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The etiology of human tumors often involves chromosomal translocations. Models that emulate translocations are essential to understanding the determinants of frank malignancy, those dictating the restriction of translocations to specific lineages, and as a basis for development of rational therapeutic methods. We demonstrate that developmentally regulated Cre-loxP-mediated interchromosomal recombination between the Mll gene, whose human counterpart is involved in a spectrum of leukemias, and the Enl gene creates reciprocal chromosomal translocations that cause myeloid tumors. There is a rapid onset and high penetrance of leukemogenesis in these translocator mice, and high proportions of cells carrying chromosomal translocations can be found in bone marrow as early as 12 days after birth. This de novo strategy is a direct recapitulation of naturally occurring human cancer-associated translocations.

Original publication




Journal article


Cancer Cell

Publication Date





449 - 458


Alleles, Amino Acid Sequence, Animals, Base Sequence, Chromosomes, DNA-Binding Proteins, Disease Models, Animal, Flow Cytometry, Genetic Techniques, Genotype, Histone-Lysine N-Methyltransferase, Humans, In Situ Hybridization, Fluorescence, Leukocytes, Mice, Models, Genetic, Molecular Sequence Data, Myeloid-Lymphoid Leukemia Protein, Neoplasms, Oncogene Proteins, Fusion, Phenotype, Proto-Oncogenes, Recombination, Genetic, Time Factors, Transcription Factors, Translocation, Genetic