View clinical trials related to Acute Myeloid Leukemia.
Filter by:This is a unique dose-escalation trial that will titrate doses of umbilical cord blood (UCB) Treg and CD3+ Teff cells with the goal of infusing as many CD3+ Teff cells as possible without conferring grade II-IV acute graft-versus-host disease (GVHD). In this study, the investigators propose to add UCB Treg and UCB CD3+ Teff cells to the two TCD UCB donor units with the goal of transplanting as many CD3+ Teff cells as possible without reintroducing risk of acute GVHD. The investigators hypothesize that Treg will permit the reintroduction of CD3+ Teff cells that will provide a bridge while awaiting HSC T cell recovery long term. The co-infusion of Treg will prevent GVHD without the need for prolonged pharmacologic immunosuppression.
The study aims at determining the feasibility of using maintenance Decitabine therapy following remission induction and consolidation in elderly Acute Myeloid Leukemia patients who are fit for aggressive therapy. Primary: Safety and tolerability of the decitabine regimen in the post remission state. Secondary: 1. Disease-free survival - To determine the one-year disease-free survival in elderly patients with acute myeloid leukemia (AML) in complete remission treated with Decitabine as post-consolidation maintenance therapy. 2. Overall survival
Evaluation of efficacy of autologous hematopoietic cell transplantation (HCT) with core-binding factor (CBF) positive acute myeloid leukemia (AML) in the first CR (CR1).
Acute leukemias are commonly seen in elderly and have no effective therapy. In recent years, small molecule inhibitors have shown a tremendous promise in cancer treatment such as chronic myeloid leukemia and lung cancer. Thus, in this proposal, we intend to use our novel patented "indole" compound to conjugated with hydroxamic acid in histone deacetylases inhibitor, suberoylanilide hydroxamic acid and further modify its structure to generate novel small-molecule anticancer compounds. By screening acute leukemic cell lines, we will look for compounds that have shown potential for future drug development. In our preliminary studies, we have identified a novel compound, MPT0E001, to have marked growth inhibitory activity, induce apoptosis and downregulate c-Myc protein level. We intend to use MPT0E001 as a basis to develop novel compounds and test them in multiple leukemic cell lines and primary leukemia samples (Specific aim 1) and identify the mechanisms for downregulation of c-Myc and other pathways such as NF-kappaB and Akt (Specific aim 2). Once we have identified the lead compounds, we will use murine model to assess the acute toxicity profiles in different dose ranges and examine the effects of blood counts and vital organs. After toxicity study, we will test the lead compounds using in vivo xenogenic murine model using both cell lines and primary leukemia. Using this approach, we hope to develop novel compounds that are able to be used in future leukemic therapy.
FLT3 overexpression in acute myeloid leukemia (AML) is often caused by mutations in this gene. These mutations cause constitutive phosphorylation of FLT3 proteins leading to increased proliferation and survival, decreased apoptosis and resistance to chemotherapeutic agents in AML cells. There are two major types of FLT3 mutations- internal tandem duplication (ITD) and point mutation at 835th amino residue. AMLs with FLT3 mutations have worse prognosis and are often resistant to conventional chemotherapy. Several small molecule compounds targeting FLT3 have been in the market or in clinical trials. Therefore, identification of these mutations at the time of diagnosis will provide a better prognostic prediction, might guide the treatment selection and follow-up strategies. In this study, the investigators will develop a sensitive molecular assay to detect FLT3 mutations for future clinical application. The investigators will collect 100 AML samples with at least 20 samples with known FLT3 mutations. The investigators will compare this assay with commonly used methods and standardize the procedure to meet the requirement of clinical pathology laboratory with reasonable cost.
The study will be conducted as a single center Phase I/II study to evaluate the safety of administering Plerixafor administered as part of a myeloablative preparative regimen (Institutional Protocol:Fludarabine 50mg/m2/da x 4 days, Busulfan 3.2mg/kg/day x 4 days, TBI 400cGy in divided fractions) for stem cell transplant recipients with AML and to determine whether or not residual leukemic stem cells can be mobilized. Three patients will be enrolled into each of 4 sequential cohorts. Patients in the first cohort will receive 1 dose of Plerixafor (240mcg/kg sc) prior to administration of the first dose of Fludarabine and Busulfan. If tolerated it is planned to escalate the number of Plerixafor doses in the subsequent cohorts to 2. 3. and 4 to be administered before the respective 2nd, 3rd, and 4th dose of chemotherapy.
This phase I clinical trial is studies the side effects and best dose of giving veliparib together with temozolomide in treating patients with acute leukemia. Veliparib may stop the growth of cancer cells by blocking some of the enzymes needed for cell growth. Drugs used in chemotherapy, such as temozolomide, work in different ways to stop the growth of cancer cells, either by killing the cells or by stopping them from dividing. Giving veliparib together with temozolomide may kill more cancer cells.
The purpose of this study is to assess the response rate at 6 months in Myelodysplastic Syndrome (MDS) patients, Chronic Myelomonocytic Leukaemia (CMML-2) patients, and Acute Myeloid Leukaemia (AML) patients with up to 30% bone marrow blasts, treated with low-dose decitabine who have previously failed therapy with 5-azacitidine.
The purpose of this study is to determine the tolerated dose of the combination of decitabine and midostaurin as induction (first cycle of chemotherapy) and consolidation (additional chemotherapy once a patient goes into remission) in people greater than 60 years with newly diagnosed AML or adult patients with relapsed/refractory disease.
The investigators' objective is to assess the efficacy of the combined treatment with enalapril and carvedilol in the prevention of left ventricular systolic dysfunction in patients with hematological malignancies submitted to intensive chemotherapy with potential cardiotoxicity. The hypothesis is that these drugs administered during chemotherapy may prevent left ventricular systolic dysfunction.