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Most therapies for lower-risk MDS do not impact the cause of disease, allowing proliferation of malignant stem and progenitor cells to continue2,3,6,9

Malignant proliferation drives ineffective hematopoiesis in lower-risk MDS1,2,27

For patients with lower-risk MDS, normal blood cell production in bone marrow is disrupted by malignant and/or dysfunctional hematopoietic stem and progenitor cells.27

Ineffective hematopoiesis contributes to:

Graphic showing that ineffective hematopoiesis leads to cytopenias in the blood and morphological dysplasia of the bone marrow

Cytopenias in the
peripheral blood2

Graphic showing that ineffective hematopoiesis leads to cytopenias in the blood and morphological dysplasia of the bone marrow

Morphological dysplasia
of the bone marrow2

The expansion of malignant and dysfunctional cells further drives ineffective hematopoiesis2

Malignant stem and progenitor cells proliferate indefinitely inside the bone marrow, creating an imbalance where malignant and dysfunctional cells eventually crowd out normal progenitor cells and disrupt normal hematopoiesis.1,2

Graphic illustrating how ineffective hematopoiesis is influenced by malignant stem and progenitor cells in the bone marrow, leading to fewer cells of poorer quality.

In MDS, affected bone marrow results in increased symptom burden, relapse, or transformation to AML.2,27,28

Many patients with lower-risk MDS will eventually progress since their treatments do not address ineffective hematopoiesis.2

Learn about limitations of current treatments

AML, acute myeloid leukemia; MDS, myelodysplastic syndromes.