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The molecular basis of Lmo2-induced T-cell acute lymphoblastic leukemia Curtis DJ; McCormack MPClin Cancer Res 2010[Dec]; 16 (23): 5618-23T-cell acute lymphoblastic leukemia (T-ALL) is commonly caused by the overexpression of oncogenic transcription factors in developing T cells. In a mouse model of one such oncogene, LMO2, the cellular effect is to induce self-renewal of committed T cells in the thymus, which persist long-term while acquiring additional mutations and eventually giving rise to leukemia. These precancerous stem cells (pre-CSC) are intrinsically resistant to radiotherapy, implying that they may be refractory to conventional cancer therapies. However, they depend on an aberrantly expressed stem cell-like self-renewal program for their maintenance, in addition to a specialized thymic microenvironmental niche. Here, we discuss potential approaches for targeting pre-CSCs in T-ALL by using therapies directed at oncogenic transcription factors themselves, downstream self-renewal pathways, and the supportive cell niche.|Adaptor Proteins, Signal Transducing[MESH]|Animals[MESH]|Cell Transformation, Neoplastic/genetics[MESH]|DNA-Binding Proteins/genetics/metabolism/*physiology[MESH]|Disease Models, Animal[MESH]|Humans[MESH]|LIM Domain Proteins[MESH]|Metalloproteins/genetics/metabolism/*physiology[MESH]|Mice[MESH]|Mice, Knockout[MESH]|Models, Biological[MESH]|Neoplastic Stem Cells/metabolism/pathology[MESH]|Precursor T-Cell Lymphoblastic Leukemia-Lymphoma/*genetics/metabolism/pathology[MESH]|Stem Cell Niche/metabolism/pathology[MESH] |
