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

doi:10.1158/2159-8290.CD-24-0093

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Community

Back to search

Article

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

Cancer discovery - 2 Dec 2024

Ben-Crentsil Nana Adjoa, Mohammed Ismail Wazim, Balasis Maria E, Newman Hannah, Quintana Ariel, Binder Moritz, Kruer Traci, Neupane Surendra, Ferrall-Fairbanks Meghan C, Fernandez Jenna, Lasho Terra L, Finke Christy M, Ibrahim Mohammed L, McGraw Kathy L, Wysota Michael, Aldrich Amy L, Ryder Christopher B, Letson Christopher T, Traina Joshua, McLemore Amy F, Droin Nathalie, Shastri Aditi, Yun Seongseok, Solary Eric, Sallman David A, Beg Amer A, Ma Li, Gaspar-Maia Alexandre, Patnaik Mrinal M, Padron Eric

Abstract excerpt

SIGNIFICANCE: 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.

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Clonal Hematopoiesis

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Dioxygenases

Share to DNA-Binding Proteins

Share to Inflammation

Share to Mice

Share to Proto-Oncogene Proteins

Share to RNA, Long Noncoding

Share to Transcription Factor RelA

Source

Open in PubMed Open full text

Identifiers

PMID: 39189614
DOI: 10.1158/2159-8290.CD-24-0093
PMCID: PMC11611684

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 6 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

RNA Shielding of p65 Is Required to Potentiate Oncogenic Inflammation in TET2-Mutated Clonal Hematopoiesis.PMID 39189614Read ↗

TET2 and TP53 Mutations Cooperatively Modulate the Response to Inflammation to Promote Leukemic TransformationSemantic proximity Read ↗

Human TET2-Mutant Clonal Hematopoiesis Expansion Is Driven by Distinct Inflammatory Signaling Responses in Stem Cells Versus Myeloid Progeny.Semantic proximity Read ↗

Stromal Gasdermin D-mediated Pyroptosis Drives Maladaptive CD4⁺ T-cell Remodeling in Tet2-Deficient HematopoiesisSemantic proximity Read ↗

TP53 mutations and TET2 deficiency cooperate to drive leukemogenesis and establish an immunosuppressive environment.Semantic proximity Read ↗

Targeting Piezo1 unleashes innate immunity against cancer and infectious diseaseSemantic proximity Read ↗

TET2 Clonal Hematopoiesis Is Associated With Anthracycline-Induced Cardiotoxicity in Patients With LymphomaSemantic proximity Read ↗

The transcriptional and epigenetic reprogramming associated with chronic IL1β-mediated expansion and myeloid priming in TET2 deficient stem and progenitor cellsSemantic proximity Read ↗

The Impact of Inflammation-Induced Tumor Plasticity during Myeloid Transformation.Semantic proximity Read ↗

Metabolic control of innate immune activation in TET2-mutant clonal hematopoiesis.Semantic proximity Read ↗

Multitargeted Reduction of Inflammation and Atherosclerosis in Tet2 -deficient CHIP via XPO1 Inhibition and Atf3 restorationSemantic proximity Read ↗

Impact of Clonal Hematopoiesis on the Carcinogenic Process of Multiple MyelomaSemantic proximity Read ↗

Down-regulation ofMALAT1is a hallmark of tissue and peripheral proliferative T cells in COVID-19Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.