View clinical trials related to Leukemia, Myeloid, Acute.
Filter by:Patients will receive oral SKLB1028 for 28 days as a course of treatment, and then to evaluate the side effects,tolerability and best dose for treating relapsed or refractory acute myeloid leukemia With FLT3 Mutations.
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.
We previously reported results of a prospective observational study demonstrating that early response defined as reduction in bone marrow (BM) blast counts to less than 5% of BM cells by the fifth day of induction therapy is a strong predictor of remission and overall survival (Ofran Y, et al. AJH, 2015). The long term survival benefit of early response was confirmed later on after a median follow-up for surviving patients of 53 months (range 17.5-84.5).
This study is to determine the safety and best dose of PRGN-3006 T Cells.
This phase I trial studies the side effects and best dose of TAK-243 in treating patients with acute myeloid leukemia, or myelodysplastic syndrome, or chronic myelomonocytic leukemia that has come back or that is not responding to treatment. TAK-243 may stop the growth of cancer cells by blocking some of the enzymes needed for cell growth.
Acute myeloid leukemia (AML) is a genetically heterogeneous disease and allogeneic hematopoietic stem cell transplantation (allo-HSCT) is a curative treatment option for AML except for AML-M3. Relapse remains the major cause of treatment failure after allo-HSCT. Molecular residual disease has been shown to be a strong risk factor for relapse after HSCT. In this study, the investigators will detect mutations before/after allo-HSCT by using next-generation sequencing (NGS) technique to measure residual disease and evaluate the prognostic impact of molecular residual disease in a cohort of AML participants receiving allo-HSCT.
The MAC-HAPLO-MUD trial is a randomized prospective phase III trial comparing HLA 10/10 matched unrelated donor and haploidentical allogeneic hematopoietic stem cell transplantation after myeloablative conditioning regimen in patients, age 15 years or older, with Acute Myeloid Leukemia (AML) or Acute Lymphoblastic Leukemia (ALL) or Myeloproliferative Syndrome (SMP) or Myelodysplastic Syndromes (SMD) and requiring allogeneic hematopoietic stem cell transplantation. Primary endpoint is the 1-year progression free survival without acute grade II-IV GvHD and without moderate and severe chronic GvHD.
Allogeneic hematopoietic stem cell transplantation (Allo-HSCT) is a curative option for patients with acute myeloid leukemia (AML). However, transplantation related toxicity and mortality as well as the existence of HLA identical sibling donor represent major limitations. Over the 20 past years, the development of reduced intensity conditioning (RIC) regimen and the use of alternative donors allowed extending the possibility of Allo-HSCT for AML, with decreased toxicity and mortality. This invited to propose this strategy to more advanced patients, making that AML recurrence has become one of the main issues after Allo-HSCT. Thus, to develop prophylactic and preemptive strategies to minimize disease recurrence after Allo-HSCT is now the main challenge in the field. Among cellular and/or pharmacological treatments after Allo-HSCT, donor lymphocyte infusion (DLI) is probably one of the most commonly used treatments after Allo-HSCT. Indeed, DLI were reported as a potential efficient immunotherapy more than 20 years ago for the treatment of patients with leukemia relapsing after Allo-HSCT. However, most of experiences were reported in the setting of relapse after Allo-HSCT and no prospective evaluation of prophylactic DLI is available so far. Thus no strong recommendation for the use of DLI after Allo-HSCT can be made. Our study proposal would like to assess the question of prophylactic DLI efficacy, as a proof of concept of early immune intervention after Allo-HSCT. The investigators, therefore, designed a prospective multicenter randomized trial evaluating the impact of early DLI on outcome after Allo-HSCT for AML.
High risk MDS (Myelodysplastic Syndrome) patients will be treated with SGI-110 after Allogeneic Stem Cell Transplantation in the hypothesis that SGI-110 maintenance given early after HSCT can prevent relapse without increasing non-relapse mortality translating in an improved disease-free survival.
This is a prospective,uncontrolled and multi-institution trial.The aim is to identify if using decitabine,cytarabine and ATO as the therapy of acute myeloid leukemia(AML) with p53 mutations has better relapse free survival and complete response than using decitabine and cytarabine. TP53 mutation is commonly associated with poor cancer patient prognosis yet no mutant p53 (mp53)-targeting regimen was clinically established. Particularly, p53 mutation is associated with extremely poor prognosis in myelodysplastic syndromes (MDS) and acute myeloid leukemia (AML) patients. Decitabine (DAC) is a FDA approved drug for MDS treatment. In two independent clinical trials reported recently, DNA demethylating drug DAC treatment yielded a surprisingly high rate of complete remission (CR) in mp53-harboring AML/MDS patients (Welch, NEJM, 2016; Chang, BJH, 2017). Notably, all of the mp53-expressing patients in the two clinical studies relapsed quickly. Arsenic trioxide (ATO) is a FDA approved drug for M3-AML treatment. Despite of the observed efficacy in treating non-APL patients, ATO is not yet approved for non-APL cancer treatment. ATO plays key role in regulating both wild-type p53 (wtp53) and mp53. Our published and unpublished data suggest ATO potentially hijacks nuclear iASPP-mediated STRaND pathway via exposing iASPP's RaDAR nuclear import code (Lu, Cancer Cell, 2013; Lu, Cell, 2014; Lu, Nat Rev Mol Cell Biol, 2016; Lu, unpublished). Our unpublished data also suggests a key role of ATO in regulating mp53 (Lu, The 17th International p53 Workshop, 2017). ATO is widely reported to be able to degrade and thus inhibit mp53's oncogenic function (Hamadeh, BBRC, 1999)(Liu, Blood, 2003). ATO suppressed cancer cell growth by targeting mp53 for degradation by Pirh2 degradation pathway (Yang, JBC, 2011; Yan, PLOS one, 2014); Here we explore the potential of combination of DAC and ATO in improving the mp53-harboring AML/MDS patients' relapse free survival (RFS) and the ability to thoroughly eliminate mp53 subclone. Basic researches aiming to explore the mechanisms how mp53 cells responds to DAC and/or ATO treatment and how mp53 cells develop resistance to DAC and/or ATO will be coupled. We designate trials aiming for a better treatment regimen for mp53 patients as 'PANDA-Trials'.