Regulation of self-renewal in normal and cancer stem cells

Authors


P. G. Pelicci, Department of Experimental Oncology, European Institute of Oncology, Via Adamello 16, 20139 Milan, Italy
Fax: +39 02 9437 5990
Tel: +39 02 9437 5040
E-mail: piergiuseppe.pelicci@ifom-ieo-campus.it

Abstract

Mutations can confer a selective advantage on specific cells, enabling them to go through the multistep process that leads to malignant transformation. The cancer stem cell hypothesis postulates that only a small pool of low-cycling stem-like cells is necessary and sufficient to originate and develop the disease. Normal and cancer stem cells share important functional similarities such as ‘self-renewal’ and differentiation potential. However, normal and cancer stem cells have different biological behaviours, mainly because of a profound deregulation of self-renewal capability in cancer stem cells. Differences in mode of division, cell-cycle properties, replicative potential and handling of DNA damage, in addition to the activation/inactivation of cancer-specific molecular pathways confer on cancer stem cells a malignant phenotype. In the last decade, much effort has been devoted to unravel the complex dynamics underlying cancer stem cell-specific characteristics. However, further studies are required to identify cancer stem cell-specific markers and targets that can help to confirm the cancer stem cell hypothesis and develop novel cancer stem cell-based therapeutic approaches.

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