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Related Experiment Video

Updated: Jul 14, 2026

Identifying Bone Marrow Microenvironmental Populations in Myelodysplastic Syndrome and Acute Myeloid Leukemia
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
PubMed
Summary

Inflammation drives myelodysplastic syndromes (MDS) by promoting clonal selection and ineffective hematopoiesis. Targeting inflammation may improve prognosis and treatment sensitivity in MDS patients.

Keywords:
IRAK4–NFκB signalingNLRP3 inflammasomeTP53 mutationsbone marrow microenvironmentclonal hematopoiesisinflammaginginflammationinnate immunitymyelodysplastic syndromesspliceosome mutations

Related Experiment Videos

Last Updated: Jul 14, 2026

Identifying Bone Marrow Microenvironmental Populations in Myelodysplastic Syndrome and Acute Myeloid Leukemia
06:33

Identifying Bone Marrow Microenvironmental Populations in Myelodysplastic Syndrome and Acute Myeloid Leukemia

Published on: November 10, 2023

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.