The protooncogene Vav1 regulates murine leukemia virus-induced T-cell leukemogenesis.

Abstract : Vav1 is expressed exclusively in hematopoietic cells and is required for T cell development and activation. Vav1-deficient mice show thymic hypocellularity due to a partial block during thymocyte development at the DN3 stage and between the double positive (DP) and single positive (SP) transition. Vav1 has been shown to play a significant role in several non-hematopoietic tumors but its role in leukemogenesis is unknown. To address this question, we investigated the role of Vav1 in retrovirus-induced T cell leukemogenesis. Infection of Vav1-deficient mice with the Moloney strain of murine leukemia virus (M-MuLV) significantly affected tumor phenotype without modulating tumor incidence or latency. M-MuLV-infected Vav1-deficient mice showed reduced splenomegaly, higher hematocrit levels and hypertrophic thymi. Notably, Vav1-deficient mice with M-MuLV leukemias presented with markedly lower TCRβ/CD3 levels, indicating that transformation occurred at an earlier stage of T cell development than in WT mice. Thus, impaired T cell development modulates the outcome of retrovirus-induced T cell leukemias, demonstrating a link between T cell development and T cell leukemogenesis.
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OncoImmunology, Taylor & Francis, 2012, 1 (5), pp.600-608. 〈10.4161/onci.20225〉
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Sandra Kaminski, Oumeya Adjali, Chantal Jacquet, Johan Garaude, Anne Keriel, et al.. The protooncogene Vav1 regulates murine leukemia virus-induced T-cell leukemogenesis.. OncoImmunology, Taylor & Francis, 2012, 1 (5), pp.600-608. 〈10.4161/onci.20225〉. 〈inserm-00726759〉

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