Active clinical trials for "Leukemia, Myeloid, Acute"

We will focus on the prognostic value of CD318 in acute myeloid leukemia patients at Assiut University Hospital

Acute Core Binding Factor leukemias represent a specific category of acute myeloid leukemias that share prognostic factors, a specific mutational profile, and a favorable response to chemotherapy. Their management now follows the reference pattern from the French trial CBF-2006 closed to inclusions since November 2010. This includes intensive chemotherapy and intensification by allogeneic marrow transplant depending on the residual disease measured by RT qPCR . These leukemias have not been the subject of multicenter clinical trials since that date. The results of this treatment regimen need to be evaluated. Known prognostic factors such as signaling mutations, clonal interference or residual disease follow-up (MRD) will be analyzed and updated in this recent cohort. The interaction between residual disease and mutational profile will be evaluated on the prognosis. Treatment with gemtuzumab-ozogamycin and first-line allogeneic transplantation will be investigated, depending on prognostic factors including associated mutations and residual disease. The course and early treatment of molecular relapses will be analyzed. The treatment and prognosis of cytological relapses will be described with in particular the role of tyrosine kinase inhibitors and therapeutic intensification.

The most reliable prognostic marker of acute myeloid leukemia(AML) is cytogenetics by karyotyping. According to cytogenetic results, the patients with AML are classified as better, intermediate and poor prognosis groups. The normal karyotype AML was reported in about 50% of all AML and classified as intermediate risk group. However, the patients with normal karyotype AML showed various prognosis. Therefore, the further studies about subgroup analysis of normal karyotype AML are needed. Recently, the understandings of human genome polypmorphism using SNP array have been accumulated. However, the advanced researches for clinical application are not enough. The study design is a retrospective and single-center study. The patients with normal karyotyping AML who were diagnosed from 1994 to 2008 at Samsung Medical Center (South Korea) will be enrolled. The stored bone marrow samples of enrolled patients are used for genome wide scanning by SNP array. The purpose of present study is to develop predictive pharmacogenemic biomarkers model associated wit clinical outcomes including efficacy and toxicity in patients with AML with normal karyotype treated with chemotherapy using pharmacogenetic SNP array. And secondly, to develop enrichment clinical trial based on predictive pharmacogenomic model.

The purpose of this study is to elucidate the role of RUNX1 in Acute Myeloid Leukemia (AML), in particular, the transcriptional regulation of genes by mutated forms of this protein. This research will study the effect of mutations found in AML patients

Myelodysplastic syndromes (MDS) are frequent diseases in elderly patients (median age: 71 years). IPSS classification defines low risk (Low and Intermediate 1), and high risk (Intermediate 2 and High) MDS. High-risk MDS (MDS-HR) have a high risk of transformation into acute leukemia with multilineage dysplasia (AML-DML). The success of Azacitidine has been mainly achieved through a rigorous empirical and clinical research, but the molecular mechanisms by which this molecule exerts its effects remain poorly characterized. The primary mode of action of Azacytidine is through DNA demethylation, and integration in to mRNA that favor traduction inhibition. The impact of this molecule on various cell death programs involved in the elimination of leukemic cells : apoptosis and autophagy is currently poorly known. The research program and clinical studies we proposed focus on two major aspects: - Main objective: Molecular mechanism of action and resistance to Azacitidine: Role of apoptosis versus autophagy. - Secondary Objective: Reversion of Azacytidine resistance using different drugs targeting apoptosis and/or autophagy. Our laboratory has identified new molecules to selectively induce different types of cell death (apoptosis or autophagy).

The main objective of this observational survey is to estimate the incidence, the typology, and the evolution of patients with acute myelobalstic leukemia, aged more than 60 years old. In this age group (aged more than 60y), three groups of patients with very different response rates and late outcome can be delineated with specific standard chemotherapy.

Whether Idarubicin can overcomes multidrug resistant 1 induced chemoresistance with higher induction remission rate than daunorubicin in de novo acute myeloid leukemia patients.Whether induction therapy with IA regimen has a higher remission quality with AML patients than that of DA regimen in high MDR1 expression AML patients.

Prospective multicenter, open-lab el, observational, single arm study of decitabine. Subjects will be elderly patients with newly diagnosed, treatment-naïve AML who are unfit to receive and not candidate for intensive induction chemotherapy (iIC)

The purpose of this project is to develop a process to identify highly personalized antigens that are uniquely expressed by the patient's own leukemia cells that can be used for cellular immune therapy.

The long-term efficacy of chemotherapy in patients with acute myeloid leukemia (AML) has been significantly improved in recent years. The combination of anthracycline plus cytarabine (Ara-C) has been a standard induction regimen for patients with AML. However, the optimal consolidation therapy after induction chemotherapy has not reached a consensus. The FLAG regimen consisting of fludarabine and high-dose cytarabine combined with G-CSF which is one of the first-line consolidation treatment options for relapsed and refractory AML. This study conducted a retrospective analysis of the intensive treatment of AML with the FLAG regimen from January 2007 to May 2018 in our hospital to evaluate the efficacy of the FLAG regimen. To provide the basis for the choice and timing of treatment for patients with AML treated with the FLAG regimen.