Mutant IDH1 inhibition induces dsDNA sensing to activate tumor immunity.

doi:10.1126/science.adl6173

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

Mutant IDH1 inhibition induces dsDNA sensing to activate tumor immunity.

Science (New York, N.Y.) - 12 Jul 2024

Wu Meng-Ju, Kondo Hiroshi, Kammula Ashwin V, Shi Lei, Xiao Yi, Dhiab Sofiene, Xu Qin, Slater Chloe J, Avila Omar I, Merritt Joshua, Kato Hiroyuki, Kattel Prabhat, Sussman Jonathan, Gritti Ilaria, Eccleston Jason, Sun Yi, Cho Hyo Min, Olander Kira, Katsuda Takeshi, Shi Diana D, Savani Milan R, Smith Bailey C, Cleary James M, Mostoslavsky Raul, Vijay Vindhya, Kitagawa Yosuke, Wakimoto Hiroaki, Jenkins Russell W, Yates Kathleen B, Paik Jihye, Tassinari Ania, Saatcioglu Duygu Hatice, Tron Adriana E, Haas Wilhelm, Cahill Daniel, McBrayer Samuel K, Manguso Robert T, Bardeesy Nabeel

Abstract excerpt

Isocitrate dehydrogenase 1 (IDH1) is the most commonly mutated metabolic gene across human cancers. Mutant IDH1 (mIDH1) generates the oncometabolite (R)-2-hydroxyglutarate, disrupting enzymes involved in epigenetics and other processes. A hallmark of IDH1-mutant solid tumors is T cell exclusion, whereas mIDH1 inhibition in preclinical models restores antitumor immunity. Here, we define a cell-autonomous mechanism...

Read the complete abstract on PubMed

Topics

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

Share to Immune Evasion

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to DNA Transposable Elements

Share to Epigenesis, Genetic

Share to Glutarates

Share to Immunity, Innate

Share to Isocitrate Dehydrogenase

Share to Nucleotidyltransferases

Share to Tumor Escape

Source

Open in PubMed Open full text

Identifiers

PMID: 38991060
DOI: 10.1126/science.adl6173
PMCID: PMC11602233

Genes

IDH1
CGAS

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Mutant IDH1 inhibition induces dsDNA sensing to activate tumor immunity.PMID 38991060Read ↗

Clinical and translational study of ivosidenib plus nivolumab in advanced solid tumors harboring IDH1 mutations.Semantic proximity Read ↗

Clinical and translational study of ivosidenib plus nivolumab in advanced solid tumors harboring IDH1 mutationsSemantic proximity Read ↗

Mutant IDH: a targetable driver of leukemic phenotypes linking metabolism, epigenetics and transcriptional regulation.Semantic proximity Read ↗

The IDH1 Mutation-Induced Oncometabolite, 2-Hydroxyglutarate, May Affect DNA Methylation and Expression of PD-L1 in GliomasSemantic proximity Read ↗

Inhibition of 2-hydroxyglutarate elicits metabolic reprogramming and mutant IDH1 glioma immunity in miceSemantic proximity Read ↗

Illuminating the cross-talk between tumor metabolism and immunity in IDH-mutated cancers.Semantic proximity Read ↗

IDH2 mutation-induced histone and DNA hypermethylation is progressively reversed by small-molecule inhibition.Semantic proximity Read ↗

Biology of IDH mutant cholangiocarcinoma.Semantic proximity Read ↗

Mutant IDH Inhibits IFNγ-TET2 Signaling to Promote Immunoevasion and Tumor Maintenance in Cholangiocarcinoma.Semantic proximity Read ↗

De Novo Pyrimidine Synthesis is a Targetable Vulnerability in IDH Mutant GliomaSemantic proximity Read ↗

The implications of IDH mutations for cancer development and therapy.Semantic proximity Read ↗

IDH mutations in cancer and progress toward development of targeted therapeutics.Semantic proximity Read ↗

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