Active clinical trials for "Leukemia, Myeloid"

To assess the incidence of IDH1 and IDH2 mutations in adult AML patients, and to explore their associations with the patients' clinical, cytogenetic, and molecular characteristics as well as with treatment response and outcome. To delineate the similarities and distinctions among mutations at IDH1-R132, IDH2-R140 and IDH2-R172 in AML, both clinically and molecularly (including cytogenetics, immunophenotyping, mutation co-occurrence patterns). The results can be references for future selection of targeted therapy (targeting IDH mutant proteins).

This will be a translational study without any therapeutic intervention, for the purpose of analyzing the diagnostic and molecular results / characterization of adult patients with AML, regardless of the treatment they receive. Newly diagnosed or relapsed/resistant AML patients will be included.

Create a network of institutions in developing countries that will perform AML diagnosis, risk classification, treatment, supportive care and follow-up evaluation according to a common protocol and will register data using common clinical research forms (CRFs) in a single database and available on the internet.

The objective of this study is to test the scale structure, reliability, validity and responsiveness to change of the QLQ-CML24 in conjuction with the QLQ-C30 for patients diagnosed with CML, and to investigate longitudinal relationship between satisfaction with information provision and QoL outcomes.

This is a multicenter, prospective, translational study, to evaluate the immunogenic profile of AML cases according to immune checkpoint molecule expression.

To assess overall survival of AML patient. To measure rate of disease free survival. rate of non relapse mortality. rate of complete remission . percentage of refractory disease. percentage of relapsed disease.

Hyper-leukocytosis > 50.109/L is observed in 15% of acute myeloid leukemia (AML). Level of hyper-leukocytosis is linearly associated with the incidence of life threatening complications that lead to the early death in 25% of these patients. The HEAL project is a prospective, uni-centric, observational study that plans to include a cohort of 50 patients presenting de novo AML with hyper-leukocytosis (HL) (> 50.109/L) and 10 controls. The aim of the study is to describe the relative proportion of various hemostasis components disturbances, endothelium alterations, platelet dysfunction and to calculate cumulative incidence of hemorrhagic and thrombotic complications as well as overall survival of patients presenting with HL AML.

The purposes of this study are to investigate the patterns of BCR-ABL mutations in CML and Ph positive ALL patients with imatinib resistance during the year of 2001-2009 in Asian institutes.

Bone marrow consists of a complex hematopoietic cellular component.When the blood progenitor cells differentiate to mature cells, they will exit unassisted to peripheral blood. On the other hand, the immature cells trapped by marrow-blood barrier. However, malignant transformation of the hematopoietic progenitor cells in AML and CML results in a blockade of their ability to terminally differentiate, causing a rapid accumulation of immature cells.Chemokines have been shown to direct the movement of cells between intravascular and extravascular compartments.The CXC chemokine CXCL12, the ligand of CXCR4, activates distinct signaling pathways that may mediate cell migration.In the preliminary research, we analyze the CXCR4 expression and the chemotactic response of CXCL12 and peripheral plasma in six leukemia cell lines (HL-60, HL-CZ, K562, U937, Raji and Jurkat) and found that three categories among them could be suggested: one is CXCR4 (-) and CXCL12 response (-), such as HL-CZ and K562 cells; the other is CXCR4 (+) and CXCL12 response (-), such as HL-60 and Raji cells; the rest is CXCR4 (+) and CXCL12 response (+), such as Jurkat and U937 cells. These results make us wonder that the leukemic cells could egress to PB from BM is due to destruction of homing process or the activation of mobilization process through CXCR4-CXCL12 axis dysfunction. Therefore,we will focus on evaluating the mechanism of CXCR4-CXCL12 axis dysfunction in the various leukemic cell lines and primary leukemic cells.

Detect the expression of marker CD56 and CD11b in newly diagnosed cases of adult AML. Study correlation between CD56 and CD11b expression with haematological parameters in cases of adult AML.