Active clinical trials for "Lymphoma"

LEE011 is a new oral drug designed to inhibit the activity of an enzyme known as CDK4/6. CDK4/6 is involved in the process that allows both normal and cancer cells to divide and multiply. Cancer cells are often driven to divide and multiply by abnormalities that increase the activity of CDK4. Hence there is hope that blocking the activity of CDK4 may slow the growth of some cancers. LEE011 has shown anti-cancer activity in several different tumor models in animals. Because CDK4 is important in both normal and cancerous cells, LEE011 is expected to decrease the ability of the bone marrow to make white blood cells, platelets, and red blood cells. Although these effects are expected to be reversible, they can increase the risk of infection, bleeding and fatigue. The primary purpose of this study is to find the highest dose of LEE011 that can be safely given to adult patients with advanced solid tumors or lymphomas for which no further effective standard treatment is available. It will provide information about the side effects that may occur following treatment. The study will also possibly provide early evidence for LEE011's anti-tumor activity.

This is a Phase 2 study to assess the efficacy of SB1518 in the treatment of patients with advanced lymphoid malignancies including Hodgkin Lymphoma, Mantle Cell Lymphoma and Indolent Lymphoma (follicular lymphoma, lymphoplasmacytic lymphoma, marginal zone lymphoma and small lymphocytic lymphoma).

Primary Objective: - To determine the maximum tolerated dose (MTD) and recommended Phase 2 dose (RP2D) for SAR245409 when administered in combination with rituximab or bendamustine plus rituximab Secondary Objectives: To determine the safety and tolerability of SAR245409 in combination with rituximab or bendamustine plus rituximab in subjects with indolent Hon-Hodgkin Lymphoma (iNHL) Mantle Cell Lymphoma (MCL) or Chronic Lymphocytic Leukemia (CLL) To determine the pharmacokinetics (PK) of SAR245409, bendamustine and rituximab when used in combination in subjects with iNHL, MCL or CLL To determine the pharmacodynamic (PD) effects of SAR245409 in combination with rituximab or bendamustine plus rituximab in subjects with iNHL, MCL or CLL To determine the antitumor activity of SAR245409 in combination with rituximab or bendamustine plus rituximab in subjects with iNHL, MCL or CLL

This multicenter, randomized, open-label, parallel-group study will evaluate the efficacy and safety of subcutaneously administered rituximab in comparison with observation only as maintenance therapy in participants with relapsed or refractory indolent Non-Hodgkin's lymphoma (NHL). All participants will receive induction therapy with rituximab (375 milligrams per square meter [mg/m^2] intravenously [IV] in Cycle 1, then 1400 mg subcutaneous [SC] every 3-4 weeks) plus standard chemotherapy for 6-8 months; followed by 24 months of maintenance I period with rituximab (1400 mg SC every 8 weeks). Participants completing therapy and showing partial or complete response will be randomized to receive either rituximab (1400 mg SC every 8 weeks) or observation with no treatment during maintenance II period and will be followed for at least 15 months. Anticipated time on study treatment is until disease progression, unacceptable toxicity or end of study, whichever occurs first.

This is an open-label, Phase 1, dose escalation study of oral ARQ 092 administered to subjects with advanced solid tumors and recurrent malignant lymphoma. The study is designed to explore the safety, tolerability, pharmacokinetics, and pharmacodynamics of ARQ 092 and to define a recommended Phase 2 dose of ARQ 092.

It is expected that addition of anti-CD20 antibody - ofatumumab would enhance the activity of the etoposide+ifosphamide with mesna+cytarabine+methotrexate+lenograstim or filgrastim (IVAC) regimen. This study is planned to determine the efficacy and safety of ofatumumab in combination with IVAC chemotherapy in patients with CD20 positive diffuse large B cell lymphoma progressing or relapsed after prior R-CHOP chemotherapy not suitable for Autologous Stem Cell Transplant (ASCT).

Stem cells can be transplanted from a healthy donor to a patient to combat blood cancers and other disorders. This process is called stem cell transplantation. Stem cells normally live in the bone marrow. A bone marrow transplantation (BMT) is when the bone marrow is directly transplanted into a patient. However, stem cells can also be stimulated to move from the bone marrow to the blood where they can be collected, a process is called mobilization. When these stem cells are transplanted it is called peripheral blood stem cell transplantation (PBSCT). Both stem cell sources are used for different reasons, but PBSCT is much more common. There is considerable debate as to which stem cell source, BMT or PBSCT, is optimal. There are differences between the two sources in important transplant outcomes. The stem cell product that is transplanted, also called the stem cell graft, contains more than just stem cells. Results from studies suggest that the variation in the cells with grafts may account for the variation in outcomes. Preliminary data from a recent study conducted by the Canadian Blood and Bone Marrow Transplant Group has associated relative frequencies of particular cell populations with leukemic relapse and another important outcome called graft versus host disease (GVHD). While the later essentially equates to a failed transplant, the former is the most common and devastating complication of stem cell transplantation. The only drug used to mobilize stem cells into the blood of health donors for collection is G-CSF. However there is a new mobilization drug recently approved called plerixafor. This drug is able to mobilize stem cells when G-CSF has failed and pre-clinical studies suggest that it may produce a superior stem cell graft to G-CSF alone. There is little information available, besides safety and efficacy data, about the effects that plerixafor has on the stem cell graft of normal healthy donors. This study will compare the stem cell graft in normal healthy donors following plerixafor mobilization versus plerixafor and G-CSF mobilization. Specifically, they will look at the cell populations that have been previously correlated with important transplantation outcomes like relapse and GVHD. The investigators suspect that the stem cell graft mobilized by plerixafor and G-CSF will provide a superior graft to that mobilized by plerixafor alone.

The purpose of this study is 2-fold: initially, in the dose escalation phase, the goal is to determine the safety profile of orally administered brigatinib, including: the maximum tolerated dose (MTD), dose limiting toxicities (DLTs), recommended phase 2 dose (RP2D), and pharmacokinetic (PK) profile. Then, once the RP2D is established, an expansion phase will assess the preliminary anti-tumor activity of brigatinib, both in non-small cell lung cancer (NSCLC) with ALK gene rearrangement (including participants with active brain metastases) or mutated EGFR, and in other cancers with abnormal targets against which brigatinib is active.

The probability to achieve CR with R-chemotherapy in patients failing a rituximab containing first line regimen is quite low, in particular in cases with non GCB profile. The bioCORAL trial suggest that ABC subset have a dismal outcome whichever the induction treatment. Thus it can be argued the addition of new molecule to the RDHAP regimen could be of value. Bortezomib appears the best candidate in this setting as ABC subtypes constitutively express NFkb, which is the target of bortezomib itself. Data from the literature suggest an encouraging activity of R-chemo+ bortezomib in non GCB-derived DLBCL, although in small series. Thus, the addition of bortezomib is here justified by the need to circumvent constitutional resistance to chemotherapy. Published experience of the association between bortezomib and cytarabine are also encouraging with acceptable cumulative toxicity.

This phase I trial studies the side effects and best dose of silicon phthalocyanine 4 and photodynamic therapy in treating patients with stage IA-IIA cutaneous T-cell non-Hodgkin lymphoma. Photodynamic therapy (PDT) uses a drug, silicon phthalocyanine 4, that becomes active when it is exposed to a certain kind of light. When the drug is active, cancer cells are killed. This may be effective against cutaneous T-cell non-Hodgkin lymphoma. Funding Source - FDA OOPD