Novel combinations to improve hematopoiesis in myelodysplastic syndrome

Khaja Syed, Sara Naguib, Zhao Jun Liu, Luisa Cimmino, Feng Chun Yang

Research output: Contribution to journalReview articlepeer-review

6 Scopus citations

Abstract

Myelodysplastic syndrome (MDS) represents a heterogeneous group of clonal hematopoietic disorders, which is characterized by cytopenias in the peripheral blood and bone marrow dysplasia due to ineffective hematopoiesis. Patients with MDS have an increased risk of transformation to acute myeloid leukemia (AML). Although the molecular basis of MDS is heterogeneous, several studies demonstrated the significant contribution of the dysregulated immune system in accelerating MDS progression. The immunosuppressive tumor microenvironment is shown to induce tolerance of MDS blasts, which may result in a further accumulation of genetic aberrations and lead to the disease progression. Increasing evidence shows an expansion of myeloid-derived suppressor cells (MDSCs), a population of inflammation-associated immature cells, in patients with MDS. Interestingly, the increased MDSC populations are shown to be correlated with a risk of disease progression in MDS. In addition, MDS is highly prevalent in aged individuals with non-hematology co-morbidities who are fragile for chemotherapy. Increasing research effort is devoting to identify novel agents to specific targeting of the MDSC population for MDS treatment.

Original languageEnglish (US)
Article number132
JournalStem Cell Research and Therapy
Volume11
Issue number1
DOIs
StatePublished - Mar 20 2020

Keywords

  • Leukemic stem cells
  • Myelodysplastic syndrome
  • Myeloid-derived suppressor cells
  • T regulatory cells
  • Therapeutic antibodies
  • Transfusion independent

ASJC Scopus subject areas

  • Medicine (miscellaneous)
  • Molecular Medicine
  • Biochemistry, Genetics and Molecular Biology (miscellaneous)
  • Cell Biology

Fingerprint

Dive into the research topics of 'Novel combinations to improve hematopoiesis in myelodysplastic syndrome'. Together they form a unique fingerprint.

Cite this