Acute myeloid leukemia

Insertional mutagenesis identifies cooperation between Setbp1 and Mllt3 in inducing myeloid leukemia development

Article metrics

Access optionsAccess options

Rent or Buy article

Get time limited or full article access on ReadCube.

from$8.99

All prices are NET prices.

Fig. 1
Fig. 2

References

  1. 1.

    Oakley K, Han Y, Vishwakarma BA, Chu S, Bhatia R, Gudmundsson KO, et al. Setbp1 promotes the self-renewal of murine myeloid progenitors via activation of Hoxa9 and Hoxa10. Blood. 2012;119:6099–108.

  2. 2.

    Piazza R, Magistroni V, Redaelli S, Mauri M, Massimino L, Sessa A, et al. SETBP1 induces transcription of a network of development genes by acting as an epigenetic hub. Nat Commun. 2018;9:2192.

  3. 3.

    Cristobal I, Blanco FJ, Garcia-Orti L, Marcotegui N, Vicente C, Rifon J, et al. SETBP1 overexpression is a novel leukemogenic mechanism that predicts adverse outcome in elderly patients with acute myeloid leukemia. Blood. 2010;115:615–25.

  4. 4.

    Lucas CM, Scott LJ, Carmell N, Holcroft AK, Hills RK, Burnett AK, et al. CIP2A- and SETBP1-mediated PP2A inhibition reveals AKT S473 phosphorylation to be a new biomarker in AML. Blood Adv. 2018;2:964–8.

  5. 5.

    Vishwakarma BA, Nguyen N, Makishima H, Hosono N, Gudmundsson KO, Negi V, et al. Runx1 repression by histone deacetylation is critical for Setbp1-induced mouse myeloid leukemia development. Leukemia. 2016;30:200–8.

  6. 6.

    Gentles AJ, Plevritis SK, Majeti R, Alizadeh AA. Association of a leukemic stem cell gene expression signature with clinical outcomes in acute myeloid leukemia. J Am Med Assoc. 2010;304:2706–15.

  7. 7.

    Du Y, Spence SE, Jenkins NA, Copeland NG. Cooperating cancer-gene identification through oncogenic-retrovirus-induced insertional mutagenesis. Blood. 2005;106:2498–505.

  8. 8.

    Jin G, Yamazaki Y, Takuwa M, Takahara T, Kaneko K, Kuwata T, et al. Trib1 and Evi1 cooperate with Hoxa and Meis1 in myeloid leukemogenesis. Blood. 2007;109:3998–4005.

  9. 9.

    Valk PJ, Verhaak RG, Beijen MA, Erpelinck CA, Barjesteh van Waalwijk van Doorn-Khosrovani S, Boer JM, et al. Prognostically useful gene-expression profiles in acute myeloid leukemia. New Engl J Med. 2004;350:1617–28.

  10. 10.

    Nakamura T, Alder H, Gu Y, Prasad R, Canaani O, Kamada N, et al. Genes on chromosomes 4, 9, and 19 involved in 11q23 abnormalities in acute leukemia share sequence homology and/or common motifs. Proc Natl Acad Sci USA. 1993;90:4631–5.

  11. 11.

    Collins EC, Appert A, Ariza-McNaughton L, Pannell R, Yamada Y, Rabbitts TH. Mouse Af9 is a controller of embryo patterning, like Mll, whose human homologue fuses with Af9 after chromosomal translocation in leukemia. Mol Cell Biol. 2002;22:7313–24.

  12. 12.

    Lin C, Smith ER, Takahashi H, Lai KC, Martin-Brown S, Florens L, et al. AFF4, a component of the ELL/P-TEFb elongation complex and a shared subunit of MLL chimeras, can link transcription elongation to leukemia. Mol Cell. 2010;37:429–37.

  13. 13.

    Li Y, Wen H, Xi Y, Tanaka K, Wang H, Peng D, et al. AF9 YEATS domain links histone acetylation to DOT1L-mediated H3K79 methylation. Cell. 2014;159:558–71.

  14. 14.

    Thorsteinsdottir U, Kroon E, Jerome L, Blasi F, Sauvageau G. Defining roles for HOX and MEIS1 genes in induction of acute myeloid leukemia. Mol Cell Biol. 2001;21:224–34.

  15. 15.

    Nguyen N, Vishwakarma BA, Oakley K, Han Y, Przychodzen B, Maciejewski JP, et al. Myb expression is critical for myeloid leukemia development induced by Setbp1 activation. Oncotarget. 2016;7:86300–12.

Download references

Acknowledgements

This work was supported by National Institutes of Health (NIH) grant RO1CA143193 (Y.D.) and USUHS Pediatrics Grant QP86GI (Y.D.). The views presented in this paper are those of the authors; no endorsement by the Uniformed Services University of the Health Sciences or the Department of Defense has been given or should be inferred.

Author information

Correspondence to Yang Du.

Ethics declarations

Conflict of interest

The authors declare that they have no conflict of interest.

Additional information

Publisher’s note: Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.

Supplementary information

Rights and permissions

Reprints and Permissions

About this article

Verify currency and authenticity via CrossMark