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The  LMO2  oncogene is deregulated in the majority of human T-cell leukemia cases and in most gene therapy-induced T-cell leukemias. We made transgenic mice with enforced expression of  Lmo2  in T-cells by the  CD2  promoter/enhancer. These transgenic mice developed highly penetrant T-ALL by two distinct patterns of gene expression: one in which there was concordant activation of  Lyl1 ,  Hhex , and  Mycn  or alternatively, with  Notch1  target gene activation. Most strikingly, this gene expression clustering was conserved in human Early T-cell Precursor ALL (ETP-ALL), where  LMO2 ,  HHEX ,  LYL1 , and  MYCN  were most highly expressed. We discovered that  HHEX  is a direct transcriptional target of  LMO2  consistent with its concordant gene expression. Furthermore, conditional inactivation of  Hhex  in  CD2-Lmo2  transgenic mice markedly attenuated T-ALL development, demonstrating that  Hhex  is a crucial mediator of  Lmo2 's oncogenic function. The  CD2-Lmo2  transgenic mice offer mechanistic insight into concordant oncogene expression and provide a model for the highly treatment-resistant ETP-ALL subtype.

LIM Domain Only-2 (LMO2) Induces T-Cell Leukemia by Two Distinct Pathways