{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,26]],"date-time":"2026-06-26T01:15:42Z","timestamp":1782436542322,"version":"3.54.5"},"reference-count":42,"publisher":"MDPI AG","issue":"16","license":[{"start":{"date-parts":[[2019,8,7]],"date-time":"2019-08-07T00:00:00Z","timestamp":1565136000000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["IJMS"],"abstract":"<jats:p>During the last decade, substantial advances have been made in the understanding of the complex molecular, immunological and cellular disturbances involved in the initiation as well as evolution of myelodysplastic syndromes (MDS). In 85% of the mainly frail and older patient population, anemia is present at the time of diagnosis and is thus a major therapeutic challenge. High rates of primary resistance to erythropoiesis-stimulating agents (ESAs), the currently only approved standard therapy to treat anemia in lower-risk MDS, demand the development of novel and efficient drugs with a good safety profile. Luspatercept, a ligand trap of activin receptor II, is able to promote late stage erythropoiesis even in patients failing prior ESA treatment. The presence of ring sideroblastic phenotype defines a subgroup of patients with higher response rates. Additionally, recent developments in clinical research using HIF-1 or telomerase modulation by roxadustat or imetelstat are promising. Other areas of translational research involve targeting the inflammasome by anti-inflammatory drugs in order to improve anemia. These efforts will hopefully pave the way for new targeted treatment options for anemic low-risk MDS patients.<\/jats:p>","DOI":"10.3390\/ijms20163853","type":"journal-article","created":{"date-parts":[[2019,8,7]],"date-time":"2019-08-07T10:56:38Z","timestamp":1565175398000},"page":"3853","update-policy":"https:\/\/doi.org\/10.3390\/mdpi_crossmark_policy","source":"Crossref","is-referenced-by-count":24,"title":["Setting Fire to ESA and EMA Resistance: New Targeted Treatment Options in Lower Risk Myelodysplastic Syndromes"],"prefix":"10.3390","volume":"20","author":[{"given":"Anne Sophie","family":"Kubasch","sequence":"first","affiliation":[{"name":"Medical Clinic and Policlinic 1, Hematology and Cellular Therapy, University Hospital Leipzig, 04103 Leipzig, Germany"},{"name":"German MDS Study Group (G-MDS), 04103 Leipzig, Germany"},{"name":"European Myelodysplastic Syndromes Cooperative Group (EMSCO Group), 01067 Dresden, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Uwe","family":"Platzbecker","sequence":"additional","affiliation":[{"name":"Medical Clinic and Policlinic 1, Hematology and Cellular Therapy, University Hospital Leipzig, 04103 Leipzig, Germany"},{"name":"German MDS Study Group (G-MDS), 04103 Leipzig, Germany"},{"name":"European Myelodysplastic Syndromes Cooperative Group (EMSCO Group), 01067 Dresden, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1968","published-online":{"date-parts":[[2019,8,7]]},"reference":[{"key":"ref_1","doi-asserted-by":"crossref","first-page":"1096","DOI":"10.1182\/blood-2018-10-844696","article-title":"Treatment of MDS","volume":"133","author":"Platzbecker","year":"2019","journal-title":"Blood"},{"key":"ref_2","doi-asserted-by":"crossref","first-page":"47","DOI":"10.1038\/s41408-018-0085-4","article-title":"Myelodysplastic syndromes current treatment algorithm 2018","volume":"8","author":"Steensma","year":"2018","journal-title":"Blood Cancer J."},{"key":"ref_3","doi-asserted-by":"crossref","first-page":"67","DOI":"10.1111\/j.1365-2141.1995.tb08909.x","article-title":"Efficacy of erythropoietin in the myelodysplastic syndromes: A meta-analysis of 205 patients from 17 studies","volume":"89","year":"1995","journal-title":"Br. 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