Abstract
Background: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,viadifferent signal transduction pathways.Conclusion: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.
Highlights
The concept that cancer develops from normal cells via the accumulation of genetic alterations, which activate carcinogenic pathways or inhibit tumor suppressor genes, has been well-known [1]
This review addresses key components of cancer stem cells (CSCs) dysregulation in the signaling pathways, and focuses on their possible clinical implications in personalized oncology approaches
In the chemotherapy-alone group, high CD44 expression was correlated with reduced survival. These findings suggest that the patients who have GI cancers with high CD44 expression can have improved survival upon receiving a combination of FOLFOX chemotherapy and vismodegib [23]
Summary
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
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