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The LMO2 and TAL1 genes were first identified via chromosomal translocations and later found to encode proteins that interact during normal erythroid development. Some T cell leukaemia patients have chromosomal abnormalities involving both genes, implying that LMO2 and TAL1 act synergistically to promote tumorigenesis after their inappropriate co-expression. To test this hypothesis, transgenic mice were made which co-express Lmo2 and Tal1 genes in T cells. Dimers of Lmo2 and Tal1 proteins were formed in thymocytes of double but not single transgenic mice. Furthermore, thymuses of double transgenic mice were almost completely populated by immature T cells from birth, and these mice develop T cell tumours approximately 3 months earlier than those with only the Lmo2 transgene. Thus interaction between these two proteins can alter T cell development and potentiate tumorigenesis. The data also provide formal proof that TAL1 is an oncogene, apparently acting as a tumour promoter in this system.


Journal article



Publication Date





1021 - 1027


Adaptor Proteins, Signal Transducing, Animals, Basic Helix-Loop-Helix Transcription Factors, Cell Differentiation, DNA-Binding Proteins, Disease Models, Animal, Humans, LIM Domain Proteins, Leukemia-Lymphoma, Adult T-Cell, Metalloproteins, Mice, Mice, Transgenic, Oncogenes, Phenotype, Protein Conformation, Proto-Oncogene Proteins, Recombinant Fusion Proteins, T-Cell Acute Lymphocytic Leukemia Protein 1, T-Lymphocyte Subsets, Thymus Gland, Transcription Factors, Translocation, Genetic