Background: Leptomeningeal metastasis is discovered at autopsy in approximately 5% of patients with systemic cancer. Until recently with the introduction of magnetic resonance imaging (MRI), premorbid diagnosis was extremely difficult. In particular, initial spinal fluid cytology is diagnostic in less than 50% of autopsy-verified patients, although repeated spinal fluid examinations may increase the yield significantly. Leptomeningeal metastasis in metastatic prostate cancer has been reported in only 14 patients previously.
Case Description: We recently studied such a patient and were able to establish a correct diagnosis based solely on the MRI and the presence of an elevated cerebrospinal fluid (CSF) prostate-specific antigen (PSA). Only 3 previous patients with leptomeningeal prostate metastasis have undergone CSF PSA evaluations.
Conclusion: We believe that, in such patients, the combination of MRI and CSF studies can overcome the lack of sensitivity of CSF cytology.
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http://dx.doi.org/10.1016/j.surneu.2005.08.026 | DOI Listing |
Eur J Nucl Med Mol Imaging
January 2025
Department of Radiation Oncology, University Medical Centre Freiburg, Robert-Koch Straße 3, 79106, Freiburg, Germany.
Purpose: Prostate-specific membrane-antigen positron emission tomography (PSMA PET) is a promising candidate for non-invasive characterization of prostate cancer (PCa). This study evaluated whether PET with tracers [Ga]Ga-PSMA-11 or [F]PSMA-1007 is capable to depict intratumour heterogeneity of histological PSMA expression.
Methods: Thirty-five patients with biopsy-proven primary PCa without evidence of metastatic disease nor prior interventions were prospectively enrolled.
Mol Oncol
January 2025
Institute of Biochemistry and Molecular Medicine, University of Bern, Bern, Switzerland.
Transient receptor potential melastatin-4 (TRPM4) ion channel expression is upregulated in prostate cancer (PCa), contributing to increased cell proliferation, migration, adhesion, epithelial-to-mesenchymal transition, cell cycle shift, and alterations of intracellular Ca signaling. GEO2R platform analysis of messenger RNA (mRNA) expression of ~ 6350 genes in normal and malignant prostate tissue samples from 15 PCa patients demonstrates that TRPM4 expression is upregulated sixfold and is among the most significantly upregulated genes in PCa. We find that absence of TRPM4 reduced PCa tumor spheroid size and decreased PCa tumor spheroid outgrowth.
View Article and Find Full Text PDFJpn J Clin Oncol
January 2025
Department of Urology, The Jikei University School of Medicine, 3-25-8, Nishishimbashi, Minato-ku, Tokyo 105-8461, Japan.
Background: Despite its demonstrated efficacy in prolonging overall survival (OS) and delaying skeletal-related events in the ALSYMPCA trial, the optimal timing of radium-223 initiation remains unclear. This study investigated factors influencing radium-223 treatment outcomes, including completion rates and survival.
Methods: This retrospective, multi-institutional study included 164 patients with metastatic castration-resistant prostate cancer (CRPC) who received radium-223 therapy.
Jpn J Clin Oncol
January 2025
Department of Urology, Kyoto University Hospital, 54 Shogoin-kawahara-cho, Sakyo-ku, Kyoto, 606-8507, Japan.
Background: Non-metastatic castration-resistant prostate cancer (PCa) has become clinically important in PCa management, with treatments aiming to delay metastasis. However, limited data exist on its prevalence and patient characteristics in real-world settings.
Methods: We retrospectively investigated the clinical records of 1929 patients who were treated for localized PCa between 2005 and 2018.
Nat Rev Urol
January 2025
Cancer Biology and Epigenetics Group, Research Center of IPO Porto (CI-IPOP)/CI-IPOP@RISE (Health Research Network), Portuguese Oncology Institute of Porto (IPO Porto)/Porto Comprehensive Cancer Center Raquel Seruca (Porto.CCC Raquel Seruca), Porto, Portugal.
Prostate cancer is a multifactorial disease influenced by various molecular features. Over the past decades, epigenetics, which is the study of changes in gene expression without altering the DNA sequence, has been recognized as a major driver of this disease. In the past 50 years, advancements in technological tools to characterize the epigenome have highlighted crucial roles of epigenetic mechanisms throughout the entire spectrum of prostate cancer, from initiation to progression, including localized disease, metastatic dissemination, castration resistance and neuroendocrine transdifferentiation.
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