Pathophysiology of Myelodysplastic Syndromes

Ineffective hematopoiesis is the major characteristic of early myelodysplastic syndromes. Its pathophysiology relies on a diversity mechanisms supported by genetic events that develop in aging hematopoietic stem cells. Deletion and mutations trigger epigenetic modifications, co-transcriptional post-transcriptional deregulations gene expression. Epistatic interactions between mutants may aggravate phenotype. Amplification minor subclones containing promote their growth suppress others drives clonal evolution. Aging also participates reprogramming immune microenvironment towards an inflammatory state, which precedes expansion immunosuppressive cells such as Tregs myeloid-derived suppressive alters anti-tumor response effector Integrating biomarkers transcription/translation deregulation contexture will help design personalized treatments.