ArticleBlood advances2020
Inflammation-driven activation of JAK/STAT signaling reversibly accelerates acute myeloid leukemia in vitro.
Article in Blood advances, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 50 citations in OpenAlex.
- Inflammation as a central driver in AML pathogenesis and therapy resistance.Science China. Life sciences · 2026Review
- Synergistic cooperation between progranulin and Jak2/Stat3 signaling determines definitive myeloid cell fate.Cell reports · 2026Article
- Leukemia cells remodel bone marrow stromal cells to generate a protumoral microenvironment via the S100A8-NOX2-ROS signaling pathway.Scientific reports · 2025Article
- Paediatric bone marrow mesenchymal stem cells support acute myeloid leukaemia cell survival and enhance chemoresistance via contact-independent mechanism.British journal of haematology · 2025Article
- Unravelling the link between circadian clock genes and brain tumors: From pathological disruptions to potential therapeutic interventions.Frontiers in pharmacology · 2025Review
- Bone marrow mesenchymal stem cell exosomes suppress JAK/STAT signaling pathway in acute myeloid leukemia in vitro.Blood research · 2024Article
- Age-associated myeloid malignancies - the role of STAT3 and STAT5 in myelodysplastic syndrome and acute myeloid leukemia.FEBS letters · 2024Review
- Article
- Trained and ready - the case for an inflammatory memory for hematopoietic stem and progenitor cells in the AML niche.Oncotarget · 2024Review
- Data-driven modeling of core gene regulatory network underlying leukemogenesis in IDH mutant AML.NPJ systems biology and applications · 2024Article
- Pretransplantation predictors of survival in nonremission acute myeloid leukemia treated with haploidentical transplantation using steroid-based GVHD prophylaxis.Annals of hematology · 2024Article
- High throughput screening aids clinical decision-making in refractory acute myeloid leukaemia.Cancer reports (Hoboken, N.J.) · 2024Article
- Review
- Large-scale genome-wide association studies reveal the genetic causal etiology between ankylosing spondylitis and risk of leukemia and lymphocytic malignancies.Frontiers in oncology · 2024Article
- Modelling acute myeloid leukemia (AML): What's new? A transition from the classical to the modern.Drug delivery and translational research · 2023Review
- Article
- Characterization of mesenchymal stem cells in pre-B acute lymphoblastic leukemia.Frontiers in cell and developmental biology · 2023Article
- Inflammatory bone marrow signaling in pediatric acute myeloid leukemia distinguishes patients with poor outcomes.Nature communications · 2022Article
- Black Seed (Nigella sativa): A Favourable Alternative Therapy for Inflammatory and Immune System Disorders.Inflammopharmacology · 2022Review
- The genesis and evolution of acute myeloid leukemia stem cells in the microenvironment: From biology to therapeutic targeting.Cell death discovery · 2022Review
Corrections and comments
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Authors and funding
8 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Acute myeloid leukemia (AML) is characterized by a high relapse rate and dismal long-term overall survival which is related to persistence of leukemia-initiating cells in their niche. Different animal models of myeloid malignancies reveal how neoplastic cells alter the structural and functional characteristics of the hematopoietic stem cell niche to reinforce malignancy. Understanding and disruption of the microenvironmental interactions with AML cells are a vital need. Malignant niches frequently go along with inflammatory responses, but their impact on cancerogenesis often remains unexplored. Here, we uncovered an aberrant production of inflammatory cytokines in untreated AML bone marrow that was proved to promote the proliferation of leukemia cells. This inflammatory response induced an activation of the Janus kinase/signal transducer and activator of transcription (JAK/STAT) signaling pathway in AML blasts as well as bone marrow stromal cells that also fostered leukemia proliferation. Inhibition of JAK/STAT signaling using the selective JAK1/2 inhibitor ruxolitinib resulted in significant antileukemic activity in AML in vitro which is mediated through both cell-autonomous and microenvironment-mediated mechanisms. However, in a xenograft transplantation model, monotherapy with ruxolitinib did not achieve substantial antileukemic activity, possibly suggesting a complementary function of JAK1/2 inhibition in AML.
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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.