ReviewJAK-STAT2012
STAT signaling in the pathogenesis and treatment of myeloid malignancies.
Review in JAK-STAT, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 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
43 citing papers in PubMed, 82 citations in OpenAlex.
- Review
- Advances of signal transducer and activator of transcription 3 inhibitors in acute myeloid leukemia (Review).Oncology letters · 2025Review
- Expression of interleukin-17 in oral tongue squamous cell carcinoma and its effect on biological behavior.Scientific reports · 2025Article
- Bi-functional CpG-STAT3 decoy oligonucleotide triggers multilineage differentiation of acute myeloid leukemia in mice.Molecular therapy. Nucleic acids · 2024Article
- Therapeutic advances of targeting receptor tyrosine kinases in cancer.Signal transduction and targeted therapy · 2024Review
- Ashwagandha-Induced Programmed Cell Death in the Treatment of Breast Cancer.Current issues in molecular biology · 2024Review
- Susceptibility of pediatric acute lymphoblastic leukemia to STAT3 inhibition depends on p53 induction.Haematologica · 2024Article
- Oncogenic STAT Transcription Factors as Targets for Cancer Therapy: Innovative Strategies and Clinical Translation.Cancers · 2024Review
- STAT3 drives the malignant progression of low-grade gliomas through modulating the expression of STAT1, FOXO1, and MYC.Frontiers in molecular biosciences · 2024Article
- AMPK-induced novel phosphorylation of RUNX1 inhibits STAT3 activation and overcome imatinib resistance in chronic myelogenous leukemia (CML) subjects.Cell death discovery · 2023Article
- Indole-based FLT3 inhibitors and related scaffolds as potential therapeutic agents for acute myeloid leukemia.BMC chemistry · 2023Review
- Targeting MET and FGFR in Relapsed or Refractory Acute Myeloid Leukemia: Preclinical and Clinical Findings, and Signal Transduction Correlates.Clinical cancer research : an official journal of the American Association for Cancer Research · 2023Article
- Splicing factor deficits render hematopoietic stem and progenitor cells sensitive to STAT3 inhibition.Cell reports · 2022Article
- Understanding Aberrant Signaling to Elude Therapy Escape Mechanisms in Myeloproliferative Neoplasms.Cancers · 2022Review
- Comprehensive analysis of the prognostic and immunotherapeutic implications of STAT family members in human colorectal cancer.Frontiers in genetics · 2022Article
- Review
- Extracellular Vesicles After Allogeneic Hematopoietic Cell Transplantation: Emerging Role in Post-Transplant Complications.Frontiers in immunology · 2020Review
- Novel Nanocomplexes Targeting STAT3 Demonstrate Promising Anti-Ovarian Cancer Effects in vivo.OncoTargets and therapy · 2020Article
- Review
- A Potent and Selective Small-Molecule Degrader of STAT3 Achieves Complete Tumor Regression In Vivo.Cancer cell · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
STAT transcription factors play a critical role in mediating the effects of cytokines on myeloid cells. As STAT target genes control key processes such as survival, proliferation and self-renewal, it is not surprising that constitutive activation of STATs, particularly STAT3 and STAT5, are common events in many myeloid tumors. STATs are activated both by mutant tyrosine kinases as well as other pathogenic events, and continued activation of STATs is common in the setting of resistance to kinase inhibitors. Thus, the targeting of STATs, alone or in combination with other drugs, will likely have increasing importance for cancer therapy.
Indexed as
Identifiers
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.