View clinical trials related to Leukemia, Myeloid, Acute.
Filter by:Activating mutations in the fms like tyrosine kinase 3 (FLT3) gene are observed in approximately 30% of patients with newly diagnosed acute myeloid leukemia (AML). Addition of the multitargeted kinase inhibitor midostaurin to standard chemotherapy prolongs event-free survival (EFS) and overall survival (OS) in patients with a FLT3 mutation. Gilteritinib is a more potent and more specific inhibitor of mutant FLT3 in comparison to midostaurin and has shown promising clinical activity in AML.
The purpose of this study is to determine the efficacy of cusatuzumab in combination with azacitidine in participants with previously untreated acute myeloid leukemia (AML) who are not eligible for intensive chemotherapy.
This first-in-human study will evaluate RVU120 (SEL120), a novel small molecule CDK8/19 inhibitor, in patients with Acute Myeloid Leukemia (AML) or High-risk Myelodysplastic Syndrome (HR-MDS), in terms of selection of the recommended dose for further clinical development and assessment of safety, tolerability, preliminary anti-leukemic activity, as well as pharmacokinetic and pharmacodynamic profiles.
This phase II trial studies how well olaparib works in treating patients with acute myeloid leukemia that has come back (relapsed) or does not respond to treatment (refractory), or myelodysplastic syndrome. Patients must also have a change in the gene called the IDH gene (IDH mutation). Olaparib may stop the growth of cancer cells by blocking some of the enzymes needed for cell growth. This study is being done to see if olaparib is better or worse in treating acute myeloid leukemia or myelodysplastic syndrome compared to the standard chemotherapy drugs.
This is a phase 1b, multi-arm, open-label study of HDM201 in combination with MBG453 or venetoclax in subjects with AML or high-risk MDS. For all subjects, TP53wt status must be characterized by, at a minimum, no mutations noted in exons 5, 6, 7 and 8. Two treatment arms will enroll subjects in parallel to characterize the safety, tolerability, PK, PD and preliminary antitumor activity of HDM201+MBG453 (treatment arm 1) and HDM201+venetoclax (treatment arm 2). - In the treatment arm 1, subjects will receive HDM201 in combination with MBG453. - In the treatment arm 2, subjects will receive HDM201 in combination with venetoclax. Venetoclax dose will be gradually increased (ramp-up) over a period of 4 to 5 days to achieve the daily target dose tested that will be subsequently continued. Upon the completion of the escalation part, MTD(s) and/or RD(s) of HDM201 in combination with MBG453 or venetoclax in AML and high-risk MDS subjects will be determined for each treatment arm.
This is a single-center pilot study of 20 patients with AML/MDS. Eligible patients will be enrolled following an informed consent between 6-20 weeks after allogeneic hematopoietic stem cell transplant. Patients will receive weekly oral ONC 201 for a total of 52 weeks.
This study is an observational study of MIF involvement in retrospectively and prospectively included adult acute myeloid leukemia (AML). Standard care samples collected at diagnosis, after one course of treatment, at time of remission controls, and at time of relapse will be used. The first objective is to determine which AMLs have pre-leukemic stem cells that overexpress MIF. Cytogenetic and molecular (NGS) profiling will be performed at diagnosis. Blood and bone marrow plasma, as well as bone marrow mononuclear cells will be collected and stored. The expression of MIF and its receptor (CD74 and CXCR4) will be analysed. Their prognostic value will be also tested. The second objective is to test whether patients in complete remission have persistent pre-leukemic stem cells that overexpress MIF. Blood and bone marrow plasma, bone marrow mononuclear cells from patients in complete remission will be collected. MIF, CD74, and CXCR4 expression by hematopoietic cells at time of diagnosis and remission will be compared to determine which patients have a persistent overexpression/secretion of MIF. In the meantime, the persistence of initiating lesions in complete remission samples will be tested by NGS, digital PCR, FISH, or RT-PCR methods. The third objective is to develop a pre-clinical model to target MIF in immuno-compromised mice (NSG mice) transplanted with primary AML cells and cells with pre-leukemic lesions. TET2 depletion leads to MIF over-expression/secretion by hematopoietic cells and improved multi-lineage NSG-repopulation capacity. MIF inhibitors and anti-MIF antibodies will be tested in these pre-clinical TET2-depleted models. Xenotransplantation of selected primary AML samples and xenotransplantation of TET2 depleted hematopoietic stem cells into NSG mice will be used. The fourth objective is to understand how MIF is deregulated in pre-leukemic stem cells and how the MIF-dependent crosstalk between mesenchymal stromal cells (MSCs) and pre-leukemic stem cells or normal hematopoietic cells works. The molecular mechanisms of MIF overexpression will be analyzed in hematopoietic stem and progenitor cells from normal and leukemic bone marrow, with a focus on cells depleted in TET2 or DNMT3A. To study the cross-talk between hematopoietic stem and progenitor cells, pre-leukemic stem cells, and bone marrow MSCs, co-culture experiments will be performed using available MSC cell lines and primary MSCs from healthy donors.
In this research study, our main goal for the ipilimumab portion of the study is to determine the highest dose of ipilimumab that can be given safely in several courses and to determine what side effects are seen in patients with Acute Myeloid Leukemia (AML), Myelodysplastic Syndromes (MDS), Myeloproliferative Neoplasms (MPN), Chronic Myelomonocytic Leukemia (CMML), or Myelofibrosis (MF).
This phase I trial studies the side effects and best dose of ruxolitinib when given together with venetoclax in treating patients with acute myeloid leukemia that has come back (relapsed) or has not responded to treatment (refractory). Ruxolitinib may stop the growth of cancer cells by blocking some of the enzymes needed for cell growth. Venetoclax is in a class of medications called B-cell lymphoma-2 (BCL-2) inhibitors. It may stop the growth of cancer cells by blocking Bcl-2, a protein needed for cancer cell survival. This study is being done to see if the combination of ruxolitinib and venetoclax works better in treating patients with acute myeloid leukemia compared to standard of care chemotherapy.
This phase I/II trial studies the best dose of venetoclax when given together with azacitidine and pevonedistat and to see how well it works in treating patients with newly diagnosed acute myeloid leukemia. Drugs used in chemotherapy, such as azacitidine, 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. Venetoclax may stop the growth of cancer cells by blocking Bcl-2, a protein needed for cancer cell survival. Pevonedistat may stop the growth of cancer cells by blocking some of the enzymes needed for cell growth. Giving azacitidine, venetoclax, and pevonedistat may work better in treating patients with acute myeloid leukemia.