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nature portfolio crispr/cas9 genome editing privacy policy medical research council medical research advertising member institutions mntfl/fl myc10hom/rag1cre cohort kaplan–meier survival curves scientific purposes author information authors supplementary table s4 myc-driven t-cell proliferation supplementary table s3 social media mntfl/fl myc10hom/rag1cre mice premalignant mntfl/flmyc10hom/rag1cre mice nature supplementary table s5 mntfl/flmyc10hom/rag1cre mice presented reprints induces mycn expression pre-malignant myc-driven myc-driven pre-malignant myc-related transcriptional repressors γ-irradiation decimates leukocytes vavp-myc transgene-driven p53 wild-type lymphoma quantitative dose-response study mntfl/fl rag1cre mice international peripheral t-cell mntfl/flmyc10hom/rag1cre mice transcription factor c-myc c-myc oncogene driven bim+/−mntfl/fl rag1cre vavp-myc transgenic mice constitutive c-myc expression pre-malignant myc10hom mice anti-apoptotic bcl-2 synergises lmo2 t-cell oncogene high-resolution genomic profiling curb myc-induced apoptosis bind e-box motifs myc-driven lymphomas require control γ-irradiated mnt+/+ facilitating myc-driven oncogenesis rag1cre-mediated mnt deletion γ-irradiated c57bl/6 mice p53/p19arf pathway mutations mnt+/+myc10hom/rag1cre mice

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         description:The importance of c-MYC in regulating lymphopoiesis and promoting lymphomagenesis is well-established. Far less appreciated is the vital supporting role of MYC’s relative MNT. Using Rag1Cre-mediated Mnt deletion in lymphoid progenitor cells, we show here that, during normal T cell development, MNT loss enhances apoptosis, at least in part by elevating expression of the pro-apoptotic BH3-only protein BIM. Moreover, using T lymphoma-prone VavP-MYC transgenic mice, we show that Mnt deletion reduces the pool of pre-malignant MYC-driven T lymphoid cells and abrogates thymic T lymphomagenesis. In addition, we establish that Mnt deletion prevents T lymphoma development in γ-irradiated mice, most likely by enhancing apoptosis of T lymphoid cells repopulating the depleted thymus. Taken together with our recent demonstration that MNT is vital for the survival of MYC-driven pre-malignant and malignant B lymphoid cells, these results suggest that MNT represents an important new drug target for both T and B lymphoid malignancies.
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      headline:MNT suppresses T cell apoptosis via BIM and is critical for T lymphomagenesis
      description:The importance of c-MYC in regulating lymphopoiesis and promoting lymphomagenesis is well-established. Far less appreciated is the vital supporting role of MYC’s relative MNT. Using Rag1Cre-mediated Mnt deletion in lymphoid progenitor cells, we show here that, during normal T cell development, MNT loss enhances apoptosis, at least in part by elevating expression of the pro-apoptotic BH3-only protein BIM. Moreover, using T lymphoma-prone VavP-MYC transgenic mice, we show that Mnt deletion reduces the pool of pre-malignant MYC-driven T lymphoid cells and abrogates thymic T lymphomagenesis. In addition, we establish that Mnt deletion prevents T lymphoma development in γ-irradiated mice, most likely by enhancing apoptosis of T lymphoid cells repopulating the depleted thymus. Taken together with our recent demonstration that MNT is vital for the survival of MYC-driven pre-malignant and malignant B lymphoid cells, these results suggest that MNT represents an important new drug target for both T and B lymphoid malignancies.
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