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Myelodysplastic syndrome

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English: FIGURE 1. Mechanism of actions for treatments in low-risk myelodysplastic syndromes (MDS). Erythropoiesis stimulating agents stimulate gene transcription of maturation and proliferation of erythrocytes through JAK/STAT and Erk1/2. Lenalidomide inhibits the CDC25C phosphatase and by decrease in CK1α levels. Inhibition of the CDC25C phosphatase leads to a stoppage of proliferation by induction of an arrest in the cell cycle at the transition between G2 and M phase. Hypomethylating agents induce DNA hypomethylation. Ivosidenib, and enasidenib inhibits IDH1 or 1DH2 genes. Thrombopoietic receptor agonists activate signaling leads to increased platelet production. Imetelstat is a drug that help maintaining normal hematopoiesis by acting as a telomerase inhibitor in cells with short telomere length and hyper telomerase activity. “Luspatercept” and “sotatercept” specific activin receptor fusion proteins that act as ligand traps to neutralize negative regulators of late-stage erythropoiesis. Roxadustat is a small molecule that can be used orally and is an inhibitor of the “hypoxia-inducible factor” (20, 21, 61–64). EPO-R, erythropoietin receptor; JAK, janus kinase; STAT, signal transducer and activator of transcription; TPO-R, thrombopoietin receptor.
Date
Source https://www.frontiersin.org/articles/10.3389/fmed.2022.967900/full
Author Selami Kocak Toprak

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current01:24, 27 February 2024Thumbnail for version as of 01:24, 27 February 20243,162 × 2,210 (290 KB)Ozzie10aaaa (talk | contribs)Uploaded a work by Selami Kocak Toprak from https://www.frontiersin.org/articles/10.3389/fmed.2022.967900/full with UploadWizard

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