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Leukemia, Lymphoid clinical trials

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NCT ID: NCT00402090 Recruiting - Clinical trials for Acute Lymphoblastic Leukemia

DHPLC Determination of TPMT Polymorphisms.

Start date: April 2005
Phase: N/A
Study type: Observational

TPMT is a key enzyme in the metabolism of thiopurines. TPMT polymorphisms have been described and are associated with a decrease activity of such enzyme. Therefore, a higher risk of developing toxicity is present in patients requiring these drugs, which are indicated in acute lymphoblastic leukemia, as well as, immunosuppressors after organ transplantation. The frequency of heterozygotes polymorphisms ranges from 3 till 12 %, in different populations. Homozygous patients have a lower frequency, estimated 1 in 300 individuals. The frequency of such polymorphisms in mestizos mexican population has not been analyzed, and we considered important to determine this frequency in healthy and patients requiring thiopurines, particularly acute lymphoblastic leukemia.

NCT ID: NCT00343369 Recruiting - Leukemia Clinical Trials

Combination Chemotherapy in Treating Young Patients With Acute Lymphoblastic Leukemia

Start date: January 2003
Phase: N/A
Study type: Interventional

RATIONALE: Drugs used in chemotherapy work in different ways to stop the growth of cancer cells, either by killing the cells or by stopping them from dividing. Giving more than one drug (combination chemotherapy) may kill more cancer cells. It is not yet known which combination chemotherapy regimen is more effective in treating acute lymphoblastic leukemia. PURPOSE: This randomized phase III trial is studying different combination chemotherapy regimens to compare how well they work in treating young patients with acute lymphoblastic leukemia.

NCT ID: NCT00328237 Recruiting - Clinical trials for Acute Myeloid Leukemia

Treatment of Hematologic Malignancies With Single-Unit or Double-Unit Cord Blood Transplantation

Start date: November 2005
Phase: Phase 2
Study type: Interventional

The purpose of this study is to evaluate the incidence of neutrophil engraftment after transplantation of one or two cord blood units meeting a predetermined total minimum cell dose of 2.0 x 10 to the seventh total nucleated cell (TNC)/kg.

NCT ID: NCT00304720 Recruiting - Multiple Myeloma Clinical Trials

Tacrolimus and MMF as Post Grafting Immunosuppression After Conditioning With Flu TBI for HLA Matched Family Donor

Start date: March 2004
Phase: Phase 2
Study type: Interventional

Primary Objective: A. To determine whether stable allogeneic hematopoietic engraftment can be safely established in patients receiving a non-myeloablative allogeneic SCT from a matched sibling donor, with fludarabine and low-dose TBI, with pre- and post-transplant immunosuppression with tacrolimus and MMF. B. To evaluate the incidence of grade II-IV GVHD associated with this treatment.

NCT ID: NCT00271063 Recruiting - Clinical trials for Acute Lymphocytic Leukemia

Study of Liposomal Annamycin in Patients With Refractory or Relapsed Acute Lymphocytic Leukemia

Start date: October 2005
Phase: Phase 1/Phase 2
Study type: Interventional

This is a Phase I/II multi-center, open label, dose escalation study to identify the maximum tolerated dose (MTD) of liposomal annamycin and to evaluate the safety of liposomal annamycin in patients with refractory or relapsed acute lymphocytic leukemia.

NCT ID: NCT00222612 Recruiting - Clinical trials for Acute Lymphoblastic Leukemia

Medical Research Council (MRC) Working Party on Leukaemia in Children UK National Acute Lymphoblastic Leukaemia (ALL) Trial: UKALL 2003

Start date: October 2003
Phase: Phase 4
Study type: Interventional

A randomised trial for children with acute lymphoblastic leukemia, using the detection of minimal residual disease to define risk groups, aiming to answer the questions: 1. Can treatment be reduced without compromising efficacy in a MRD-defined low risk group? 2. Does further post-remission intensification improve outcome for a MRD-defined high risk group? 3. Measure the Quality of Life impact of the different treatment arms on the children and their families.

NCT ID: NCT00199186 Recruiting - Clinical trials for Philadelphia Positive Acute Lymphoblastic Leukemia

Study Comparing Imatinib With Chemotherapy as Induction in Elderly Patients With Philadelphia Positive Acute Lymphoblastic Leukemia (ALL)

Start date: March 2002
Phase: Phase 2
Study type: Interventional

The aims of the study are to determine whether single agent imatinib (STI571; Glivec) is more effective as up-front remission induction therapy than conventional multi-agent induction chemotherapy for elderly patients with Philadelphia positive (Ph+)ALL, whether this treatment is better tolerated, and whether subsequent combination therapy with imatinib and chemotherapy of approximately a 1 year duration is tolerable and effective with respect to maintaining remissions.

NCT ID: NCT00192673 Recruiting - Clinical trials for Acute Lymphoblastic Leukemia

Poly(Ethylene Glycol)(PEG)-Asparaginase During Two Treatment Courses

Start date: June 2005
Phase: Phase 4
Study type: Interventional

The purpose of this study is 1. to determine the correct dose for intramuscular administration 2. to compare the frequency of antibody formation after intramuscular administration of native E.coli asparaginase and PEG-asparaginase during two treatment courses in the treatment of childhood lymphoblastic leukemia

NCT ID: NCT00188084 Recruiting - Clinical trials for Adult Acute Lymphoblastic Leukemia

Description and Prognostic Evaluation of Four Biological Parameters of Blast Cells in Adult Acute Lymphoblastic Leukemia

Start date: November 2003
Phase: N/A
Study type: Observational

Adult acute lymphoblastic leukemia treatment approaches relie on risk stratification, including cytogenetics. We want to study at diagnosis several blast cells parameters on frozen samples of GRAALL protocols enrolled patients: 1. A CD45-DNA double staining analysed by flow cytometry will allow mesurement for each blastic clone of DNA ploidy, percentage of cells in S-phase, CD45 fluorescence index. 2. The proteine P16 metabolic way, involved in cell cycle regulation, will be studied by Western Blot analysis. The comparison between these parameters, and main haematological data, will be followed by a prognostic analysis, based on blast corticosensibility in vivo, chimiosensibility, complete remission, and survival. Combination of the studied parameters will allow to appreciate a clonal diversity. This will help to predict, at diagnosis, high probability of resistance to treatment.

NCT ID: NCT00155844 Recruiting - Clinical trials for Acute Lymphocytic Leukemia

Studies on the Significance of CXCR4-CXCL12 on Leukemic Cells Passing Through"Marrow-Blood Barrier"

Start date: February 2003
Phase: N/A
Study type: Observational

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.