Metastatic castrate-resistant prostate cancer with a late, complete and durable response to docetaxel chemotherapy: a case report

Abstract

Introduction: Although treatment options for men with metastatic castrate-resistant prostate cancer have improved in recent years, the outlook for patients remains poor, with overall survival in the region of 2 years. Response rates with chemotherapy are modest and disease progression is usually observed within months of stopping treatment.

Case presentation: We present a case of a 72-year-old White man of British origin with metastatic castrate-resistant prostate cancer with bulky lymphadenopathy and a serum prostate-specific antigen of 295 μg/L. He received treatment with docetaxel chemotherapy plus prednisolone, but received just 3 cycles before treatment was stopped due to toxicity and lack of response (prostate-specific antigen was 276 μg/L 4 weeks after the last dose and there was a confirmed stable appearance on computed tomography scan). Unexpectedly, at follow-up 4 months later, the patient was clinically better; his prostate-specific antigen had dramatically improved to 4.1 μg/L and a re-staging computed tomography scan revealed complete resolution of his bulky lymphadenopathy. At the time, he was receiving a luteinising hormone-releasing hormone analogue but no other disease-modulating treatment. He remains well and asymptomatic, with his most recent serum prostate-specific antigen measuring 0.14 μg/L, 18 months after last receiving chemotherapy.

Conclusion: We report a case of complete and durable regression of metastatic castrate-resistant prostate cancer following palliative chemotherapy which, to the best of our knowledge, has not previously been reported in the literature.

Figure 1

Histology from prostate biopsy. Core biopsies of the patient’s prostate gland at diagnosis revealed a typical prostatic adenocarcinoma, Gleason score 4+4=8. Hematoxylin and eosin-stained section.

Figure 2

Serial abdominal computed tomography scans. (A) Baseline computed tomography scan performed 3 days prior to the start of chemotherapy. Bulky retroperitoneal lymph nodes are visible (arrow). (B) End-of-treatment computed tomography scan performed 28 days following the last dose of chemotherapy. The lymphadenopathy persists (arrow) and was deemed stable by Response Evaluation Criteria In Solid Tumours criteria. (C) Follow-up computed tomography scan, performed 203 days following the last dose of chemotherapy. This scan was requested in view of the dramatic fall in PSA. Complete resolution of the lymphadenopathy is observed, with only a small residuum left (arrow).

Figure 3

Line plots of change in serum prostate-specific antigen with time. (A) Change in serum prostate-specific antigen from diagnosis (log 10 scale). The patient achieved almost 6 years of disease control with androgen-deprivation therapy before developing a castrate-resistant state. The prostate-specific antigen can be seen to initially rise despite bicalutamide, then subsequently to rise despite a switch to goserelin, and finally despite maximum androgen blockade (bicalutamide plus goserelin). The patient then went on to receive three cycles of docetaxel plus prednisolone chemotherapy. A dramatic and sustained fall in prostate-specific antigen was observed 4 months after last receiving chemotherapy. This section of the plot has been expanded in Figure 3B for clarity. (B) Change in serum prostate-specific antigen (log 10 scale) in relation to chemotherapy. The prostate-specific antigen remained stable during chemotherapy (>250μg/L) and for at least 34 days following the last dose. However, at follow-up 4 months following his last dose of chemotherapy, his serum prostate-specific antigen had fallen to 4.1μg/L. When last seen, his latest prostate-specific antigen reading was 0.14μg/L, 18 months since his last cycle of chemotherapy. Abbreviation: PSA, prostate-specific antigen.