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Contrôle de l’Expression Génétique et Oncogenèse Virale

Our main research interest is to decipher the molecular mechanisms underlying oncogenesis, with a particular interest in the role of genetic instability in the process. Towards this goal we focused our attention on leukemogenesis driven by infection with the human T-cell lymphotropic virus type 1 (HTLV-1). This retrovirus is the causative agent of adult T cell leukemia/lymphoma (ATL) which is an aggressive and fatal form of leukemia characterized by the uncontrolled proliferation of activated mature CD4+ T cells. Two regulatory proteins expressed by the virus, Tax and HBZ (HTLV-1 bZIP), play key roles in the leukemogenic process by deregulating important cellular pathways. These two viral proteins therefore represent interesting tools to understand the normal and pathological functioning of specific cellular pathways. Following identification of INT6/EIF3E as a cellular target of Tax, we are also studying the function of this protein. INT6, through its involvement in many different cellular pathways (DNA damage response (DDR), nonsense-mediated mRNA decay (NMD), protein translation, regulation of protein degradation by the ubiquitin proteasome pathway, etc...),  also represents an interesting model to understand how alteration of its functions is able to generate oncogenic effects.

By developing different research axes (DNA repair / RNA stability / translation regulation) we hope to reach an integrated view of the various deregulated pathways at the origin of tumorigenesis. Our studies are carried out with various biochemichal, molecular and cellular approaches including highthroughput analyses and a model of humanized mice.