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Gene expression alterations during development of castration-resistant prostate cancer are detected in circulating tumor cells

Journal article
Authors Andreas Josefsson
Karin Larsson
E. Freyhult
Jan-Erik Damber
Karin Welén
Published in Cancers
Volume 12
Issue 1
ISSN 2072-6694
Publication year 2020
Published at Sahlgrenska Cancer Center
Institute of Clinical Sciences, Department of Urology
Language en
Keywords Biomarker, CRPC, CTC, Hormone-sensitive prostate cancer, Liquid biopsy, Resistance mechanisms, abiraterone acetate, androgen receptor, bicalutamide, cabazitaxel, cyclophosphamide, docetaxel, enzalutamide, midkine, radium chloride ra 223, aged, AGR2 gene, AKR1C3 gene, androgen deprivation therapy, apoptosis, AR gene, Article, BCL2 gene, cancer prognosis, cancer recurrence, cancer specific survival, carcinogenesis, castration resistant prostate cancer, circulating tumor cell, clinical article, disease association, down regulation, EPCAM gene, epithelial mesenchymal transition, FOLH1 gene, gene, gene expression profiling, gene mutation, HER2 gene, human, human cell, human tissue, KLK3 gene, KRT19 gene, male, molecular phylogeny, PSCA gene, real time polymerase chain reaction, signal transduction, SRD5A1 gene, steroidogenesis, survival rate, survival time, Sweden, TACSTD2 gene, TWIST1 gene
Subject categories Cancer and Oncology, Urology and Nephrology


Development of castration-resistant prostate cancer (CRPC) is associated with alterations in gene expression involved in steroidogenesis and androgen signaling. This study investigates whether gene expression changes related to CRPC development can be identified in circulating tumor cells (CTCs). Gene expression in paired CTC samples from 29 patients, before androgen deprivation therapy (ADT) and at CRPC relapse, was compared using a panel including 47 genes related to prostate cancer progression on a qPCR platform. Fourteen genes displayed significantly changed gene expression in CTCs at CRPC relapse compared to before start of ADT. The genes with increased expression at CRPC relapse were related to steroidogenesis, AR-signaling, and anti-apoptosis. In contrast, expression of prostate markers was downregulated at CRPC. We also show that midkine (MDK) expression in CTCs from metastatic hormone-sensitive prostate cancer (mHSPC) was associated to short cancer-specific survival (CSS). In conclusion, this study shows that gene expression patterns in CTCs reflect the development of CRPC, and that MDK expression levels in CTCs are prognostic for cancer-specific survival in mHSPC. This study emphasizes the role of CTCs in exploring mechanisms of therapy resistance, as well as a promising biomarker for prognostic and treatment-predictive purposes in advanced mHSPC. © 2019 by the authors. Licensee MDPI, Basel, Switzerland.

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