Molecular Mechanisms Underlying the Progression of Prostate Cancer
A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".
Deadline for manuscript submissions: 20 March 2025 | Viewed by 11671
Special Issue Editors
Interests: castration-resistant prostate cancer; epigenetics and epitranscriptomics; transcriptional regulation; chromatin architecture; drug development
Special Issue Information
Dear Colleagues,
Prostate cancer is the most diagnosed cancer among men in the US, except for skin cancer. It is also the second leading cause of cancer death in American men. Commonly used for patients with metastatic prostate cancer, androgen deprivation therapies (ADTs), which can be achieved by surgical or medical castration to lower androgen levels, have been initially effective. Unfortunately, a majority of prostate tumors invariably relapse and progress to become ADT-resistant, which is referred to as castration-resistant prostate cancer (CRPC). Approximately 20% of lethal metastatic CRPC have a neuroendocrine phenotype following the development of resistance to hormone therapy, and thus are called neuroendocrine prostate cancer (NEPC). NEPC is characterized by low androgen receptor (AR) signaling, castration resistance, and elevated levels of neuroendocrine markers. Unfortunately, without an effective therapy, most patients die within one year upon progression to NEPC. Mechanisms by which prostate cancer progresses to CRPC and further progresses to treatment-emergent NEPC are largely unclear, dramatically hindering the therapeutic development for these lethal forms of the disease.
For this Special Issue, we sincerely invite you to submit research articles or reviews that describe recent advances and novel findings in molecular mechanisms, cell signaling, or biological processes that underlie prostate cancer progression, especially focusing on castration resistance, neuroendocrine differentiation, cellular plasticity, epigenetic regulation, hypoxia and angiogenesis, novel imaging, or therapeutic modalities for NEPC.
Dr. Kexin Xu
Dr. Wenliang Li
Guest Editors
Manuscript Submission Information
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Keywords
- prostate cancer progression
- CRPC
- NEPC
- molecular mechanisms
- cell signaling
- treatment options
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