Cited by 273Inflammasome and immune disordersAcute Myeloid Leukemia ResearchBlood disorders and treatments

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The central role of inflammatory signaling in the pathogenesis of myelodysplastic syndromes

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Sallman, David A., List, Alan·2019·Blood

DOI 10.1182/blood-2018-10-844654PMC PMC7022316

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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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Authors: Sallman, D. A., & List, A.
Affiliations: Moffitt Cancer Center (US)
ORCID: Sallman, David A.
List, Alan
Venue: Blood
Publisher: American Society of Hematology
Published: 2019-03-07
Volume: 133
Issue: 10
Pages: 1039-1048
ISSN: 0006-4971 (ISSN-L)
1528-0020
DOI: 10.1182/blood-2018-10-844654
PMC: PMC7022316
OpenAlex: W2913296480
Cited by: 273
References: 81
Citations by year: 2026: 26 · 2025: 27 · 2024: 39 · 2023: 47 · 2022: 38 · 2021: 59 · 2020: 23 · 2019: 14
FWCI: 2.96
Type: journal article
Language: en
Open access: bronze
doi.org
Locations: Blood (publishedVersion)
PubMed Central (publishedVersion)
PubMed (publishedVersion)
Funders: National Cancer Institute (P30CA076292)
Topics: Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Inflammasome and immune disorders
Health Sciences › Medicine › Hematology › Acute Myeloid Leukemia Research
Health Sciences › Medicine › Hematology › Blood disorders and treatments
Keywords: myelodysplastic syndrome, NLRP3 inflammasome, S100A9, pyroptosis, bone marrow microenvironment, myeloid-derived suppressor cells, innate immune activation, clonal hematopoiesis, cardiovascular morbidity, caspase-1, reactive oxygen species, Wnt/β-catenin signaling, disease biomarkers, disease-modifying therapy
MeSH terms: Pyroptosis, NLR Family, Pyrin Domain-Containing 3 Protein, Bone Marrow, Bone Marrow Cells, Hematopoiesis, Humans, Immunity, Innate, Inflammation, Mutation, Myelodysplastic Syndromes, Phenotype, Signal Transduction, Reactive Oxygen Species, Inflammasomes

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The central role of inflammatory signaling in the pathogenesis of myelodysplastic syndromes

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