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Figure S1 from RNA Shielding of p65 Is Required to Potentiate Oncogenic Inflammation in TET2-Mutated Clonal Hematopoiesis

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posted on 2024-12-02, 08:41 authored by Nana 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 1 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

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ARTICLE ABSTRACT

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.