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      The translation factor eIF-4E promotes tumor formation and cooperates with c-Myc in lymphomagenesis.

      Nature medicine
      Animals, Apoptosis, Cocarcinogenesis, Eukaryotic Initiation Factor-4E, genetics, physiology, Gene Expression, Genes, myc, Lymphoma, B-Cell, etiology, pathology, Mice, Mice, Transgenic, Protein Kinases, TOR Serine-Threonine Kinases

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          Abstract

          The mammalian target of rapamycin, mTOR, regulates cell growth and proliferation. Here we show that the initiation factor of translation (eIF-4E), a downstream effector of mTOR, has oncogenic effects in vivo and cooperates with c-Myc in B-cell lymphomagenesis. We found that c-Myc overrides eIF-4E-induced cellular senescence, whereas eIF-4E antagonizes c-Myc-dependent apoptosis in vivo. Our results implicate activation of eIF-4E as a key event in oncogenic transformation by phosphoinositide-3 kinase and Akt.

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