Bipolar androgen therapy followed by immune checkpoint inhibitors in metastatic castration resistant prostate cancer: A report of 4 cases.
- Author:
Sheng Jie LIU
1
;
Hui Min HOU
1
;
Zheng Tong LV
1
;
Xin DING
1
;
Lu WANG
1
;
Lei ZHANG
1
;
Ming LIU
1
Author Information
1. Department of Urology, Beijing Hospital; National Center of Gerontology; Institute of Geriatric Medicine, Chinses Academy of Medical Sciences, Beijing 100070, China.
- Publication Type:Journal Article
- Keywords:
Bipolar androgen therapy;
Efficacy;
Immune checkpoint inhibitors;
Prostate cancer;
Safety
- MeSH:
Aged;
Aged, 80 and over;
Androgens/therapeutic use*;
Humans;
Immune Checkpoint Inhibitors;
Male;
Nitriles/therapeutic use*;
Prostate-Specific Antigen;
Prostatic Neoplasms, Castration-Resistant/drug therapy*;
Testosterone/therapeutic use*;
Treatment Outcome
- From:
Journal of Peking University(Health Sciences)
2022;54(4):766-769
- CountryChina
- Language:Chinese
-
Abstract:
The relationship between androgen and prostate cancer treatment has plagued the field of urologic oncology. To investigate the efficacy and safety of bipolar androgen therapy (BAT) followed by immune checkpoint inhibitor therapy in patients with metastatic castration resistant prostate cancer (mCRPC). In August 2020, Beijing Hospital conducted an investigator-initiated study: Bipolar androgen therapy followed by immune checkpoint inhibitor therapy in metastatic castration resistant prostate cancer. Up to now, the study has included 4 patients who completed the entire cycle of treatment. The mean age of the patients was 74.5 (68 to 82) years old, the mean prostate-specific antigen (PSA) was 20.8 (9.9 to 8.36) μg/L, the mean testosterone was 0.50 (0.00 to 1.81) μg/L, and the Gleason score were 10 and 9, 7, 7 respectively. The pain scale score before treatment was 1.5 (1 to 2). In this study, 4 patients completed the entire cycle of treatment, and the treatment effect of the patients showed great heterogeneity. PSA in case 1 decreased from 24.0 μg/L to 0.47 μg/L, testosterone increased from 0.175 6 μg/L to 2.62 μg/L. PSA in case 2 increased from 9.939 μg/L to 168.536 μg/L, and testosterone increased from 0.0 μg/L increased to 2.85 μg/L. PSA increased from 13.31 μg/L to 39.278 μg/L in case 3, testosterone increased from 0.0 μg/L to 2.54 μg/L. and PSA increased from 36.0 μg/L to 350.2 μg/L in the case 4, testosterone increased from 1.81 μg/L to 3.85 μg/L. Except for one patient who showed significant PSA remission, the PSA levels of the remaining three patients remained high overall. There were no adverse reactions reported in 4 patients. In the follow-up, case 1 continued to use PD-1 monoclonal antibody (median progression free survival time was 10 months). Two patients who had previously been resistant to enzalutamide received enzalutamide again after the whole cycle of treatment, and their PSA decreased again, which indicated that the patient was sensitive to enzalutamide again. BAT had a certain therapeutic effect on mCRPC patients, and the safety was controllable. Its tumor control effect still needed long-term follow-up verification in large-sample clinical trials. BAT has a certain therapeutic effect on mCRPC patient, especially the resensitivity of tumors to enzalutamide can be restored. Immune checkpoint inhibitors may have therapeutic potential in patients with prostate cancer treated with BAT and enzalutamide.
