Related Experiment Video
Updated: Jul 14, 2026
06:33
Identifying Bone Marrow Microenvironmental Populations in Myelodysplastic Syndrome and Acute Myeloid Leukemia
Published on: November 10, 2023
Inflammatory Signatures in MDS: The Missing Link Between Genetics, Microenvironment, and Therapy.
Adele Bottaro1, Maria Elisa Nasso1, Giuseppe Mirabile1
1Hematology Unit, Department of Human Pathology in Adulthood and Childhood "Gaetano Barresi", University of Messina, Via Consolare Valeria, 98125 Messina, Italy.
Cells
|July 13, 2026
Summary
Inflammation drives myelodysplastic syndromes (MDS) by promoting clonal selection and ineffective hematopoiesis. Targeting inflammation may improve prognosis and treatment sensitivity in MDS patients.
Area of Science:
- Hematology
- Immunology
- Stem Cell Biology
Background:
- Myelodysplastic syndromes (MDS) involve ineffective hematopoiesis within a context of chronic inflammation and immune dysregulation.
- Aging-associated inflammaging and bone marrow microenvironment remodeling actively shape MDS progression.
Purpose of the Study:
- To review the interplay between inflammation and MDS pathogenesis.
- To explore how inflammation influences clonal selection, hematopoiesis, and disease evolution.
Main Methods:
- Narrative review integrating insights from translational immunology, stem cell biology, multi-omics, and clinical studies.
- Examination of reciprocal interactions between inflammation and MDS.
Main Results:
- Chronic inflammation selects for and expands mutation-bearing clones in hematopoietic stem cells.
- Persistent inflammation, immune dysfunction, and stromal alterations worsen ineffective hematopoiesis and clonal dominance.
- Genetic lesions (e.g., TP53, spliceosome mutations) amplify inflammation and confer clonal advantage.
- Peripheral blood inflammatory markers correlate with MDS prognosis and treatment response.
Conclusions:
- Inflammation is a key factor in MDS initiation, progression, and treatment sensitivity.
- Integrating inflammatory signatures with genomic profiling can refine risk stratification.
- Therapeutic strategies targeting inflammation may restore marrow homeostasis and limit disease evolution.
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