ArticleCell death & disease2024
A novel function of STAT3β in suppressing interferon response improves outcome in acute myeloid leukemia.
Article in Cell death & disease, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
6 citing papers in PubMed.
- Uncompetitive Allosteric Inhibition of PTP1B by BP-1-102 Reveals a Potential Dual-Target Strategy toward the PTP1B-STAT3 Oncogenic Axis: Biochemical and Computational Evidence.ACS medicinal chemistry letters · 2026Article
- A STAT3 degrader demonstrates efficacy in venetoclax resistant acute myeloid leukemia.Leukemia · 2026Article
- Loss of STAT3 in acute myeloid leukemia favors tissue infiltration linked to CXCR4 signaling.Blood neoplasia · 2025Article
- RETRACTED: Duloxetine, an SNRI, Targets pSTAT3 Signaling:International journal of molecular sciences · 2025Article
- STAT3 Signaling Pathway in Health and Disease.MedComm · 2025Review
- DDR1 promotes metastasis of cervical cancer and downstream phosphorylation signal via binding GRB2.Cell death & disease · 2024Article
Corrections and comments
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Authors and funding
17 authors.
Funding
Abstract
Signal transducer and activator of transcription 3 (STAT3) is frequently overexpressed in patients with acute myeloid leukemia (AML). STAT3 exists in two distinct alternatively spliced isoforms, the full-length isoform STAT3α and the C-terminally truncated isoform STAT3β. While STAT3α is predominantly described as an oncogenic driver, STAT3β has been suggested to act as a tumor suppressor. To elucidate the role of STAT3β in AML, we established a mouse model of STAT3β-deficient, MLL-AF9-driven AML. STAT3β deficiency significantly shortened survival of leukemic mice confirming its role as a tumor suppressor. Furthermore, RNA sequencing revealed enhanced STAT1 expression and interferon (IFN) signaling upon loss of STAT3β. Accordingly, STAT3β-deficient leukemia cells displayed enhanced sensitivity to blockade of IFN signaling through both an IFNAR1 blocking antibody and the JAK1/2 inhibitor Ruxolitinib. Analysis of human AML patient samples confirmed that elevated expression of IFN-inducible genes correlated with poor overall survival and low STAT3β expression. Together, our data corroborate the tumor suppressive role of STAT3β in a mouse model in vivo. Moreover, they provide evidence that its tumor suppressive function is linked to repression of the STAT1-mediated IFN response. These findings suggest that the STAT3β/α mRNA ratio is a significant prognostic marker in AML and holds crucial information for targeted treatment approaches. Patients displaying a low STAT3β/α mRNA ratio and unfavorable prognosis could benefit from therapeutic interventions directed at STAT1/IFN signaling.
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Registered trials
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.