ReviewBlood2019
The central role of inflammatory signaling in the pathogenesis of myelodysplastic syndromes.
Review in Blood, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 172 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
172 citing papers in PubMed, 266 citations in OpenAlex.
- A phase 1b/2 study of ceralasertib, a selective inhibitor of ATR, in patients with relapsed or refractory MDS and CMML.Blood advances · 2026Trial
- EASIX for prediction of survival in lower-risk myelodysplastic syndromes.Blood cancer journal · 2019Trial
- Assessing the Frequency of VEXAS-Related Canonical UBA1 Mutations in Myelodysplastic Syndrome Patients.European journal of haematology · 2026Article
- Lung-Predominant Hyperinflammatory Syndrome in Therapy-Related Myelodysplastic Syndrome Responsive to Interleukin-1 Blockade.Hematology reports · 2026Article
- Canakinumab or emavusertib for anemia in lower-risk MDS: results of the CANFIRE and LUCAS phase 2, open-label, multicenter trials.Communications medicine · 2026Article
- Therapeutic Silencing of Tmprss6 Reduces Iron-Induced Inflammation and Prolongs Survival in MDS Mice.American journal of hematology · 2026Article
- PANoptosis in the pathogenesis of myelodysplastic syndromes.Molecular oncology · 2026Review
- Inflammatory signatures in the spectrum of myeloid diseases.HemaSphere · 2026Article
- Inflammatory Signatures in MDS: The Missing Link Between Genetics, Microenvironment, and Therapy.Cells · 2026Review
- Nanobody-engineered CLL-1 CAR T cells: A strategy for safer targeting in acute myeloid leukemia.Molecular therapy. Oncology · 2026Article
- Time-Dependent Prognostic Value of the mEASIX Score in Patients with Myelodysplastic Syndromes.Diagnostics (Basel, Switzerland) · 2026Article
- Article
- Stromal Gasdermin D-mediated Pyroptosis Drives Maladaptive CD4bioRxiv : the preprint server for biology · 2026Article
- Clinical decisions in clonal hematopoiesis: a contemporary review for clinicians.Haematologica · 2026Review
- A machine learning-driven framework integrating cell death and senescence signatures for multi-target drug design and immunotherapy optimization in ovarian cancer.NPJ precision oncology · 2026Article
- Preclinical efficacy of tasquinimod in myelodysplastic neoplasms: Restoring erythropoiesis and mitigating bone loss.HemaSphere · 2026Article
- TGFβ-activated kinase-1 knockdown in hematopoietic stem-progenitor cells causes PANoptosis and myelodysplastic syndrome-like disease in mice.Haematologica · 2026Article
- Aberrant Kupffer-like differentiation of hematopoietic stem cell is critical for the MDS pathogenesis in Setd2-deficient mice.Cell death and differentiation · 2026Article
- The role of macrophages and cytokines in the occurrence and development of MDS.Clinical and experimental medicine · 2026Review
- Targeting IL-1/IRAK1/4 signaling in acute myeloid leukemia stem cells following treatment and relapse.Leukemia · 2026Article
112 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
In cancer biology, tumor-promoting inflammation and an inflammatory microenvironment play a vital role in disease pathogenesis. In the past decade, aberrant innate immune activation and proinflammatory signaling within the malignant clone and the bone marrow (BM) microenvironment were identified as key pathogenic drivers of myelodysplastic syndromes (MDS). In particular, S100A9-mediated NOD-like receptor protein 3 (NLRP3) inflammasome activation directs an inflammatory, lytic form of cell death termed pyroptosis that underlies many of the hallmark features of the disease. This circuit and accompanying release of other danger-associated molecular patterns expands BM myeloid-derived suppressor cells, creating a feed-forward process propagating inflammasome activation. Furthermore, somatic gene mutations of varied functional classes license the NLRP3 inflammasome to generate a common phenotype with excess reactive oxygen species generation, Wnt/β-catenin-induced proliferation, cation flux-induced cell swelling, and caspase-1 activation. Recent investigations have shown that activation of the NLRP3 inflammasome complex has more broad-reaching importance, particularly as a possible disease-specific biomarker for MDS, and, mechanistically, as a driver of cardiovascular morbidity/mortality in individuals with age-related, clonal hematopoiesis. Recognition of the mechanistic role of aberrant innate immune activation in MDS provides a new perspective for therapeutic development that could usher in a novel class of disease-modifying agents.
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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.