Introduction: As an acute-phase protein synthesized in response to systemic inflammation, the C-reactive protein (CRP) has been shown to be an independent prognostic factor for patients with castration-resistant prostate cancer (CRPC). The aim of this study was to investigate the association between CRP and progression-free survival (PFS), overall survival (OS) and radiological response in CRPC patients treated with docetaxel.

Methods: 115 histologically confirmed CRPC patients who were treated with docetaxel chemotherapy from 2008 to 2013 were selected. Univariable and multivariable Cox regression models were used to predict the association of CRP as a dichotomous variable with PFS and OS after chemotherapy initiation.

Results: None of the clinicopathological features were associated with the CRP. In Kaplan-Meier analysis, the median PFS (9.8 vs. 7.5 months, p < 0.001) and OS (26.5 vs. 13.5 months, p = 0.002) were higher in patients who did not have an elevated CRP than in those with an elevated CRP. In univariable analysis, the pretreatment CRP was significantly associated with PFS (p < 0.001) and OS (p = 0.003).In multivariable analysis, patients with a CRP > 8 mg/l were at significantly higher risk of tumor progress (hazard ratio (HR) 2.184; 95% confidence interval (CI) 1.401-3.403; p = 0.001) and death (HR 2.003; 95% CI 1.285-3.121; p = 0.002) than patients with a CRP ≤ 8 mg/l.

Conclusions: CRP may be an important biomarker of PFS and OS in CRPC patients treated with docetaxel. The findings require validation in further prospective, large cohort-size studies.

Download full-text PDF

Source
http://dx.doi.org/10.1159/000446098DOI Listing

Publication Analysis

Top Keywords

crpc patients
12
patients treated
12
crp
10
c-reactive protein
8
patients
8
patients castration-resistant
8
castration-resistant prostate
8
prostate cancer
8
association crp
8
treated docetaxel
8

Similar Publications

Systems-level liquid biopsy in advanced prostate cancer.

Endocr Relat Cancer

January 2025

S Dehm, Masonic Cancer Center, University of Minnesota, Minneapolis, United States.

Treatment for castration-resistant prostate cancer (CRPC) primarily involves the suppression of androgen receptor (AR) activity using androgen receptor signaling inhibitors (ARSIs). While ARSIs have extended patient survival, resistance inevitably develops. Mechanisms of resistance include genomic aberrations at the AR locus that reactivate AR signaling, or lineage plasticity that drives emergence of AR-independent phenotypes.

View Article and Find Full Text PDF

Background: Adverse pathology (AP) is often used as an intermediate end point for long-term outcomes in men with prostate cancer (PCa) who are active surveillance candidates. The association between a commonly used AP definition and long-term outcomes was tested, which identified definitions more strongly linked to a high risk of metastasis.

Methods: Data were reviewed from the Shared Equal Access Regional Cancer Hospital cohort of men undergoing radical prostatectomy (RP) from 1988 to 2020 at nine Veterans Affairs hospitals.

View Article and Find Full Text PDF

Drug repositioning in castration-resistant prostate cancer using systems biology and computational drug design techniques.

Comput Biol Chem

December 2024

Bioinformatics Research Center, Basic Sciences Research Institute, Mashhad University of Medical Sciences, Mashhad, Iran; Department of Medical Biotechnology and Nanotechnology, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran. Electronic address:

Background And Objective: Castration-resistant prostate cancer (CRPC) is caused by resistance to androgen deprivation treatment and leads to the death of patients and there is almost no chance of survival. Therefore, finding a cure to overcome CRPC is challenging and important, but discovering a new drug is very time-consuming and expensive. To overcome these problems, we used Drug repositioning (drug repurposing) strategy in this study.

View Article and Find Full Text PDF

Inhibiting HnRNP L-mediated alternative splicing of EIF4G1 counteracts immune checkpoint blockade resistance in Castration-resistant prostate Cancer.

Neoplasia

December 2024

General Surgery Center Department of Thyroid Surgery, Zhujiang Hospital, Southern Medical University, Guangzhou 510280, PR China; Department of Urology, Zhujiang Hospital, Southern Medical University, Guangzhou 510280, PR China. Electronic address:

Immunotherapy with checkpoint inhibitors produced significant clinical responses in a subset of cancer patients who were resistant to prior therapies. However, Castration-resistant prostate cancer (CRPC) is seriously lack of T cell infiltration, which greatly limits the clinical application of immunotherapy, but the mechanism is unclear. In the present study, in silico analyses and experimental data show that HnRNP L was significantly negatively correlated with CD4+ and CD8+ T cells infiltration in patients; besides, we found deficiency of HnRNP L recruites CD4+ and CD8+ T cells infiltration and impairs tumorigenesis.

View Article and Find Full Text PDF

PARP inhibitors (PARPi) have received regulatory approval for the treatment of several tumors, including prostate cancer (PCa), and demonstrate remarkable results in the treatment of castration-resistant prostate cancer (CRPC) patients characterized by defects in homologous recombination repair (HRR) genes. Preclinical studies showed that DNA repair genes (DRG) other than HRR genes may have therapeutic value in the context of PARPi. To this end, we performed multiple CRISPR/Cas9 screens in PCa cell lines using a custom sgRNA library targeting DRG combined with PARPi treatment.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!