Smoking is associated with prostate cancer mortality and disease progression after treatment for clinically nonmetastatic prostate cancer with curative intent. We investigated the effect of smoking on biochemical recurrence and metastasis in a retrospective cohort of 214 radiation-recurrent prostate cancer patients who underwent salvage radical prostatectomy. High cumulative smoking exposure was associated with the biologic and clinical aggressiveness of prostate cancer and was an independent predictor of biochemical recurrence after adjusting for established clinicopathologic features. These data support the body of evidence that smoking is detrimental beyond the initial diagnosis of prostate cancer, even when the disease is more advanced.Introduction:
The purpose of the present study was to investigate the association of smoking with biochemical recurrence (BCR) and metastasis in radiation-recurrent prostate cancer (PCa) patients undergoing salvage radical prostatectomy (SRP).Patients and Methods:
A total of 214 patients treated with SRP for radiation-recurrent PCa in 5 tertiary referral centers were included from January 2007 to December 2015. Kaplan-Meier analyses were used to assess the time to BCR and metastasis. Pre- and postoperative multivariable Cox proportional hazard regression models were fitted.Results:
Overall, 120 (56.1%), 49 (22.9%), and 45 (21%) patients were never, former, and current smokers, respectively. Low-, medium-, and high-cumulative smoking exposure was registered in 59.8%, 16.4%, and 23.8% of cases, respectively. Patients with high cumulative smoking exposure had a significantly greater rate of a pathologic Gleason score of ≥ 8 (P = .01) and extracapsular extension (P = .004). Smoking status, cumulative smoking exposure, intensity, and duration were significantly associated with BCR-free survival (P < .001 for all). Smoking status, cumulative smoking exposure, and smoking intensity were significantly associated with metastasis-free survival (P = .03 for all). High cumulative smoking exposure was independently associated with BCR in both pre- (hazard ratio, 2.23; P = .001) and postoperative (hazard ratio, 1.64; P = .04) multivariable models adjusted for the effects of established clinicopathologic features. Smoking cessation did not affect either BCR- or metastasis-free survival (P = .56 and P = .40, respectively).Conclusion:
High cumulative smoking exposure was associated with the biologic and clinical aggressiveness of PCa in patients treated with SRP for radiation-recurrent disease. Smoking is a modifiable risk factor that detrimentally affected the outcomes, even in patients with advanced PCa.