Stephen Arnovitz

TL;DR: It is shown that FTO, as an m6A demethylase, plays a critical oncogenic role in acute myeloid leukemia (AML) and provides profound insights into leukemogenesis and drug response.

TL;DR: In contrast to the frequent down-regulation (or loss-of-function mutations) and critical tumor-suppressor roles of the three TET genes observed in various types of cancers, here it is shown that TET1 is a direct target of MLL-fusion proteins and is significantly up-regulated in M LL-rearranged leukemia, leading to a global increase of 5-hydroxymethylcytosine level.

TL;DR: It is shown that MLL fusion proteins negatively regulate production of miR-150, an miRNA widely repressed in acute leukemia, by blocking mi R-150 precursors from being processed to mature miRNAs through MYC/LIN28 functional axis.

TL;DR: In vitro and in vivo studies indicated that ectopic expression of miR-181b significantly promoted apoptosis and inhibited viability/proliferation of leukemic cells and delayed leukemogenesis; such effects could be reversed by forced expression of PBX3.

TL;DR: The results uncover a previously unappreciated miRNA-regulation mechanism by which a single miRNA may target both oncogenes and tumour suppressors, simultaneously, or, sequentially, in tumourigenesis and normal development per cell differentiation, indicating that miRNA regulation is much more complex than previously thought.