ReviewOncology letters2025
Advances of signal transducer and activator of transcription 3 inhibitors in acute myeloid leukemia (Review).
Review in Oncology letters, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
3 citing papers in PubMed.
- Dihydrotanshinone I as a novel signal transducer and activator of transcription 3 inhibitor for glioblastoma treatment.Journal of translational medicine · 2026Article
- Preliminary Effects of Benralizumab in an AML Cell Model with Promyelocytic Features Expressing IL-5R: An Exploratory Proof-of-Concept Study.Biomedicines · 2026Article
- Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Signal transducer and activator of transcription 3 (STAT3), a crucial transcription factor, exerts a notable influence by hyperactivating or acquiring functional mutations in the occurrence and progression of cancers. Hyperactive STAT3 is also implicated in a range of hematopoietic malignancies, especially acute myeloid leukemia (AML). The function of STAT3 is associated with the phosphorylated parallel dimer structure, enabling them to stimulate the transcription of specific genes. AML is a highly heterogeneous hematological malignancy, which is challenging in terms of therapy. The current efficacy of chemotherapy and targeted therapy remains suboptimal. Targeted inhibition of STAT3 has the potential to enhance the efficacy of AML treatment, thereby possibly improving the prognosis of individuals suffering from AML. The present review summarizes the development of inhibitors against STAT3 and discusses their applicability as AML therapeutics, which could inspire new possibilities for enhancing AML treatment strategies.
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What OpenQuestion holds
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.