View clinical trials related to Myelodysplastic Syndrome.
Filter by:In a recent analysis of a large transfusion database (Transfusion Research Utilization, Surveillance and Tracking database [TRUST]), the investigators found that the transfusion of ABO non-identical RBCs to group A individual was associated with an increased risk of death in-hospital compared to patients transfused with ABO identical RBCs (Red Blood Cells). Our finding was corroborated in a separate study of low birth weight neonates who received only group O RBCs (e.g., group O neonates received ABO identical RBCs but group A, B, and AB neonates received ABO non-identical RBCs). A subgroup of neonates who received ABO non-identical transfusions had higher mortality (Z. Sohl, personal communication, April 30th, 2020). Similar adverse clinical outcomes have been reported in a number of studies where patients have received ABO non-identical RBCs and/or platelets. Together, these findings raise the concern that the longstanding policy of transfusing group O non-identical RBCs and platelets may increase the risk of harm for some patients. In Hamilton, Ontario hospitals, approximately 20% of transfused patients receive ABO non-identical RBCs every year because of inventory shortages, urgent requests, and specific phenotype requirements. The negative impact of this practice could have widespread national and international implications for transfusion policy. The ability to undertake critical exploratory analyses in transfusion medicine is enabled by large research and administrative data sets that include all Hamilton hospitals. The initial finding of potential harm with ABO non-identical RBCs is hypothesis-generating and requires confirmation through external datasets and translational studies to support a biological mechanism. If confirmed, this hypothesis can then be tested in a clinical trial.
An open-label study available to all eligible participants from Study B1371019 and participants originating from Study B1371012 continuing on study intervention with azacitidine with or without glasdegib.
This phase II trial studies the effect of adding pomalidomide to usual chemotherapy treatment (daunorubicin and cytarabine liposome) in treating patients with newly diagnosed acute leukemia with myelodysplastic syndrome-related changes. Pomalidomide may stop the growth of blood vessels, stimulate the immune system, and kill cancer cells. Chemotherapy drugs, such as daunorubicin and cytarabine liposome, work in different ways to stop the growth of cancer cells, either by killing the cells, by stopping them from dividing, or by stopping them from spreading. Adding pomalidomide to chemotherapy treatment with daunorubicin and cytarabine liposome may be effective in improving some treatment outcomes in patients with newly diagnosed acute leukemia with myelodysplastic syndrome-related changes.
This research study tests a new medicine for mobilizing stem cells so they can be collected and used for allogeneic stem cell transplant for treatment of hematological malignancies. MGTA-145, the new medicine, will be given with plerixafor.
This study will evaluate whether a geriatric assessment can lead to better treatment outcomes in older patients (age 60+) with a myeloid malignancy including acute myeloid leukemia, ,myelodysplastic syndromes, myeloproliferative neoplasms, or related blood disorders who are going to receive chemotherapy or another treatment to prepare the body for an allogeneic hematopoietic stem cell transplant (allo-HCT). The geriatric assessment includes looking at patients' cognitive function (thinking processes), physical function, mobility (ability to move the body), mood, nutrition, and current medications to help decide the type of treatment they'll receive. Another purpose of this study is to see whether use of the geriatric assessment improves participants' quality of life. We will evaluate participants' quality of life through questionnaires.
This phase I/II trial identifies the best dose of seclidemstat when given together with azacitidine in treating patients with myelodysplastic syndrome or chronic myelomonocytic leukemia. Seclidemstat may stop the growth of cancer cells by blocking some of the enzymes needed for cell growth. Azacitidine may help block the formation of growths that may become cancer. Giving seclidemstat and azacytidine may kill more cancer cells.
This study aims to use clinical and biological characteristics of acute leukemias to screen for patient eligibility for available pediatric leukemia sub-trials. Testing bone marrow and blood from patients with leukemia that has come back after treatment or is difficult to treat may provide information about the patient's leukemia that is important when deciding how to best treat it, and may help doctors find better ways to diagnose and treat leukemia in children, adolescents, and young adults.
Allo-HSCT is the most effective way to cure MDS and AML secondary to MDS. At present, the best conditioning regimen for MDS and AML secondary to MDS undergoing allo-HSCT remains in discussion. In this prospective study, the safety and efficacy of G-CSF+DAC+BUCY and G-CSF+DAC+BF conditioning regimens in RAEB-1, REAB-2 and AML secondary to MDS undergoing allo-HSCT are evaluated.
This phase II trial studies the effect of venetoclax together with busulfan, cladribine, and fludarabine in treating patients with high-risk acute myeloid leukemia or myelodysplastic syndrome who are undergoing stem cell transplant. Chemotherapy drugs, such as venetoclax, busulfan, cladribine, and fludarabine, work in different ways to stop the growth of cancer cells, either by killing the cells, by stopping them from dividing, or by stopping them from spreading. Adding venetoclax to the current standard of care stem cell transplant regimen of busulfan, fludarabine, and cladribine may help to control high-risk acute myeloid leukemia or myelodysplastic syndrome.
This is a Phase Ⅰ/II, Open-label Study to Investigate the Pharmacokinetics, Safety, and Efficacyof ATG 016 Monotherapy in IPSS-R Intermediate Risk and above Myelodysplastic Syndrome (MDS) Patients after Failure of Hypomethylating Agent (HMA)-based Therapy.