ReviewCancers2019
STAT3: A Promising Therapeutic Target in Multiple Myeloma.
Review in Cancers, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
52 citing papers in PubMed, 86 citations in OpenAlex.
- STAT3 inhibition eradicates multiple myeloma stem-like cells and induces immunogenic cell death.Blood science (Baltimore, Md.) · 2026Article
- Stromal and endothelial transcriptional changes during progression from MGUS to myeloma and after treatment response.Nature communications · 2026Article
- A bibliometric analysis of the research landscape of lenalidomide resistance in multiple myeloma.Discover oncology · 2026Article
- Non-coding RNAs as predictive factors of oncological outcomes in plasma cell myeloma.Oncology reviews · 2026Review
- Targeting STK17B kinase activates ferroptosis and suppresses drug resistance in multiple myeloma.Blood · 2026Article
- Targeting Wnt/β-catenin signaling enhances the efficacy of anti-CD38 immunotherapy in multiple myeloma.Neoplasia (New York, N.Y.) · 2025Article
- Human preclinical multiple myeloma in vitro models for disease modeling and therapy screening.Journal of biological engineering · 2025Review
- Targeting of SKP2 to combat drug resistance in multiple myeloma.Scientific reports · 2025Article
- PRL-3: unveiling a new horizon in cancer therapy.Acta pharmacologica Sinica · 2025Review
- Syntenin inhibition impairs stroma-tumor communication in multiple myeloma and improves bortezomib treatment efficiency.HemaSphere · 2025Article
- Breaking Barriers: The Role of the Bone Marrow Microenvironment in Multiple Myeloma Progression.International journal of molecular sciences · 2025Review
- Combined MEK1/2 and ATR inhibition promotes myeloma cell death through a STAT3-dependent mechanism in vitro and in vivo.British journal of haematology · 2024Article
- Pathways to therapy resistance: The sheltering effect of the bone marrow microenvironment to multiple myeloma cells.Heliyon · 2024Review
- Fabrication of Nickel/Zinc Oxide Nanocomposites from Citrus sinensis Extract Prompts Apoptosis Through Impeding JAK/STAT3 Signaling in Gastric Cancer.Applied biochemistry and biotechnology · 2024Article
- An IL-1β-driven neutrophil-stromal cell axis fosters a BAFF-rich protumor microenvironment in individuals with multiple myeloma.Nature immunology · 2024Article
- Factors determining the sensitivity to proteasome inhibitors of multiple myeloma cells.Frontiers in pharmacology · 2024Review
- KS18, a Mcl-1 inhibitor, improves the effectiveness of bortezomib and overcomes resistance in refractory multiple myeloma by triggering intrinsic apoptosis.Frontiers in pharmacology · 2024Article
- Oxidative stress regulation and related metabolic pathways in epithelial-mesenchymal transition of breast cancer stem cells.Stem cell research & therapy · 2023Review
- HAPLN1 matrikine: a bone marrow homing factor linked to poor outcomes in patients with MM.Blood advances · 2023Article
- Dysregulation of Non-Coding RNAs: Roles of miRNAs and lncRNAs in the Pathogenesis of Multiple Myeloma.Non-coding RNA · 2023Review
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 at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Multiple myeloma (MM) is an incurable plasma cell malignancy for which novel treatment options are required. Signal Transducer and Activator of Transcription 3 (STAT3) overexpression in MM appears to be mediated by a variety of factors including interleukin-6 signaling and downregulation of Src homology phosphatase-1 (SHP-1). STAT3 overexpression in MM is associated with an adverse prognosis and may play a role in microenvironment-dependent treatment resistance. In addition to its pro-proliferative role, STAT3 upregulates anti-apoptotic proteins and leads to microRNA dysregulation in MM. Phosphatase of regenerating liver 3 (PRL-3) is an oncogenic phosphatase which is upregulated by STAT3. PRL-3 itself promotes STAT-3 phosphorylation resulting in a positive feedback loop. PRL-3 is overexpressed in a subset of MM patients and may cooperate with STAT3 to promote survival of MM cells. Indirectly targeting STAT3 via JAK (janus associated kinase) inhibition has shown promise in early clinical trials. Specific inhibitors of STAT3 showed
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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.