View clinical trials related to Acute Myeloid Leukemia.
Filter by:Hematopoietic stem cell transplantation is a curative treatment for a number of benign and malignant hematologic diseases. One of the key parts of hematopoietic stem cell transplantation is the prophylaxis of graft-versus-host disease. Since the end of the 1970s, with the introduction of cyclosporine, calcineurin inhibitors (cyclosporine and tacrolimus) have become part of almost all prophylactic regimens, even though they are a group of drugs with a poor toxicity profile that requires monitoring. constant serum level. Since 2008, post-transplant cyclophosphamide has been introduced with great success, associated with a calcineurin inhibitor and mycophenolate, in the prophylaxis of graft-versus-host disease in haploidentical transplantation (50% matched). Since then, in view of this enormous success, efforts have been made to incorporate post-transplant cyclophosphamide in matched related and unrelated transplants, or with a mismatch. This is a prospective, 2-arm, non-randomized study. Arm 1, with related donors, and arm 2, with unrelated donors. Patients will be allocated in these arms according to donor availability (patients with a matched-sibling donor will receive a matched-sibling transplant; patients with no related donors but with unrelated donors, an unrelated transplant). Patients who are ready for transplantation with matched-sibling or unrelated donors will be recruited to participate in the study. The stem cell collection target will be 5E6 CD34/kg recipient weight for peripheral source. If a quantity greater than this is collected, the remainder will be cryopreserved according to the institutional protocol. Graft-versus-host disease prophylaxis will be performed on D+3 and D+4 with cyclophosphamide and with ATG on D-1 or on D-2 and D-1, depending on ATG de-escalation, for matched-sibling transplants, according to prespecified criteria based on the 3+3 approach; and on D+3 and D+4 with cyclophosphamide and with ATG on D-2 and D-1, for unrelated donors.
The goal of this study is to determine the safety and antitumor effects of REM-422, a MYB mRNA degrader, in people with Higher Risk MDS and relapsed/refractory AML
Acute myeloid leukemia (AML) is a malignant disorder of the bone marrow and the most common form of acute leukemia in adults. Patient with AML have the shortest survival compared to other forms of leukemia. In the past 6 years, several new therapies have been approved. Biomarkers are in urgent need to guide therapeutic regimen selection in order to maximize the benefit of available therapies and minimize treatment toxicity. Current standard practice is to perform bone marrow biopsy at end of treatment cycle (each cycle around 28 days), and based on bone marrow finding, to decide further treatment plan. It is invasive and time consuming. The research we are proposing here is to investigate whether tracking leukemia stem cells (LSC) in peripheral blood during early treatment cycle may provide a non-invasive method to predict therapeutic outcome at end of treatment cycle. Our retrospective study have found that LSC fractional change, defined by two LSC markers, named CLL1 and CD45RA, is highly correlated with therapeutic outcome. Further more, CLL1 and CD45RA positive LSC fraction demonstrates a high concordance between bone marrow and peripheral blood, offering the opportunity to track CLL1 and CD45RA positive LSC fraction non-invasively in peripheral blood during treatment. This pilot study will allow us to decide whether testing CLL1 and CD45RA positive LSC in peripheral blood during leukemia treatment is feasible in clinical practice. This result will lay the foundation for designing future trials using CLL1 and CD45RA positive LSC fractional change to optimize therapeutic strategy for patients with AML.
To find a recommended dose of HC-7366 that can be given in combination with azacitidine and venetoclax to patients with AML. The safety and effects of this drug combination will also be studied.
This study investigates the immune profile of patients receiving treatment with venetoclax plus azacitidine for acute myeloid leukemia (AML). Studying the information gathered from the immune profile from blood and bone marrow samples may help researchers understand the associated responses to the treatment of patients undergoing therapy of venetoclax plus azacitidine and create future immune based treatment approaches.
We apply for this clinical study to evaluate the efficacy of "combined recombinant human interference'- α- 1b, interleukin-2, and thalidomide" regimen in obtaining MRD positive AML patients in CR,as well as the efficacy of the "Venentoclax and azacitidine" regimen and the "combined recombinant human interference'- α- 1b, interleukin-2, and thalidomide" regimen in alternately maintaining the treatment of MRD negative AML patients. The study included two cohorts. The first cohort consisted of AML patients who obtained CR or CRi but MRD positive after induction chemotherapy and consolidation chemotherapy. They were randomly given two cycles of "recombinant human interference'- α- 1b, interleukin-2, and thalidomide" or "VA" regimen treatment, and the MRD conversion rates of the two groups were analyzed. In the second cohort , after induction chemotherapy and consolidation chemotherapy, AML patients with CR or CRi and negative MRD were obtained, and were given "recombinant human interference'- α- 1b, interleukin-2, and thalidomide", Venentoclax and Azacitidine triple alternative maintenance treatment, to analyze the impact of maintenance treatment scheme on long-term survival of aml patients.
This study evaluates the efficacy and safety of the combination of idarubicin and cytarabine induction followed by intermediate-dose cytarabine consolidation with venetoclax in the treatment of newly diagnosed adult acute myeloid leukemia (AML). This study includes the induction and consolidation phases of AML treatment.
Acute myeloid leukemia (AML) is a malignancy of aging endowed with poor prognosis. The combination of the hypomethylating agent azacitidine (AZA) with the BCL-2 inhibitor venetoclax (VEN) is the first-line treatment of older AML patients but is endowed with substantial resistance. The project leverages functional precision oncology, single-cell studies and mouse experiments to dissect the mechanisms of primary and adaptive resistance to AZA/VEN. The primary objective is to prospectively validate an ex vivo drug sensitivity testing (DST) assay as predictor of primary resistance to first-line AZA/VEN in 100 unfit AML patients. The study will also explore whether newer DST assays with enhanced niche mimicry can improve on the standard assay. By serially interrogating the short-term fate of both leukemic and immune cells upon AZA/VEN exposure in patients primed towards refractoriness, transient or prolonged remission, the aim is to dissect the cell-intrinsic and immune-mediated mechanisms of primary versus adaptive resistance. A parallel flow cytometry study will interrogate the role of senescence in AZA/VEN activity. These translational studies will be mirrored by experiments in a transplantable AML model derived from syngeneic mice harboring the age-related Tet2-/- leukemia-predisposing genotype. Lineage tracing single-cell experiments will backtrack AZA/VEN resistance to determine whether it is driven by selection or adaptation. The actionable stress sensor Pml will be invalidated in the same model to determine whether Pml-driven senescence contributes to AZA/VEN anti-leukemic activity in vivo. The project will pave the way to the clinical implementation of functional precision oncology in a high-risk malignancy. By simultaneously interrogating cell-intrinsic and immune-mediated drug resistance in vivo in a prospective patient cohort mirrored by controlled mice experiments, the project will provide a framework for the integrative analysis of drug resistance in cancers.
The goal of this clinical trial is to estimate the rate (probability) of complete remission or complete remission with incomplete count recovery (CR/CRi) with negative MRD after induction I and II, event-free survival (EFS), and cumulative incidence (probability) of relapse (CIR), in patients receiving molecular/precision medicine and MRD-driven remission inductions, and to assess secondarily if there is an improvement over the AML2018 protocol.
Chidamide in combination with venetoclax and azacitidine (VAC) were expected to improve remission rate of patients following to VA regimen treatment failure.