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Phenotypic and genotypic characterization of single circulating tumor cells in the follow‐up of high‐grade serous ovarian cancer
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Phenotypic and genotypic characterization of single circulating tumor cells in the follow‐up of high‐grade serous ovarian cancer
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Journal Article
Phenotypic and genotypic characterization of single circulating tumor cells in the follow‐up of high‐grade serous ovarian cancer
2026
Overview
Single circulating tumor cell (sCTC) analysis enables the determination of predominant CTC phenotypes and genotypes. We previously demonstrated the feasibility of sCTC detection and genomic characterization in high‐grade serous ovarian cancer (HGSOC) by combining immune‐magnetic enrichment and image‐based sorting, followed by whole‐genome amplification (WGA) and next‐generation sequencing‐based copy number alteration analysis (CNA). Here we aimed to improve our workflow by incorporating HGSOC‐specific markers, folate receptor alpha (FRα), and markers to identify epithelial (cytokeratin) and mesenchymal (vimentin) phenotypes for the phenotypic as well as genotypic analysis of sCTCs over the course of treatment in 42 HGSOC patients. We detected a significant reduction of FRα‐positive cells (P = 0.0205) and an expansion of cells with a high nuclear staining and no target antigen expression (P = 0.002). Before treatment, sCTCs showed an enrichment in CNAs of Chromosomes 2, 7, and 12, while CNA dynamics of sCTCs suggested a potential selection of distinct CNAs specific to the homologous recombination pathway. sCTCs revealed persistent CNAs in the CDK4 and emerging ones in the ALK oncogene. Notably, primary tumors revealed considerable fractions of shared genomic aberrations. Single circulating tumor cells (sCTCs) from high‐grade serous ovarian cancer patients were enriched, imaged, and genomically profiled using WGA and NGS at different time points during treatment. sCTCs revealed enrichment of alterations in Chromosomes 2, 7, and 12 as well as persistent or emerging oncogenic CNAs, supporting sCTC identity. Notably, primary tumors revealed considerable fractions of shared genomic aberrations.
Publisher
John Wiley & Sons, Inc,Wiley
Subject
/ Antigens
/ Biomarkers, Tumor - genetics
/ Cystadenocarcinoma, Serous - blood
/ Cystadenocarcinoma, Serous - genetics
/ Cystadenocarcinoma, Serous - pathology
/ DNA Copy Number Variations - genetics
/ Ethylenediaminetetraacetic acid
/ Female
/ Folate Receptor 1 - metabolism
/ Genomes
/ Genomics
/ Genotype
/ high‐grade serous ovarian cancer
/ Humans
/ Keratin
/ Mutation
/ Neoplastic Cells, Circulating - metabolism
/ Neoplastic Cells, Circulating - pathology
/ Ovarian Neoplasms - genetics
/ Ovarian Neoplasms - pathology
/ Patients
/ single circulating tumor cells
/ Tumors
/ Vimentin
