ReviewCellular and molecular life sciences : CMLS2025
IL-1 signaling and inflammasomes in acute myeloid leukemia: mechanisms and therapeutic opportunities.
Review in Cellular and molecular life sciences : CMLS, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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
2 citing papers in PubMed.
- Dysregulation of IL-37/SIGIRR Axis in De Novo acute myeloid leukemia patients: association with treatment response.Molecular biology reports · 2026Article
- LncRNA GAS5 inhibits the remodeling of the tumor microenvironment by binding to miR-93-5p, thereby suppressing the development of osteosarcoma.Journal of orthopaedic surgery and research · 2026Article
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
Abstract
Acute myeloid leukemia (AML) is a heterogenous disease characterized by the accumulation of immature myeloid blasts with distinct genetic mutations in the bone marrow and peripheral blood. AML co-evolve with other components of specialized bone marrow niches within a microenvironment enriched in cytokines and inflammatory cells; among these, interleukin-1 (IL-1) may act as a tumor driver. This review examines two complementary aspects of AML biology in relation to IL-1. First, we describe the functional activity of IL-1 and the signaling pathways triggered by the IL-1 receptor in malignant cells, along with preclinical and clinical studies targeting this pathway in AML. Second, we discuss the mechanisms regulating the release of mature IL-1β through the activation of different inflammasomes. Inflammasomes, particularly NLRP3, are emerging as key contributors to AML pathophysiology. Beyond IL-1 release, NLRP3 may interface with cellular stress responses and pyroptosis, thereby influencing both AML cells and their microenvironment through multiple mechanisms. Inflammasome signaling may act as a driver of therapy resistance while also representing a promising therapeutic target.
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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.