To build a practical model for predicting the progression to castration-resistant prostate cancer (CRPC) after androgen deprivation therapy (ADT).In all, 185 patients with prostate cancer who had received ADT as the primary therapy at our institution, from 2003 to 2014, were retrospectively enrolled. The following clinical variables were included in the analysis: age, clinical tumor, node, metastasis stage, Gleason score, risk groups of prostate cancer, prostate-specific antigen (PSA) at the initiation of ADT, PSA nadir after ADT, velocity of PSA decline, and the time to PSA nadir. Cox proportional-hazards regression models were calculated to estimate effects of these variables on the time of progression to CRPC.On univariate and multivariate analyses, the presence of distant metastasis before ADT (hazard ratio [HR] 6.030, 95% confidence interval (CI) 3.229-11.263, P = .001), higher PSA nadir (HR 1.185, 95% CI 1.080-1.301, P = .001), a velocity of PSA decline >11 ng/mL per month (HR 2.124, 95% CI 1.195-3.750, P = .001), and a time to PSA nadir ≤9 months (HR 0.276, 95% CI 0.162-0.469, P = .004) were significantly associated with an increased risk of progression to CRPC.Patients with a rapidly decreasing PSA level in the initial phase of ADT are more likely to progress to CRPC. Our findings provide a practical approach to screen patients during ADT for early identification of those likely to progress to CRPC, allowing treatment to be modified to improve outcomes.
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http://dx.doi.org/10.1097/MD.0000000000007823 | DOI Listing |
JCO Precis Oncol
January 2025
Medical Research Service, Department of Veterans Affairs, Tennessee Valley Healthcare System, Nashville, TN.
Purpose: Considerable genetic heterogeneity is currently thought to underlie hereditary prostate cancer (HPC). Most families meeting criteria for HPC cannot be attributed to currently known pathogenic variants.
Methods: To discover pathogenic variants predisposing to prostate cancer, we conducted a familial case-control association study using both genome-wide single-allele and identity-by-descent analytic approaches.
Cancer Res Commun
January 2025
University of Minnesota, Minnesota, MN, United States.
Neuroendocrine neoplasms (NENs) encompass a diverse set of malignancies with limited precision therapy options. Recently, therapies targeting DLL3 have shown clinical efficacy in aggressive NENs, including small cell lung cancers and neuroendocrine prostate cancers. Given the continued development and expansion of DLL3-targeted therapies, we sought to characterize the expression of DLL3 and identify its clinical and molecular correlates across diverse neuroendocrine and non-neuroendocrine cancers.
View Article and Find Full Text PDFAsian Pac J Cancer Prev
January 2025
Department of Biotechnology, Kakatiya University, Warangal, Telangana, India.
Objective: A new library of Thiazolidine-2,4-dione-biphenyl Derivatives derivatives (10a-j) was designed and synthesized. All compounds were characterized by spectral data. Further, these were evaluated for their in vitro anticancer activity.
View Article and Find Full Text PDFAsian Pac J Cancer Prev
January 2025
Postgraduate Program in Oncology, Haroldo Juaçaba Hospital, Ceará Cancer Institute (ICC), Brazil.
Objective: This study aimed to investigate the influence of p16 immunohistochemical expression on the biochemical recurrence rate of pT2-pT3 prostate cancer.
Materials And Methods: A total of 488 pT2-pT3 stage prostate adenocarcinomas undergoing radical prostatectomy were included in this study. Following a review of Gleason classification and retrieval of sociodemographic and clinicopathological data, as well as the date of last consultation and biochemical recurrence, immunohistochemistry for p16 was performed.
FASEB J
January 2025
Prostate Cancer/Genitourologic Program, Oncology, The Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Among the known nuclear exportins, CRM1 is the most studied prototype. Dysregulation of CRM1 occurs in many cancers, hence, understanding the role of CRM1 in cancer can help in developing synergistic therapeutics. The study investigates how CRM1 affects prostate cancer growth and survival.
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