615P Circulating tumor cells (CTC) gene expression and plasma androgen receptor (AR) copy number (CN) in cabazitaxel-treated metastatic castration-resistant prostate cancer (mCRPC)

2021 ◽  
Vol 32 ◽  
pp. S654-S655
Author(s):  
G. Gurioli ◽  
V. Conteduca ◽  
N. Brighi ◽  
E. Scarpi ◽  
U. Basso ◽  
...  
Keyword(s):  
Gene Expression ◽  
Prostate Cancer ◽  
Androgen Receptor ◽  
Tumor Cells ◽  
Circulating Tumor Cells ◽  
Copy Number ◽  
Castration Resistant Prostate Cancer ◽  
Castration Resistant

scholarly journals Gene Expression Alterations during Development of Castration-Resistant Prostate Cancer Are Detected in Circulating Tumor Cells

Cancers ◽  
2019 ◽  
Vol 12 (1) ◽  
pp. 39 ◽  
Author(s):  
Andreas Josefsson ◽  
Karin Larsson ◽  
Eva Freyhult ◽  
Jan-Erik Damber ◽  
Karin Welén
Keyword(s):  
Gene Expression ◽  
Prostate Cancer ◽  
Tumor Cells ◽  
Circulating Tumor Cells ◽  
Cancer Progression ◽  
Expression Patterns ◽  
Therapy Resistance ◽  
Castration Resistant Prostate Cancer ◽  
Cancer Specific Survival ◽  
Castration Resistant

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.

scholarly journals Detection of Androgen Receptor Mutations in Circulating Tumor Cells in Castration-Resistant Prostate Cancer

2010 ◽  
Vol 56 (9) ◽  
pp. 1492-1495 ◽  
Author(s):  
Yuqiu Jiang ◽  
John F Palma ◽  
David B Agus ◽  
Yixin Wang ◽  
Mitchell E Gross
Keyword(s):  
Prostate Cancer ◽  
Androgen Receptor ◽  
Tumor Cells ◽  
Circulating Tumor Cells ◽  
Relative Abundance ◽  
Direct Sequencing ◽  
Receptor Gene ◽  
Missense Mutations ◽  
Castration Resistant Prostate Cancer ◽  
Castration Resistant

BACKGROUND Coding mutations in the AR (androgen receptor) gene have been identified in tissue samples from patients with advanced prostate cancer and represent a possible mechanism underlying the development of castration-resistant prostate cancer (CRPC). There is a paucity of tumor-derived tissue available for molecular studies of CRPC patients. Circulating tumor cells (CTCs) in the blood of CRPC patients represent a possible avenue for interrogating the disease of such patients. METHODS Circulating tumor cells were captured with the CellSearch® Circulating Tumor Cell (CTC) Kit and with the CellSearch Profile Kit plus Qiagen's AllPrep DNA/RNA Micro Kit for the measurement of the CTC count per 7.5 mL of blood and for the isolation of nucleic acids, respectively. The AR gene was amplified by the PCR, and mutation status and relative abundance were analyzed by applying Transgenomic's WAVE® denaturing HPLC technology followed by direct sequencing. RESULTS AR mutations were detected in 20 of 35 CRPC patients; 19 missense mutations, 2 silent mutations, 5 deletions, and 1 insertion were observed. The relative abundance of the mutants in the amplified products ranged from 5% to 50%. Many of the AR mutations were identified in surgical biopsies or at autopsy and were associated with resistance to androgen-directed therapies. CONCLUSIONS AR mutations can be identified in CTC-enriched peripheral blood samples from CRPC patients. This approach has the potential to open new perspectives in understanding CTCs and the mechanisms for tumor progression and metastasis in CRPC.

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