Research ArticleLEUKEMIA

MAFB enhances oncogenic Notch signaling in T cell acute lymphoblastic leukemia

See allHide authors and affiliations

Sci. Signal.  14 Nov 2017:
Vol. 10, Issue 505, eaam6846
DOI: 10.1126/scisignal.aam6846

You are currently viewing the editor's summary.

View Full Text

Log in to view the full text

Log in through your institution

Log in through your institution

New targets, better mouse model for leukemia

T cell acute lymphoblastic leukemias (T-ALLs) are often caused by mutations in the gene encoding Notch1, which mediates cell-cell contact signaling in embryonic development and adult tissue maintenance. However, mice expressing these mutants frequently fail to develop T-ALL. Pajcini et al. found that the transcription factors MAFB and ETS2 increased the expression of Notch1 target genes in mouse and human T-ALL cells by recruiting histone acetyltransferases. Expressing MAFB enhanced the development of Notch1-mutant T-ALL in mice. Because Notch1 is critical for the maintenance of various healthy adult tissues, developing a way to inhibit MAFB or its interacting partners may be a more targeted therapy for leukemia patients.