The standard first-line treatment of castration-resistant prostate cancer (CRPC) is docetaxel-based chemotherapy. However, CRPC may not respond to docetaxel due to drug resistance or other causes. Several new therapeutic agents have been developed, some of which are approved by FDA or on clinical trials. The mechanisms of action of these agents include stabilizing microtubules, inhibiting hormone synthesis, blocking androgen receptor, bone targeting or immune regulation. In this article we review the novel therapeutic options for CPRC after docetaxel failure.
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http://dx.doi.org/10.3785/j.issn.1008-9292.2014.01.002 | DOI Listing |
Prostate Cancer Prostatic Dis
December 2024
Department of Radiation Oncology, Peking University First Hospital, 100034, Beijing, China.
Background: Metastatic prostate cancer (PCa) has much lower survival and ultimately develops castration resistance, which expects novel targets and therapeutic approaches. As a result of iron-dependent lipid peroxidation, ferroptosis triggers programmed cell death and has been associated with castration-resistant prostate cancer (CRPC).
Subjects: To better understand how ferroptosis can be used to treat CRPC, we reviewed the following: First, ferroptosis mechanisms and characteristics.
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 PDFWorld J Urol
December 2024
Department of Urology, University Hospital Frankfurt, Goethe University Frankfurt am Main, Frankfurt, Germany.
Purpose: No currently available phase III trial compared docetaxel vs. androgen receptor pathway inhibitors (ARPI) regarding cancer-control outcomes in metastatic hormone-sensitive prostate cancer (mHSPC). Moreover, few is known about the effect of sequential therapies in mHSPC and subsequent metastatic castration resistant prostate cancer (mCRPC).
View Article and Find Full Text PDFCell Mol Life Sci
December 2024
Research Service, VA Northern California Health Care System, Mather, CA, USA.
Neoadjuvant therapy (NAT) has been studied in clinically localized prostate cancer (PCa) to improve the outcomes from radical prostatectomy (RP) by 'debulking' of high-risk PCa; however, using androgen deprivation therapy (ADT) at this point risks castration resistant PCa (CRPC) clonal proliferation. Our goal is to identify alternative NAT that reduce hormone sensitive PCa (HSPC) without affecting androgen receptor (AR) transcriptional activity. PCa is associated with increased expression and activation of the epidermal growth factor receptor (EGFR) family, including HER2 and ErbB3.
View Article and Find Full Text PDFNeoplasia
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.
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