ArticleLeukemia2023
STING activation in TET2-mutated hematopoietic stem/progenitor cells contributes to the increased self-renewal and neoplastic transformation.
Article in Leukemia, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 27 citations in OpenAlex.
- Clonal hematopoiesis of indeterminate potential (CHIP)-a pivotal contributor of aging and related disorders.Annals of translational medicine · 2026Review
- Clonal Hematopoiesis and Gut Microbiota-Derived TMAO as Candidate Amplifiers of Cardiovascular Inflammation: The CHIDT Hypothesis.Antioxidants (Basel, Switzerland) · 2026Review
- Cell autonomous inflammation in VEXAS is mediated by cGAS-STING.bioRxiv : the preprint server for biology · 2026Article
- Clinical decisions in clonal hematopoiesis: a contemporary review for clinicians.Haematologica · 2026Review
- Inflammageing and clonal haematopoiesis interplay and their impact on human disease.Nature reviews. Molecular cell biology · 2026Review
- Tet2 deficiency orchestrates Alzheimer's pathogenesis through oxidative mtDNA-driven cGAS-STING activation.Journal of neuroinflammation · 2026Article
- Clonal Hematopoiesis (CHIP) in Pulmonary Embolism and CTEPH: Evidence, Mechanisms, and Risk Stratification.International journal of molecular sciences · 2026Review
- TET2 in epigenetic control of immune cells: Implications for inflammatory responses and age-related pathologies.The Journal of biological chemistry · 2026Review
- Vulnerability of SRSF2-mutated chronic myelomonocytic leukemia to perturbation of the cGAS-STING pathway.Blood advances · 2026Article
- TET2: a critical regulatory hub with broad therapeutic implications across human diseases.Frontiers in immunology · 2026Review
- cGAS-STING signaling pathway as a therapeutic target in human diseases.Chinese medical journal · 2025Review
- Leukemic Transdifferentiation: From Pathological Plasticity to Dendritic Cell-Based Immunotherapy.Biomedicines · 2025Review
- Setd2 ensures the establishment of a precise basal inflammatory state within murine hematopoietic stem/progenitor cells.Cell death & disease · 2025Article
- Review
- Ten-Eleven Translocation Family Proteins: Structure, Biological Functions, Diseases, and Targeted Therapy.MedComm · 2025Review
- STING mediates increased self-renewal and lineage skewing in DNMT3A-mutated hematopoietic stem/progenitor cells.Leukemia · 2025Article
- TET2 deficiency increases the competitive advantage of hematopoietic stem and progenitor cells through upregulation of thrombopoietin receptor signaling.Nature communications · 2025Article
- The rewired immune microenvironment in leukemia.Nature immunology · 2025Review
- Exploring a new direction in targeted cancer therapy through hyperbaric oxygen therapy combined with biomedical engineering techniques.Frontiers in oncology · 2025Review
- TET2 mutation in acute myeloid leukemia: biology, clinical significance, and therapeutic insights.Clinical epigenetics · 2024Review
Corrections and comments
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Authors and funding
22 authors at 7 institutions in 5 countries.
Funding
Abstract
Somatic loss-of-function mutations of the dioxygenase Ten-eleven translocation-2 (TET2) occur frequently in individuals with clonal hematopoiesis (CH) and acute myeloid leukemia (AML). These common hematopoietic disorders can be recapitulated in mouse models. However, the underlying mechanisms by which the deficiency in TET2 promotes these disorders remain unclear. Here we show that the cyclic guanosine monophosphate-adenosine monophosphate synthase (cGAS)-stimulator of interferon genes (STING) pathway is activated to mediate the effect of TET2 deficiency in dysregulated hematopoiesis in mouse models. DNA damage arising in Tet2-deficient hematopoietic stem/progenitor cells (HSPCs) leads to activation of the cGAS-STING pathway which in turn promotes the enhanced self-renewal and development of CH. Notably, both pharmacological inhibition and genetic deletion of STING suppresses Tet2 mutation-induced aberrant hematopoiesis. In patient-derived xenograft (PDX) models, STING inhibition specifically attenuates the proliferation of leukemia cells from TET2-mutated individuals. These observations suggest that the development of CH associated with TET2 mutations is powered through chronic inflammation dependent on the activated cGAS-STING pathway and that STING may represent a potential target for intervention of relevant hematopoietic diseases.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.