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- W1550028495 abstract "The classical clonal evolution theory of neoplastic development supports the notion that cellular transformation results from random mutations and subsequent clonal selection. However, recent advancements in identification of the malignant populations responsible for tumor maintenance and recurrence have lent support to the cancer stem cell (CSC) hypothesis as a model of carcinogenesis, and posit that tumor growth is driven by a rare subpopulation of cells with stem cell-like properties. Cancer stem cells are commonly thought of as derivatives of a normal tissue stem cell that undergoes genetic alterations, which allow for sustained aggressive and clonal characteristics, self-renewal capacity and the ability to differentiate into all populations within a malignancy. Cancer stem cells alone, as compared to the bulk of cells in a tumor, are considered to be responsible for tumor initiation, metastasis and resistance to treatment. Moreover, CSCs are believed to share many properties with normal stem cells providing them with an overall insensitivity to conventional radioand chemotherapy. Therefore, successful targeting of such a highly tumorigenic yet rare population must be considered in order to improve the therapeutic efficacy of the currently available anti-cancer therapy. Here, we provide a summary of recent progress towards development of biomarkers that identify CSCs, the molecular mechanisms behind the conventional anti-cancer therapy resistance, and the development of therapeutic strategies to selectively target CSC populations." @default.
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- W1550028495 date "2011-08-01" @default.
- W1550028495 modified "2023-09-23" @default.
- W1550028495 title "Therapeutic Strategies Targeting Cancer Stem Cells" @default.
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- W1550028495 doi "https://doi.org/10.5772/19016" @default.
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