Abstract
Selecting a well-suited method for isolating/characterizing circulating tumor cells (CTCs) is challenging. Evaluating sensitive and specific markers for prostate cancer (PCa)-specific CTC identification and analysis is crucial. We used the CellCollector EpCAM-functionalized system (CC-EpCAM) and evaluated and developed a PCa-functionalized version (CC-PCa); we then compared CTC isolation techniques that exploit the physical and biological properties of CTCs. We established two cohorts of metastatic PCa patients (mPCa; 15 in cohort 1 and 10 in cohort 2). CTC cultivation experiments were conducted with two capturing methods (Ficoll and ScreenCell). The most sensitive detection rates and highest CTC counts were reached with the CC-PCa and ScreenCell system. Patients with ≥5 CTCs isolated with CC-EpCAM had an overall survival (OS) of 0.93 years, and patients with ≥5 CTCs isolated with CC-PCa had an OS of 1.5 years in cohort 1. Nevertheless, we observed the highest sensitivity and specificity for 24-month survival by the Ficoll with CD45 depletion and ScreenCell system with May-Grunwald Giemsa (MGG) staining. The EpCAM molecule is an essential factor related to OS for CTC isolation based on biological properties in mPCa patients. The best-suited CTC capture system is not limited to one characteristic of cells but adapted to downstream analysis.
Highlights
Circulating tumor cells (CTCs) have been one of the most discussed biomarkers for monitoring cancer progression in the last decade
The epithelial cell adhesion molecules (EpCAM) molecule is an essential factor related to overall survival (OS) for CTC isolation based on biological properties in metastatic PCa patients (mPCa) patients
We developed a PCaspecific functionalization of the CellCollector system (CC-prostate cancer (PCa))
Summary
Circulating tumor cells (CTCs) have been one of the most discussed biomarkers for monitoring cancer progression in the last decade. Epithelial–mesenchymal transition (EMT) is a significant mechanism by which CTCs invade the surrounding stroma and blood circulation [3] In this process, CTCs lose epithelial markers, such as epithelial cell adhesion molecules (EpCAM) and E-cadherin, and show a mesenchymal phenotype. CTCs lose epithelial markers, such as epithelial cell adhesion molecules (EpCAM) and E-cadherin, and show a mesenchymal phenotype This morphological change is generally reversible via epithelial–mesenchymal transition (MET), which includes the activation of mixed epithelial/mesenchymal CTC hybrid phenotypes [1,4]. These CTC phenotypes are present in the blood of patients with prostate cancer (PCa) [5]
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