ĬSCs share a number of properties with normal stem cells (SCs). The CSC and clonal evolution models are not mutually exclusive, as CSCs can also evolve over time, generating different clonal subpopulations within the tumor. A third model, clonal evolution, states that heterogeneity comes from genetic or epigenetic changes that arise during cancer progression. In contrast, the CSC model suggests that a hierarchy exists among tumor cells, with CSCs at the top, producing the bulk of the tumor cells while maintaining their own renewal. Previously, cancers were thought to be made up of equipotent malignant cells which either renewed or differentiated stochastically, giving rise to a heterogeneous tumor. The discovery of CSCs led to a major shift in cancer modeling. Within the last two decades, CSCs have become a subject of intense research as a potential target for cancer therapeutics. Since then, CSCs have been discovered in many solid tumors. They were first discovered in acute myeloid leukemia (AML) in the late 1990s. This review discusses numerous strategies to eliminate CSCs by targeting surface biomarkers, regulating CSC-associated oncogenes and signaling pathways, inhibiting drug-efflux pumps involved in drug resistance, modulating the tumor microenvironment and immune system, and applying drug combination therapy using nanomedicine.Ĭancer stem cells (CSCs) are a small subset of cancer cells with the ability to self-renew and initiate tumor growth. We further discuss multiple targeting approaches currently in preclinical or clinical testing that show great potential for targeting CSCs. In this review, the authors characterize and compare different CSC-specific biomarkers that are present in various types of tumors. Thus, a better understanding of the properties and mechanisms underlying CSC resistance to treatments is necessary to improve patient outcomes and survival rates. Compelling evidence suggests that cancer stem cells (CSCs) have a crucial impact in current shortcomings of cancer therapy because they are largely responsible for tumor initiation, relapse, metastasis, and chemo-resistance. The therapeutic limitations of conventional chemotherapeutic drugs present a challenge for cancer therapy these shortcomings are largely attributed to the ability of cancer cells to repopulate and metastasize after initial therapies.
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