scholarly journals PD-L1promoter methylation is a prognostic biomarker for biochemical recurrence-free survival in prostate cancer patients following radical prostatectomy

Oncotarget ◽  
2016 ◽  
Vol 7 (48) ◽  
pp. 79943-79955 ◽  
Author(s):  
Heidrun Gevensleben ◽  
Emily Eva Holmes ◽  
Diane Goltz ◽  
Jörn Dietrich ◽  
Verena Sailer ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Radical Prostatectomy ◽  
Cancer Patients ◽  
Biochemical Recurrence ◽  
Prognostic Biomarker ◽  
Recurrence Free Survival ◽  
Free Survival

Impact of testosterone replacement therapy after radical prostatectomy on prostate cancer outcomes.

2019 ◽  
Vol 37 (7_suppl) ◽  
pp. 100-100
Author(s):  
Reith Sarkar ◽  
J Kellogg Parsons ◽  
John Paul Einck ◽  
Arno James Mundt ◽  
A. Karim Kader ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Overall Survival ◽  
Radical Prostatectomy ◽  
Cancer Patients ◽  
Biochemical Recurrence ◽  
Testosterone Replacement ◽  
Testosterone Replacement Therapy ◽  
Recurrence Free Survival ◽  
Free Survival

100 Background: Currently there is little data to guide the use of post-radical prostatectomy (RP) testosterone replacement therapy in prostate cancer. We sought to evaluate the impact of post-RP testosterone replacement on prostate cancer outcomes in a large national cohort. Methods: We conducted a population-based cohort study using the Veterans Affairs Informatics and Computing Infrastructure. We identified node-negative and non-metastatic prostate cancer patients diagnosed between 2001-2015 treated with RP. We excluded patients for missing covariate and follow-up data. We then coded receipt of testosterone replacement after RP as a time-dependent covariate. Other covariates included: age, Charlson Comorbidity index, diagnosis year, body mass index, race, PSA, clinical T/N/M stage, Gleason score, and receipt of hormone therapy. Biochemical recurrence was defined as a post-RP PSA≥0.2. We evaluated prostate cancer-specific survival, overall survival, and biochemical recurrence free survival using multivariable Cox regression. Results: Our cohort included 28,651 patients, of whom 469 (1.6%) received testosterone replacement after RP. Median follow up was 7.4 years. There were no differences in clinical T stage, median post-RP PSA (testosterone: 0 non-testosterone: 0; p = 0.18), or hormone therapy use between treatment groups. Testosterone patients were more likely to be of younger age, have higher comorbidity, non-black, have a lower median pre-treatment PSA (5.0 vs 5.8; p < 0.001), and have higher BMI. The median time from RP to TRT was 3.0 years. After controlling for potential confounders, we found no difference in prostate cancer specific mortality (HR 0.73; 95% CI 0.32-1.62; p = 0.43), overall survival (HR 1.11; 95% CI 0.86-1.44; p = 0.43), non-cancer mortality (HR 1.17; 95% CI 0.89-1.55; p = 0.26) biochemical recurrence free survival (HR 1.07; 95% CI 0.84-1.36; p = 0.59) between testosterone users and non-users. Conclusions: Our results suggest that testosterone replacement is safe in prostate cancer patients who have undergone RP, though prospective data is necessary to confirm this finding.

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