ReviewBlood reviews2019
Flaming and fanning: The Spectrum of inflammatory influences in myelodysplastic syndromes.
Review in Blood reviews, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
31 citing papers in PubMed, 54 citations in OpenAlex.
- 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
- Bone marrow microenvironment in myelodysplastic neoplasms: insights into pathogenesis, biomarkers, and therapeutic targets.Cancer cell international · 2025Review
- Article
- Constitutive systemic inflammation in Shwachman-Diamond Syndrome.Molecular medicine (Cambridge, Mass.) · 2025Article
- VEXAS: A review of current understandings and emerging treatment strategies.Frontiers in immunology · 2025Review
- Relevance of blood tumor markers in inpatients with significant involuntary weight loss and elevated levels of inflammation biomarkers.BMC cancer · 2024Article
- Toll-Like Receptor 4, 2, and Interleukin 1 Receptor Associated Kinase4: Possible Diagnostic Biomarkers in Myelodysplastic Syndrome Patients.Advanced biomedical research · 2024Article
- The immunobiology of myelodysplastic neoplasms: a mini-review.Frontiers in immunology · 2024Review
- When inflammatory stressors dramatically change, disease phenotypes may transform between autoimmune hematopoietic failure and myeloid neoplasms.Frontiers in immunology · 2024Review
- ETV6 represses inflammatory response genes and regulates HSPC function during stress hematopoiesis in mice.Blood advances · 2023Article
- Biglycan as a mediator of proinflammatory response and target for MDS and sAML therapy.Oncoimmunology · 2023Article
- Mutant Samd9l expression impairs hematopoiesis and induces bone marrow failure in mice.The Journal of clinical investigation · 2022Article
- Myeloid-Derived Suppressor Cells: New Insights into the Pathogenesis and Therapy of MDS.Journal of clinical medicine · 2022Review
- Molecular Threat of Splicing Factor Mutations to Myeloid Malignancies and Potential Therapeutic Modulations.Biomedicines · 2022Review
- Review
- Concurrent ankylosing spondylitis and myelodysplastic syndrome: A case report.World journal of clinical cases · 2022Article
- Immune Dysfunction, Cytokine Disruption, and Stromal Changes in Myelodysplastic Syndrome: A Review.Cells · 2022Review
- Circulating HMGB1 is increased in myelodysplastic syndrome but not in other bone marrow failure syndromes: proof-of-concept cross-sectional study.Therapeutic advances in hematology · 2022Article
- The immunological role of mesenchymal stromal cells in patients with myelodysplastic syndrome.Frontiers in immunology · 2022Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
The myelodysplastic syndromes (MDS) represent neoplasms derived from the expansion of mutated clonal hematopoietic cells which often demonstrate aberrant differentiation potential with resultant cytopenias and a propensity to evolve into acute myelogenous leukemia. While multiple mutations have been identified which may serve as drivers of the MDS clone, there is accumulating evidence that MDS clones and subclones are subject to modulation by the marrow microenvironment and its inflammatory milieu. There is also a strong link between autoimmune disorders and MDS. In this review, we examine the role of inflammatory cytokines, toll like receptors, pyroptosis, stromal cells, and cellular inflammatory mediators in MDS initiation, propagation, and progression. These contributions in a background of mutational, epigenetic, and aging changes in the marrow are also reviewed. Such inflammatory mediators may be subject to therapeutic agents which will enhance suppression of the MDS clone with potential to improve therapeutic outcomes in this disease which is usually incurable in aged patients not eligible for stem cell transplantation.
Indexed as
Identifiers
What OpenQuestion holds
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.