posted on 2024-12-02, 08:41authored byNana Adjoa Ben-Crentsil, Wazim Mohammed Ismail, Maria E. Balasis, Hannah Newman, Ariel Quintana, Moritz Binder, Traci Kruer, Surendra Neupane, Meghan C. Ferrall-Fairbanks, Jenna Fernandez, Terra L. Lasho, Christy M. Finke, Mohammed L. Ibrahim, Kathy L. McGraw, Michael Wysota, Amy L. Aldrich, Christopher B. Ryder, Christopher T. Letson, Joshua Traina, Amy F. McLemore, Nathalie Droin, Aditi Shastri, Seongseok Yun, Eric Solary, David A. Sallman, Amer A. Beg, Li Ma, Alexandre Gaspar-Maia, Mrinal M. Patnaik, Eric Padron
Contains data related to Figure 2 but which were not included in the main figure
Funding
Moffitt Cancer Center (MCC)
National Cancer Institute (NCI)
United States Department of Health and Human Services
This work identifies MALAT1 as a requisite downstream effector of oncogenic feedforward inflammatory circuits necessary for the development of TET2-mutated CH and fulminant myeloid malignancy. We elucidate a novel mechanism by which MALAT1 “shields” p65 from dephosphorylation to potentiate this circuit and nominate MALAT1 inhibition as a future therapeutic strategy.