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RATIONALE: Giving chemotherapy (ICE) with monoclonal antibodies, such as rituximab, stops the growth of cancer cells by stopping them from dividing or by killing them and helps get better autologous stem cell product. Giving colony-stimulating factors, such as filgrastim (G-CSF), and plerixafor helps stem cells move from the patient's bone marrow to the blood so they can be collected and stored for future autologous transplant.
PURPOSE: This phase II trial is studying how well giving rituximab, ICE combination chemotherapy, and G-CSF together with plerixafor works in treating patients with non-Hodgkin lymphoma undergoing mobilization of autologous peripheral blood stem cells.
I. Determine the number of days of apheresis required to reach >= 5 x 106 CD34 cells/kg.
II. Determine the number of CD34 cells/kg collected in a maximum of 7 days if >= 5 x 106 CD34 cells/kg is not obtained.
Patients receive rituximab IV on day 1, etoposide IV on days 2-4, and carboplatin and ifosfamide IV on day 3. Patients also receive filgrastim (G-CSF) subcutaneously (SC) once daily beginning on day 6 and continuing until apheresis is completed and plerixafor SC once daily beginning 24 hours after recovery from nadir and continuing until apheresis is completed. Patients may undergo up to 7 apheresis procedures until the optimal number of CD34+ cells are collected.
After completion of study treatment, patients are followed periodically for up to 12 months.
Endpoint Classification: Efficacy Study, Intervention Model: Single Group Assignment, Masking: Open Label, Primary Purpose: Treatment
Adult Non-Hodgkin Lymphoma
filgrastim, plerixafor, rituximab, ifosfamide, carboplatin, etoposide, leukapheresis
Fred Hutchinson Cancer Research Center
Not yet recruiting
Fred Hutchinson Cancer Research Center
Published on BioPortfolio: 2014-08-27T03:14:51-0400
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A semisynthetic derivative of PODOPHYLLOTOXIN that exhibits antitumor activity. Etoposide inhibits DNA synthesis by forming a complex with topoisomerase II and DNA. This complex induces breaks in double stranded DNA and prevents repair by topoisomerase II binding. Accumulated breaks in DNA prevent entry into the mitotic phase of cell division, and lead to cell death. Etoposide acts primarily in the G2 and S phases of the cell cycle.
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