Cancer often arises from a combination of multiple genetic changes, each conferring characteristics that predispose cells to cause disease. T-cell acute lymphoblastic leukemia (T-ALL) can result from mutations leading to the overexpression of oncogenic transcription factors, such as LMO2, during cell development in the thymus. LMO2 operates indirectly, binding to other transcription factors to regulate their activity. However, the mechanism of LMO2 action in cancer formation is unknown. McCormack et al. show that LMO2 is constitutively expressed in the thymus and induces stem cell-like properties to previously committed T cells. Its expression expands the time of T-cell self-renewal in mice, predisposing the cells to become leukemic. This mouse model of T-ALL provides insight into how LMO2 functions as an oncogene in human cancer, and should help in identifying therapeutics that target self-renewal properties of leukemia-initiating cells.
Cancer: oncogene induces cell self-renewal
Cancer: oncogene induces cell self-renewal. Dis Model Mech 8 March 2010; 3 (3-4): 122. doi:
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