The DNA hypomethylating agents (HMAs) azacitidine and decitabine are currently the most frequently administered disease-modifying therapies for patients with higher-risk myelodysplastic syndromes (MDS). However, azacitidine and decitabine are not curative, the median response duration is 11-15 months, and only 10-20 % of patients experience complete hematologic and cytogenetic response. Moreover, once an HMA fails the patient, the prognosis is poor, with a median survival of less than 6 months unless the patient undergoes hematopoietic stem cell transplantation (HSCT). Recent insights into the genetic basis of MDS have enhanced biological understanding and prognostication accuracy, but these developments have not yet led to regulatory approval of new therapies. While there are multiple potential approaches to patients with MDS for whom HMAs have failed, including supportive care alone, cytotoxic therapy, lenalidomide, histone deacetylase inhibitors, and HSCT, favorable responses to these approaches are limited and new therapies are greatly needed. Here, we review clinical and biological data about the population of patients failed by HMAs, evaluate currently available approaches to patients in this clinical situation, and discuss prospects for development of novel active agents.
Download full-text PDF |
Source |
---|---|
http://dx.doi.org/10.1007/s11899-015-0273-2 | DOI Listing |
Genes Chromosomes Cancer
January 2025
Laboratory of Cancer Genetics and Tumor Biology, Translational Medicine Research Unit, Medical Research Center Oulu and Biocenter Oulu, University of Oulu, Oulu, Finland.
Myelodysplastic neoplasia with complex karyotype (CK-MDS) poses significant clinical challenges and is associated with poor survival. Detection of structural variants (SVs) is crucial for diagnosis, prognostication, and treatment decision-making in MDS. However, the current standard-of-care (SOC) cytogenetic testing, relying on karyotyping, often yields ambiguous results in cases with CK.
View Article and Find Full Text PDFClin Lymphoma Myeloma Leuk
January 2025
Divisions of Hematology, Department of Internal Medicine, National Taiwan University Hospital, Taipei, Taiwan; Department of Laboratory Medicine, National Taiwan University Hospital, Taipei, Taiwan.
Background: Myelodysplastic syndromes/neoplasms (MDS) are a diverse group of clonal myeloid disorders. Advances in molecular technology lead to the development of new classification systems. However, large-scale epidemiological studies on MDS in Asian countries are currently scarce.
View Article and Find Full Text PDFNat Commun
January 2025
The Picower Institute for Learning and Memory, MIT, Cambridge, MA, USA.
Many essential proteins require pyridoxal 5'-phosphate, the active form of vitamin B6, as a cofactor for their activity. These include enzymes important for amino acid metabolism, one-carbon metabolism, polyamine synthesis, erythropoiesis, and neurotransmitter metabolism. A third of all mammalian pyridoxal 5'-phosphate-dependent enzymes are localized in the mitochondria; however, the molecular machinery involved in the regulation of mitochondrial pyridoxal 5'-phosphate levels in mammals remains unknown.
View Article and Find Full Text PDFDiseases
January 2025
Department of Haematology, Faculty of Medicine, School of Health Sciences, University of Ioannina, 45500 Ioannina, Greece.
T cells, as integral components of the adaptive immune system, recognize diverse antigens through unique T cell receptors (TCRs). To achieve this, during T cell maturation, the thymus generates a wide repertoire of TCRs. This is essential for understanding cancer evolution, progression, and the efficacy of immunotherapies.
View Article and Find Full Text PDFHemasphere
January 2025
Université Paris Cité, Institut Cochin, INSERM U1016, CNRS UMR8104 Assistance Publique-Hôpitaux de Paris.Centre, Laboratory of Hematology, Hôpital Cochin Paris France.
Lower risk (LR) myelodysplastic syndromes (MDS) are heterogeneous hematopoietic stem and progenitor disorders caused by the accumulation of somatic mutations in various genes including epigenetic regulators that may produce convergent DNA methylation patterns driving specific gene expression profiles. The integration of genomic, epigenomic, and transcriptomic profiling has the potential to spotlight distinct LR-MDS categories on the basis of pathophysiological mechanisms. We performed a comprehensive study of somatic mutations and DNA methylation in a large and clinically well-annotated cohort of treatment-naive patients with LR-MDS at diagnosis from the EUMDS registry (ClinicalTrials.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!