scholarly journals High levels of DEPDC1B predict shorter biochemical recurrence‑free survival of patients with prostate cancer

Author(s):  
Shoumin Bai ◽  
Ting Chen ◽  
Tao Du ◽  
Xianju Chen ◽  
Yiming Lai ◽  
...  
2008 ◽  
Vol 14 (3) ◽  
pp. 758-763 ◽  
Author(s):  
Joseph R. Sterbis ◽  
Chunling Gao ◽  
Bungo Furusato ◽  
Yongmei Chen ◽  
Syed Shaheduzzaman ◽  
...  

2019 ◽  
Vol 37 (7_suppl) ◽  
pp. 99-99
Author(s):  
Reith Sarkar ◽  
J Kellogg Parsons ◽  
John Paul Einck ◽  
Arno James Mundt ◽  
A. Karim Kader ◽  
...  

99 Background: Currently there is little data to guide the use of testosterone replacement therapy in prostate cancer patients who have received radiation therapy (RT). We sought to evaluate the impact of post-RT 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 RT. We excluded patients for missing covariate and follow-up data. Receipt of testosterone was coded 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. We evaluated prostate cancer-specific survival, overall survival, and biochemical recurrence free survival using multivariable Cox regression. Results: Our cohort included 41,544 patients, of whom 544 (1.3%) received testosterone replacement after RT. There were no differences in Charlson comorbidity, clinical T stage, median pre-treatment PSA or Gleason score between treatment groups. Testosterone patients were more likely to be of younger age, non-black, have a lower median post-treatment PSA nadir (0.1 vs. 0.2; p < 0.001), have higher BMI, and have used hormone therapy (46.7% vs 40.3%; p = 0.003). Median duration of ADT usage was equivalent between treatment groups (testosterone: 185 days vs. non-testosterone: 186 days, p = 0.77). The median time from RT to TRT was 3.52 years. After controlling for differences in covariates between treatment groups, we found no difference in prostate cancer specific mortality (HR 1.02; 95% CI 0.62-1.67; p = 0.95), overall survival (HR 1.02; 95% CI 0.84-1.24; p = 0.86), non-cancer mortality (HR 1.02; 95% CI 0.82-1.27; p = 0.86) biochemical recurrence free survival (HR 1.07; 95% CI 0.90-1.28; p = 0.45). Conclusions: Our results suggest that testosterone replacement is safe in prostate cancer patients who have received RT. Prospective data are required to confirm the safety of post-RT testosterone replacement.


2018 ◽  
Vol Volume 11 ◽  
pp. 1077-1086 ◽  
Author(s):  
Donggen Jiang ◽  
Chutian Xiao ◽  
Tuzeng Xian ◽  
Liantao Wang ◽  
Yunhua Mao ◽  
...  

2021 ◽  
Vol 11 ◽  
Author(s):  
Rui Zhou ◽  
Yuanfa Feng ◽  
Jianheng Ye ◽  
Zhaodong Han ◽  
Yuxiang Liang ◽  
...  

Tumor-adjacent normal (TAN) tissues, which constitute tumor microenvironment and are different from healthy tissues, provide critical information at molecular levels that can be used to differentiate aggressive tumors from indolent tumors. In this study, we analyzed 52 TAN samples from the Cancer Genome Atlas (TCGA) prostate cancer patients and developed a 10-gene prognostic model that can accurately predict biochemical recurrence-free survival based on the profiles of these genes in TAN tissues. The predictive ability was validated using TAN samples from an independent cohort. These 10 prognostic genes in tumor microenvironment are different from the prognostic genes detected in tumor tissues, indicating distinct progression-related mechanisms in two tissue types. Bioinformatics analysis showed that the prognostic genes in tumor microenvironment were significantly enriched by p53 signaling pathway, which may represent the crosstalk tunnels between tumor and its microenvironment and pathways involving cell-to-cell contact and paracrine/endocrine signaling. The insight acquired by this study has advanced our knowledge of the potential role of tumor microenvironment in prostate cancer progression.


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