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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 
 
 
 
 

Myeloid leukemia with promyelocytic features in transgenic mice expressing hCG-NuMA-RARalpha.

Acute promyelocytic leukemia (APL) is characterized by the accumulation of abnormal promyelocytes in the bone marrow (BM), and by the presence of a reciprocal chromosomal translocation involving retinoic acid receptor alpha (RARalpha). To date, five RARalpha partner genes have been identified in APL. NuMA-RARalpha was identified in a pediatric case of APL carrying a translocation t(11;17)(q13;q21). Using a construct containing the NuMA-RARalpha fusion gene driven by the human cathepsin G promoter (hCG-NuMA-RARalpha), two transgenic mouse lines were generated. Transgenic mice were observed to have a genetic myeloproliferation (increased granulopoiesis in BM) at an early age, and rapidly developed a myeloproliferative disease-like myeloid leukemia. This leukemia was morphologically and immunophenotypically indistinguishable from human APL, with a penetrance of 100%. The phenotype of transgenic mice was consistent with a blockade of neutrophil differentiation. NuMA-RARalpha is therefore sufficient for disease development in this APL model.[1]

References

  1. Myeloid leukemia with promyelocytic features in transgenic mice expressing hCG-NuMA-RARalpha. Sukhai, M.A., Wu, X., Xuan, Y., Zhang, T., Reis, P.P., Dubé, K., Rego, E.M., Bhaumik, M., Bailey, D.J., Wells, R.A., Kamel-Reid, S., Pandolfi, P.P. Oncogene (2004) [Pubmed]
 
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