Discover Community Create You

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

Article

IDH2/R140Q mutation confers cytokine-independent proliferation of TF-1 cells by activating constitutive STAT3/5 phosphorylation.

Cell communication and signaling : CCS - 12 Feb 2024

Yang Jie, Chen Jiao, Chang Jingjie, Sun Xiaoyan, Wei Qingyun, Cai Xueting, Cao Peng

Abstract excerpt

BACKGROUND: R140Q mutation in isocitrate dehydrogenase 2 (IDH2) promotes leukemogenesis. Targeting IDH2/R140Q yields encouraging therapeutic effects in the clinical setting. However, therapeutic resistance occurs in 12% of IDH2/R140Q inhibitor treated patients. The IDH2/R140Q mutant converted TF-1 cells to proliferate in a cytokine-independent manner. This study investigated the signaling pathways involved in...

Read the complete abstract on PubMed

Topics

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

Share to Cell Proliferation
Share to Granulocyte-Macrophage Colony-Stimulating Factor

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Leukemia, Myeloid, Acute

Share to Mutation

Share to Phosphorylation

Share to STAT3 Transcription Factor

Share to STAT5 Transcription Factor

Source

Open in PubMed Open full text

Identifiers

PMID: 38347540
DOI: 10.1186/s12964-023-01367-y
PMCID: PMC10863291

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

IDH2/R140Q mutation confers cytokine-independent proliferation of TF-1 cells by activating constitutive STAT3/5 phosphorylation.PMID 38347540Read ↗

Isocitrate dehydrogenase mutations are associated with altered IL-1β responses in acute myeloid leukemia.Semantic proximity Read ↗

Regulation of cell cycle by the novel GATA1/TAL1/Sphingomyelin Synthase 1 ( <i>SGMS1</i> ) transcriptional axis. Implications for anti-leukemic strategiesSemantic proximity Read ↗

JAK/STAT blockade reverses the malignant phenotype of Hodgkin and Reed-Sternberg cells.Semantic proximity Read ↗

Ceramide-induced integrated stress response overcomes Bcl-2 inhibitor resistance in acute myeloid leukemiaSemantic proximity Read ↗

DNA-Binding domain mutations confer severe outcome at an early age among STAT1 gain-of-function patients.Semantic proximity Read ↗

Targeting Integrated Stress Response by ISRIB combined with imatinib attenuates STAT5 signaling and eradicates therapy-resistant Chronic Myeloid Leukemia cellsSemantic proximity Read ↗

Direct STAT3 and STAT5 Inhibition Overcomes Treatment Resistance in a Murine-Derived in vitro Model of Acute Lymphoblastic Leukaemia Driven by <italic>ETV6::JAK2</italic>.Semantic proximity Read ↗

[leukocyte-associated immunoglobulin-like receptor 1 (LAIR-1) inhibits proliferation and promotes apoptosis of human HEL cells with JAK2 V617F mutation by blocking the JAK/STAT and PI3K/AKT signaling pathways].Semantic proximity Read ↗

Proliferation and survival signaling from both Jak2-V617F and Lyn involving GSK3 and mTOR/p70S6K/4EBP1 in PVTL-1 cell line newly established from acute myeloid leukemia transformed from polycythemia vera.Semantic proximity Read ↗

GIFT4 fusokine converts leukemic B cells into immune helper cells.Semantic proximity Read ↗

SOCS1 cooperates with FLT3-ITD in the development of myeloproliferative disease by promoting the escape from external cytokine controlSemantic proximity Read ↗

Phospholipid metabolic adaptation promotes survival of IDH2 mutant acute myeloid leukemia cells.Semantic proximity Read ↗

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