Journal article
Cancer Cell, 2017
APA
Click to copy
Chen, Y., Chen, Y., Anastassiadis, K., Kranz, A., Stewart, A. F., Arndt, K., … Ernst, P. (2017). MLL2, not MLL1, Plays a Major Role in Sustaining MLL-rearranged Acute Myeloid Leukemia. Cancer Cell.
Chicago/Turabian
Click to copy
Chen, Yufei, Yufei Chen, K. Anastassiadis, A. Kranz, A. F. Stewart, Kathrin Arndt, Claudia Waskow, et al. “MLL2, Not MLL1, Plays a Major Role in Sustaining MLL-Rearranged Acute Myeloid Leukemia.” Cancer Cell (2017).
MLA
Click to copy
Chen, Yufei, et al. “MLL2, Not MLL1, Plays a Major Role in Sustaining MLL-Rearranged Acute Myeloid Leukemia.” Cancer Cell, 2017.
BibTeX Click to copy
@article{yufei2017a,
title = {MLL2, not MLL1, Plays a Major Role in Sustaining MLL-rearranged Acute Myeloid Leukemia},
year = {2017},
journal = {Cancer Cell},
author = {Chen, Yufei and Chen, Yufei and Anastassiadis, K. and Kranz, A. and Stewart, A. F. and Arndt, Kathrin and Waskow, Claudia and Yokoyama, A. and Jones, Kenneth L. and Neff, T. and Lee, Yoora and Ernst, P.}
}
Summary The MLL1 histone methyltransferase gene undergoes many distinct chromosomal rearrangements to yield poor-prognosis leukemia. The remaining wild-type allele is most commonly, but not always, retained. To what extent the wild-type allele contributes to leukemogenesis is unclear. Here we show using rigorous, independent animal models that endogenous MLL1 is dispensable for MLL-rearranged leukemia. Potential redundancy was addressed by co-deleting the closest paralog, Mll2. Surprisingly, Mll2 deletion alone had a significant impact on survival of MLL-AF9-transformed cells and additional Mll1 loss further reduced viability and proliferation. We show that MLL1/MLL2 collaboration is not through redundancy but regulation of distinct pathways. These findings highlight the relevance of MLL2 as a drug target in MLL-rearranged leukemia and suggest its broader significance in AML.