Department of Environmental Medicine and Epidemiology, Medical University of Silesia (SUM), Zabrze, Poland
Recent research evidence has revealed that cancer cells contain a subpopulation of cancer stem cells (CSCs) that can remain even after traditional oncology therapies (e.g.: surgical resection of a tumor, radiation therapy (RT), and chemotherapy (ChT)), and can subsequently regenerate the original tumor or metastases, which are resistant to standard anticancer treatments. Such a resistance can be activated in various CSC populations, via different signal transduction pathways.
The signaling pathways (e.g.: NANOG, Wnt/β-catenin, Hedgehog, Notch, signal transducer and activator of transcription 3 (STAT 3), and phosphoinositide 3-kinase (PI3K)) play a crucial role in the CSCs, leading to tumorigenesis and metastatic spread. Therefore, their detailed analysis, including innovative biomarkers, is necessary to develop the effective, novel therapies that will specifically target CSCs, in patients with aggressive cancers. This review briefly outlines the concept of CSCs, and key components of CSC dysregulation in the signaling pathways. Furthermore, it describes some innovative strategies, such as: Single-Cell Sequencing (SCS), Circulating Tumor Cells (CTCs), Disseminated Tumor Cells (DTCs), cell-free DNA (cfDNA), and circulating tumor DNA (ctDNA) that may have critical importance in the detection, early diagnosis, prognosis and monitoring of patients with various, difficult to treat malignancies (e.g.: breast or gastrointestinal cancers). It also focuses on some barriers to achieving the clinical management goals (for both patients with cancers and the interdisciplinary treatment teams), as well as suggests some solutions, how to overcome them, in personalized oncology approaches.
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* Address correspondence to this author at the Department of Environmental Medicine and Epidemiology, Medical University of Silesia (SUM), Zabrze, Poland, Tel: 33 814 1426; 692 576 729; E-mails: firstname.lastname@example.org; email@example.com