. et al. Pathologic response as an early endpoint for survival following neoadjuvant androgen deprivation therapy plus abiraterone acetate for metastatic prostate cancer. Eur J Med Res 30, 238 (2025). https://doiorg.publicaciones.saludcastillayleon.es/10.1186/s40001-025-02521-7

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European Journal of Medical Research

ISSN: 2047-783X

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