View clinical trials related to Lymphoma, Non-Hodgkin.
Filter by:Nowadays, therapy with monoclonal antibodies is considered to be a standard treatment that increases the rate of remissions and the overall survival in patients with follicular lymphoma. Nevertheless there are an important number of patients who do not benefit from this therapy. A way to improve the efficiency of monoclonal antibodies therapy could be to improve the activity of the effector arm of the immune system. A strategy that has been proposed to obtain this improvement is the utilization of lymphocyte activated killer (LAK) cells. In addition, the combination of LAK cells with monoclonal antibodies might obtain an additive effect across the stimulation of the antibody dependent cellular cytotoxicity (ADCC)activity. The present clinical assay proposes to study the feasibility, safety and effectiveness of treatment with autologous effector cells expanded ex vivo associated with a standard maintenance treatment with rituximab in patients with follicular lymphoma in remission after first-line treatment. In addition, we plan to analyse various biological parameters that can predict the susceptibility of patients to treatment with rituximab. Specifically, we propose to study the polymorphisms of Fc receptor, polymorphisms related to the ability of complement activation, to study both the complement activity and peripheral blood cell subpopulations that can mediate directly or indirectly dependent antibody cytotoxic effect. We will also try to correlate any of these biological parameters with the response to treatment.
This phase I/II trial studies the side effects and best dose of genetically engineered lymphocyte therapy and to see how well it works after peripheral blood stem cell transplant (PBSCT) in treating patients with high-risk, intermediate-grade, B-cell non-Hodgkin lymphoma (NHL). Genetically engineered lymphocyte therapy may stimulate the immune system in different ways and stop cancer cells from growing. Giving rituximab together with chemotherapy before a PBSCT stops the growth of cancer cells by stopping them from dividing or killing them. Giving colony-stimulating factors, such as filgrastim (G-CSF), or plerixafor helps stem cells move from the bone marrow to the blood so they can be collected and stored. More chemotherapy or radiation therapy is given to prepare the bone marrow for the stem cell transplant. The stem cells are then returned to the patient to replace the blood-forming cells that were destroyed by the chemotherapy. Giving genetically engineered lymphocyte therapy after PBSCT may be an effective treatment for NHL.
Lenalidomide has been shown to have single agent activity in indolent Non-Hodgkin's Lymphoma. It is approved for the treatment of multiple myeloma and myelodysplastic syndrome. Rituximab is effective as a single agent and in combination with chemotherapy for indolent Non-Hodgkin's Lymphoma. The purpose of this study is to see how well giving lenalidomide together with rituximab works in treating patients with previously untreated indolent Non Hodgkin's Lymphoma. Lenalidomide will taken at 20 mg daily, days 1-21 of a 28 day cycle, to be continued until the disease progresses, unacceptable side effects or after twelve cycles if the patient is responding well. Rituximab 375 mg/m2/wk x 4 weeks will begin on Day 15 of cycle 1. After 4 cycles of therapy, if patients respond well to treatment, patients will receive a second course of Rituximab. Blood samples will be collected to assess how the immune system is functioning.
The purpose of this study is to see how a new drug, named PUH71, accumulates in the different parts of the body & inside tumors and how long PUH71 lasts in the blood, when given to study participants in tiny amounts. The results of this study will help researchers (1) plan how they will use PUH71 as an experimental new drug (at much-higher doses) for the treatment of cancer, in clinical trials; and (2) know whether PUH71 might be used as a drug for detecting tumors with scanner machines.
Whole body diffusion-weighted imaging is a functional magnetic resonance imaging technique that characterizes tissue by probing changes in water diffusion secondary to differences in the tissue microstructure. These changes in water diffusion result in differences in signal intensity on diffusion-weighted-images that are quantified with the apparent diffusion coefficient (ADC). In malignant lesions, the extravascular extracellular space (EES) will be diminished, due to the increased number of cells. This will restrict water diffusion, identified by increased signal intensity (SI) on native DWI images and low ADC. Several studies indicate the value of DWI for differentiation of benign and malignant lymph nodes, detection of tumor recurrence and for ADC-based prediction of treatment outcome in various solid tumours (Koh DM et al, Am J Roentgenol 2007). Patients with a new diagnosis of Hodgkin or Non-Hodgkin Lymphoma (only diffuse large B-cell lymphoma, follicular lymphoma, mantle cell lymphoma and PTLD) will be included in the study. These patients will receive a WB-DWI scan before treatment, once or twice during treatment (depending on the type of lymphoma) and after the completion of the treatment. The MRI scan will be performed on a 3 Tesla-MRI system without contrast administration and without exposing the patient to radiation. Whole body diffusion-weighted images will be prospectively interpreted by two experienced radiologists, blinded to all clinical and imaging data. Findings will be correlated to FDG-18F-2-fluoro-2-deoxy-D-glucose fluorodeoxyglucose , biopsies performed in clinical routine (bone marrow always - soft tissue lesions if indicated) and imaging follow-up. The purpose of this study is: - to evaluate Whole body diffusion-weighted imaging for staging of lymphoma - to evaluate Whole body diffusion-weighted imaging as an early predictive biomarker for treatment outcome - to evaluate Whole body diffusion-weighted imaging for differentiating residual tumor from post therapy changes
The body has different ways of fighting infection and disease. No single way seems perfect for fighting cancer. This research study combines two different ways of fighting disease: antibodies and T cells. Antibodies are proteins the protect the body from diseases caused by germs or toxic substances. They work by binding those germs or substances, which stops them from growing and causing bad effects. T cells, also called T lymphocytes, are special infection-fighting blood cells that can kill other cells, including tumor cells or cells that are infected with germs. Both antibodies and T cells have been used to treat patients with cancers: they both have been shown promise, but have not been strong enough to cure most patients. This study combines the two methods. We have found from previous research that we can put a new gene into T cells that will make them recognize cancer cells and kill them. We now want to see if we can attach a new gene to T cells that will help them do a better job at recognizing and killing lymphoma cells. The new gene we will put in T cells makes an antibody called anti-CD30. The antibody alone has not been strong enough to cure most patients. For this study, the anti-CD30 antibody has been changed so that instead of floating free in the blood it is now joined to the T cells. When an antibody is joined to a T cell in this way it is called a chimeric receptor. These chimeric receptor-T cells seem to kill some of the tumor, but they don't last very long and so their chances of fighting the cancer are unknown. We have found that T cells that are also trained to recognize the EBV virus (that causes infectious mononucleosis) can stay in the blood stream for many years. These are called EBV specific Cytotoxic T Lymphocytes. By joining the anti-CD30 antibody to the EBV CTLs, we believe that we will also be able to make a cell that can last a long time in the body and recognize and kill lymphoma cells. We call the final cells CD30 chimeric receptor EBV CTLs. T We hope that these new cells may be able to work longer and target and kill lymphoma cells. However, we do not know that yet.
This partially randomized phase III trial studies the side effects of different combinations of risk-adapted chemotherapy regimens and how well they work in treating younger patients with newly diagnosed standard-risk acute lymphoblastic leukemia or B-lineage lymphoblastic lymphoma that is found only in the tissue or organ where it began (localized). Drugs used in chemotherapy work in different ways to stop the growth of cancer cells, either by killing the cells, by stopping them from dividing, or by stopping them from spreading. Giving more than one drug (combination chemotherapy), giving the drugs in different doses, and giving the drugs in different combinations may kill more cancer cells.
Relapse remains a principle cause of treatment failure for patients with aggressive lymphoma after autologous transplantation. Non-myeloablative allogeneic transplantation allows patients to receive an infusion of donor cells in an attempt to induce a graft versus lymphoma effect. This study will assess the feasibility, safety and efficacy of the combination of autologous stem cell transplantation followed by non-myeloablative transplantation for patients with poor-risk aggressive lymphoma.
The study hypotheses is that the introduction of dose escalated treosulfan, in substitution to busulfan or melphalan, will reduce toxicity after allogeneic transplantation while improving disease eradication in patients with lymphoid malignancies not eligible for standard transplantation.
The goal of this multi-center Phase II study is to add bortezomib to the highly active regimen of bendamustine and rituximab. In this study, bortezomib will be administered on a weekly schedule (Days 1, 8, 15) and will be added to bendamustine/rituximab given in 4-week cycles. This combination uses the standard bendamustine dosing schedule, and is more convenient than the 5-week regimen of these 3 drugs currently being studied.