Abstract
Metastases and cancer recurrence are the main causes of cancer death. Circulating Tumor Cells (CTCs) and disseminated tumor cells are the drivers of cancer cell dissemination. The assessment of CTCs’ clinical role in early metastasis prediction, diagnosis, and treatment requires more information about their biology, their roles in cancer dormancy, and immune evasion as well as in therapy resistance. Indeed, CTC functional and biochemical phenotypes have been only partially characterized using murine metastasis models and liquid biopsy in human patients. CTC detection, characterization, and enumeration represent a promising tool for tailoring the management of each patient with cancer. The comprehensive understanding of CTCs will provide more opportunities to determine their clinical utility. This review provides much-needed insights into this dynamic field of translational cancer research.
Highlights
For metastasis formation, cancer cells must leave the primary tumor and disseminate
The acquired genetic and epigenetic alterations, mesenchymal phenotype, clustering, and tumor microenvironment-associated clues seem to induce stem cell-like features in circulating tumor cell (CTC) [15]. These findings suggest that CTCs with CSC and metastasis-initiating cells (MICs) features more reach and colonize distant organs and subsequently induce metastasis formation
Of CTCs; (b3) The distinct electrical charges of CTCs and cells blood cells separating cell(b2) Size and (b1) Density:not density is lower than that of red blood andallow white bloodthese cells; types; and (b4) Inertial focusing: CTCs are passively separated using microfluidic devices based on deformability: filters with pores of 7- 8μm in diameter allow the passage of blood components, but not their size through the application of inertial forces of CTCs; (b3)that
Summary
For metastasis formation, cancer cells must leave the primary tumor and disseminate. To this aim, epithelial tumor cells might go through epithelial-to-mesenchymal transition (EMT), lose their polarity and cell-cell/matrix adhesion, secrete specific enzymes (e.g., cathepsin D) to digest the extracellular matrix (ECM), and gain migratory properties [1,2] (Figure 1a). It has been reported that the detection of rare CTC clusters indicates a higher metastatic potential endothelial growth factor; TAM, tumor-associated macrophages; ECM, extra cellular matrix; CAF, compared with high numbers of single CTCs [40]. The acquired genetic and epigenetic alterations (i.e., clonal selection), mesenchymal phenotype, clustering, and tumor microenvironment-associated clues (e.g., hypoxia) seem to induce stem cell-like features in CTCs [15]. These findings suggest that CTCs with CSC and MIC features more reach and colonize distant organs and subsequently induce metastasis formation
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