Faculty, Staff and Student Publications

Publication Date

12-2-2024

Journal

Cancer Discovery

DOI

10.1158/2159-8290.CD-24-0093

PMID

39189614

PMCID

PMC11611684

PubMedCentral® Posted Date

6-2-2025

PubMedCentral® Full Text Version

Author MSS

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.

Keywords

Dioxygenases, Proto-Oncogene Proteins, Humans, DNA-Binding Proteins, Inflammation, Clonal Hematopoiesis, Mice, Animals, Mutation, RNA, Long Noncoding, Transcription Factor RelA

Published Open-Access

yes

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