Circulating Tumor Cells as a Marker for Progression‐free Survival in Metastatic Castration‐naïve Prostate Cancer

Josefsson, Andreas; Linder, Anna; Site, Despina Flondell; Canesin, Giacomo; Stiehm, Anna; Anand, Aseem; Bjartell, Anders; Damber, Jan‐Erik; Welén, Karin

doi:10.1002/pros.23325

Cited by 28 publications

(25 citation statements)

References 26 publications

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“…We have previously reported the prognostic value of detection of EGFR and ARV7 in hormone-sensitive metastatic prostate cancer, in a patient cohort partly overlapping the present study [40,41]. Our previous data could not be confirmed in this study where the multiplex gene expression analysis enables more careful normalization and accurate exclusion of samples with low CTC content.…”

Section: Discussioncontrasting

confidence: 75%

“…CTCs were isolated from blood and detected using the AdnaTest ProstateCancerSelect/Detect (Qiagen Hannover GmbH, Langenhagen, Germany) as previously described [41]. Briefly, patient blood samples were collected immediately prior to surgery in AdnaCollect tubes and kept refrigerated (4 • C) for no more than 24 h until CTC isolation.…”

Section: Ctc Isolation and Cdna Synthesismentioning

confidence: 99%

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

Josefsson

Larsson

Freyhult

et al. 2019

Cancers

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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.

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Section: Discussioncontrasting

confidence: 75%

Section: Ctc Isolation and Cdna Synthesismentioning

confidence: 99%

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

Josefsson

Larsson

Freyhult

et al. 2019

Cancers

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“…We also add 1 point in cases of visceral metastasis. M1 stage showed a strong association with early progression, and circulating tumor cells were detected more frequently in M1 patients . In localized prostate cancer, circulating tumor cells did not show a significant correlation with pathological T stage, and no studies have proven that circulating tumor cells predict unfavorable prognosis .…”

Section: Discussionmentioning

confidence: 99%

Simple risk assessment in prostate cancer patients treated with primary androgen deprivation therapy: The Korean Cancer Study of the Prostate risk classification

et al. 2018

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Objectives To investigate the progression to castration‐resistant prostate cancer after primary androgen deprivation therapy, and to build a simple risk prediction model for primary androgen deprivation therapy patients based on the Japan Cancer of the Prostate Risk Assessment criteria. Methods A total of 602 patients who received primary androgen deprivation therapy were entered into the Korean Cancer Study of the Prostate database. The effect of prognostic factors was determined by multivariate analysis. For each patient, the weight of all factors was totaled to give Korean Cancer Study‐prostate scores; patients were divided into three risk groups according to their score. The probability of castration‐resistant prostate cancer, cancer‐specific survival and overall survival was estimated by Kaplan–Meier analysis. Results On multivariate analysis for castration‐resistant prostate cancer, the significant variables were initial prostate‐specific antigen (>40 ng/mL; 1 point), biopsy Gleason score (≥9; 1 point), clinical N1 (1 point), and non‐regional lymph node (1 point), bone (1 point) and visceral (1 point) metastasis. The Korean Cancer Study‐prostate scoring model was calculated on a scale of 0–6 (0: low, 1–2: intermediate, ≥3: high risk). The risk groups stratified castration‐resistant prostate cancer (P < 0.0001), cancer‐specific survival (P < 0.0001) and overall survival (P < 0.0001) by Kaplan–Meier curve. The Korean Cancer Study‐prostate model predicted castration‐resistant prostate cancer with a c‐index of 0.7242, cancer‐specific survival with a c‐index of 0.7036 and overall survival with a c‐index of 0.5890. The 5‐year estimated castration‐resistant prostate cancer/cancer‐specific death rates were 10.3%/6.3% in the low‐risk group, 48.4%/22.2% in the intermediate‐risk group and 81.7%/53.1% in the high‐risk group. Conclusions The Korean Cancer Study‐prostate risk classification, a modified Japan Cancer of the Prostate Risk Assessment model, is a simple scoring model for predicting oncological outcomes after primary androgen deprivation therapy.

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“…These two integrin markers were increased with tumor progression from localized T1-T2 tumors (44 patients) to hormone-refractory metastatic tumors (28 patients) and were associated with decreased metastasis progression free survival [63]. In a study of 53 patients, CTC enumeration using both the CellSearch method and the AdnaTest kit isolating EpCAM + and HER2 + cells demonstrated that EpCAM + cell numbers in the circulation correlated with the presence of metastases [64]. Interestingly, E-cadherin expression was associated with bone metastasis in 109 patients, but not soft tissue metastasis in 56 patients [65], suggesting that mesenchymal-epithelial transition (a reversion from EMT) may be occurring, which is required for escape from the dormancy normally associated with bone metastatic growth.…”

Section: Cancer Stem Cells Control Colonization and Metastatic Growthmentioning

confidence: 99%

“…CD117 + CTC numbers, in particular, remained high 3 months after radical prostatectomy in the circulation of 12 patients who experienced biochemical recurrence 6–18 months later [37], indicating that CSCs in the circulation may be used to predict therapeutic failure earlier. In another study of 50 patients with CTCs measured before and after androgen deprivation therapy by the CellSearch apparatus, it was shown that CTC levels were associated with rising PSA and decreased progression free survival [64]. In addition, staining of potential CTCs from 27 patients with metastatic castration-resistant prostate cancer demonstrated that patients with neuroendocrine prostate cancer have significantly different CTCs with lower AR and cytokeratin expression and smaller size [67].…”

Section: Cancer Stems Cells In Recurrence and Resistance To Treatmentmentioning

confidence: 99%

Prostate Cancer Stem Cell Markers Drive Progression, Therapeutic Resistance, and Bone Metastasis

Harris

Kerr

2017

Stem Cells International

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Metastatic or recurrent tumors are the primary cause of cancer-related death. For prostate cancer, patients diagnosed with local disease have a 99% 5-year survival rate; however, this 5-year survival rate drops to 28% in patients with metastatic disease. This dramatic decline in survival has driven interest in discovering new markers able to identify tumors likely to recur and in developing new methods to prevent metastases from occurring. Biomarker discovery for aggressive tumor cells includes attempts to identify cancer stem cells (CSCs). CSCs are defined as tumor cells capable of self-renewal and regenerating the entire tumor heterogeneity. Thus, it is hypothesized that CSCs may drive primary tumor aggressiveness, metastatic colonization, and therapeutic relapse. The ability to identify these cells in the primary tumor or circulation would provide prognostic information capable of driving prostate cancer treatment decisions. Further, the ability to target these CSCs could prevent tumor metastasis and relapse after therapy allowing for prostate cancer to finally be cured. Here, we will review potential CSC markers and highlight evidence that describes how cells expressing each marker may drive prostate cancer progression, metastatic colonization and growth, tumor recurrence, and resistance to treatment.

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Circulating Tumor Cells as a Marker for Progression‐free Survival in Metastatic Castration‐naïve Prostate Cancer

Cited by 28 publications

References 26 publications

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

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

Simple risk assessment in prostate cancer patients treated with primary androgen deprivation therapy: The Korean Cancer Study of the Prostate risk classification

Prostate Cancer Stem Cell Markers Drive Progression, Therapeutic Resistance, and Bone Metastasis

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