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Leukemia clinical trials

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NCT ID: NCT01919619 Completed - Lymphoma Clinical Trials

Lenalidomide and Ipilimumab After Stem Cell Transplant in Treating Patients With Hematologic or Lymphoid Malignancies

Start date: November 4, 2013
Phase: Phase 2
Study type: Interventional

This pilot clinical trial studies the side effects of lenalidomide and ipilimumab after stem cell transplant in treating patients with hematologic or lymphoid malignancies. Biological therapies, such as lenalidomide, may stimulate or suppress the immune system in different ways and stop cancer cells from growing. Immunotherapy with monoclonal antibodies, such as ipilimumab, may help the body's immune system attack the cancer, and may interfere with the ability of tumor cells to grow and spread. Giving lenalidomide with ipilimumab may be a better treatment for hematologic or lymphoid malignancies.

NCT ID: NCT01916785 Completed - Clinical trials for Chronic Myelogenous Leukemia, BCR/ABL Positive

OPTIM DASATINIB (Optimized Tyrosine Kinase Inhibitors Monotherapy)

OPTIM-DASA
Start date: May 2009
Phase: Phase 2
Study type: Interventional

This protocol is a multicentric interventional phase II study from the French CML Intergroup (FILMC). The core of the protocol is to explore the efficacy and safety of an optimization strategy consisting in the modulation of the dasatinib daily dose according to the results of repeated plasmatic levels of dasatinib. The objective of this strategy is to improve the overall results of the treatment of early CP-CML in order to avoid the development of resistance and BCR-ABL tyrosine kinase mutations. The study will be conducted in selected FILMC and Canadian centers. The study is sponsored by the Hôpitaux de Versailles and supported by Bristol-Myers Squibb. The dasatinib treatment will be provided by Bristol-Myers Squibb until marketing authorization is granted in that indication.

NCT ID: NCT01915992 Recruiting - Leukemia Clinical Trials

Natural Killer Cells Functions, Tumoral Escape to Immune System and Regulation of Natural Cytotoxixity Receptors in Haematological Malignancies

Start date: February 2013
Phase: N/A
Study type: Interventional

The NK cells participate in the innate immunity against infectious agents or transformed cells that are recognized as "no self" by the absent, weak or abnormal expression of human leukocyte antigen (HLA) class I molecules. According to the "missing self hypothesis", a negative signal is delivered to NK cells when their inhibitory receptors are engaged by the specific HLA class I molecules. NK activation requires a positive signal delivered by the engagement of activating receptors, more particularly of the "Natural cytotoxicity receptors" or NCRs who are directly involved in the natural cytotoxicity of Natural Killer. The activating receptors include NKp46, NKp44 and NKp30, also called NCR 1, 2 and 3 respectively. NKp46 and NKp30 are constitutively expressed on the surface of the NK, the expression of NKp44 is observed only after activation of cells NK. NK cells from most (80%) healthy donors express a high quantity of NCR on their surface, corresponding to the NCRbright phenotype while only 20 % present the NCRdull phenotype. In sharp contrast, most patients (80%) having leukaemia have the NCRdull while only 20 % patients have the NCRbright phenotype. The culture of NK from healthy donors ( NCRbright) with leukaemic cells result in decreased expression of the NKp30 while there is no difference on expression if these same NK are cultivated with cells from healthy donors. Moreover, study of AML patients showed that the NCRdull phenotype was acquired during leukemia development because it was observed its complete (for NKp46) or partial (for NKp30) reversibility in patients achieving complete remission (CR). Reversibility of the NCRdull phenotype after CR suggested that leukemia cells might be involved in NCR down-regulation. In line with these observations, we aim to study the mechanism of NCR down-regulation by cultivating NK NCRbright from healthy donors with leukaemic cells or healthy haematopoietic cells, in order to observe the appearance of the NCRdull phenotype and verify by qPCR if this down-regulation is transcriptionnal. If this hypothesis is be verified, we will study the regulation of NCR by focusing on the implication of genes NCR transcription factors via bio-informatic analysis of putative transcription factors fixation sequences in the promoters of these genes, followed by the verification of the capacity of identified sequences to bind transcription factors. Ultimately, we will verify the real implications of these transcription factors by studying the effect of their silencing by RNA interference experiments.

NCT ID: NCT01914484 Completed - Clinical trials for Chronic Phase Chronic Myeloid Leukemia

Phase I/II Study of Nilotinib/Ruxolitinb Therapy for TKI Resistant Ph-Leukemia

Start date: August 1, 2013
Phase: Phase 1/Phase 2
Study type: Interventional

This is the study to test combination regimen of Nilotinib and Ruxolitinib therapy for the treatment of patients with Philadelphia positive chronic myeloid leukemia (CML) or acute lymphoblastic leukemia (ALL) who is resistant to multiple tyrosine kinase inhibitor therapies with BCR-ABL kinase inhibition activity. Ruxolitinib is a tyrosine kinase inhibitor blocking alternative pathway independent of BCR-ABL mediated pathway, thus having a potential to overcome tyrosine kinase inhibitor resistance in Philadelphia positive CML or ALL patients. Phase I study will be conducted to define a recommended phase II dose (RPTD) and phase II study will examine the hypothesis that combinational approach will increase response rate of resistant CML/ALL patients, thus evaluating efficacy of the combination regimen.

NCT ID: NCT01913093 Completed - Clinical trials for Childhood Leukemia Survivors

N-PhenoGENICS: Neurocognitive-Phenome, Genome, Epigenome and Nutriome In Childhood Leukemia Survivors

NPG
Start date: July 2013
Phase:
Study type: Observational

To find possible therapeutic targets to help prevent long-term brain and behavioural side effects in survivors of childhood leukemia that may have been caused by chemotherapy (Treatment-Related late Adverse Neuro-Cognitive Effects: TRANCE). The study hypothesis is that genetic variations of the elements in the folate-related cycles and methotrexate disposition networks are associated with the deficit phenotype (TRANCE) of childhood leukemia survivors.

NCT ID: NCT01912274 Completed - Clinical trials for Acute Myeloid Leukemia

Safety and Efficacy Study of Pracinostat With Azacitadine in Elderly Patients With Newly Diagnosed Acute Myeloid Leukemia (AML)

Start date: December 24, 2013
Phase: Phase 2
Study type: Interventional

The purpose of this study is to determine the safety and effectiveness of pracinostat when combined with azacitadine for patients who are 65 years of age or older and have Acute Myelogenous Leukemia (AML)

NCT ID: NCT01910623 Completed - Clinical trials for Acute Promyelocytic Leukemia

Long-Term Quality of Life in Patients With Acute Promyelocytic Leukemia

QOL-APL0512
Start date: February 2013
Phase: N/A
Study type: Observational

This study will focus on acute promyelocytic leukemia patients who have been diagnosed more than 5 years ago and their present quality of life. The possible late effects of cancer treatment can include several issues and, thus, there has been an increasing interest worldwide in studying the long-term impact of these in patients' life.

NCT ID: NCT01910428 Terminated - Clinical trials for Acute Lymphoblastic Leukemia

L-asparaginase Encapsulated in Red Blood Cells (Eryaspase) for Treatment of Adult Patients With ALL or LBL

Start date: October 2013
Phase: Phase 1
Study type: Interventional

Asparaginase (Asp) is used during the induction phase of ALL treatment for children and young adults. Its efficacy is counterbalanced by its toxicity, mainly in patients 40 years or older. The efficacy rate in older adult population is lower than for children or young adults. A recent review on outcomes in older adults with ALL pointed out that there were significantly more drug reductions, omissions or delays in the older group as compared to younger adults and that asparaginase was the drug most commonly omitted. The investigational product ERYASPASE is a dispersion for infusion of homologous red blood cells (RBC) encapsulating E. coli L-asparaginase. A previous European phase I/II clinical study in children and adults (<55 yo) at first relapse of ALL was conducted to determine the optimal dose of homologous RBC encapsulating native E. coli Asp (GRASPA®) in 24 patients with relapsed ALL. The activity and safety profiles of 3 doses of GRASPA® (50, 100 and 150 IU/kg) in combination with standard chemotherapy were compared to free native Asp. The global safety profile is also improved, reducing hypersensitivity, liver toxicity and coagulation disorders. Study showed that a single dose of GRASPA® 150 IU/kg induced a depletion in plasmatic asparagine for 18.6 days, i.e. similar to that obtained with 8 injections of 10,000 IU/m² of free native Asp. A reduction in the incidence and severity of the allergic reactions and coagulation disorders were observed with GRASPA® (Domenech 2011). A French phase II study designed to determine the maximum tolerated dose of GRASPA® in combination with a polychemotherapy regimen in ALL patients older than 55 yo at first diagnosis has been performed, and showed that both 100 and 150 IU/kg doses fulfilled the predefined criteria for efficacy and tolerability but the better profile of 100 IU/kg dose was considered the optimal dose in this setting. A phase II/III trial in adult and children patients with relapsed ALL is currently ongoing. Based on these results, the combination of ERYASPASE with the CALGB chemotherapy regimen appears to be an attractive combination for the treatment of adults patients with ALL/LBL.

NCT ID: NCT01910012 Completed - Clinical trials for Acute Myeloid Leukemia

PH 2 ADI-PEG 20 Acute Myeloid Leukemia

Start date: January 6, 2015
Phase: Phase 2
Study type: Interventional

Certain cancers require the amino acid arginine. Arginine deiminase (ADI) is an enzyme from microbes that degrade arginine. ADI has been formulated with polyethylene glycol and has been used to treat patients that have cancers that require arginine. In this study, the investigators will evaluate the response rate, as determined by the revised International Working Group recommendations.

NCT ID: NCT01908387 Terminated - Multiple Myeloma Clinical Trials

Phase 1 Study of CC-486 in Japanese Subjects With Hematological Neoplasms

Start date: July 2013
Phase: Phase 1
Study type: Interventional

To identify the maximum tolerated dose (MTD) of oral azacitidine on different treatment schedules in Japanese subjects with hematological neoplasms