Background Endothelial progenitor cells (EPCs) are immature cells able to proliferate and contribute to endothelial repair, vascular homeostasis, neovascularization, and angiogenesis. It therefore seems likely that circulating EPCs have therapeutic potential in ischemic and vascular diseases. In this study we evaluated the efficiency of EPC mobilization and collection by large volume leukapheresis in subjects with hematological diseases, treated with plerixafor in association with G‐CSF. Methods Twenty‐two patients with lymphoid malignancies underwent rHuG‐CSF and plerixafor treatment followed by leukapheresis. Blood samples before and after treatment and apheresis liquid sample were taken and analyzed by flow cytometry in order to quantified EPC. Results The percentage of CD34+ cells and EPCs among circulating total nuclear cells (TNCs) increased significantly by approximately 2‐fold and 3‐fold, respectively, after plerixafor treatment. Consequently, the absolute number of CD34+ cells and EPCs were increased 4‐fold after plerixafor treatment. The median PB concentration of EPCs before and after treatment were 0.77/μL (0.31‐2.15) and 3.41/μL (1.78‐4.54), respectively, P < .0001. The total EPCs collected per patient were 3.3×107 (0.8×107–6.8×107). Conclusion We have shown that plerixafor in combination with G‐CSF allows the mobilization and collection of large amounts of EPCs along with CD34+ cells in lymphoid neoplasm patients. The possibility to collect and to store these cells could represent a promising therapeutic tool for the treatment of ischemic complications without the need of in vitro expansion.

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4520 Between June 1995 and June 2011, we performed 133 Autologous Stem Cell Transplantation (ASCT) in patients with NHL. Long term results of treatment and outcome were analyzed. The data presented were obtained from the Statistical Center of the Center for International Blood and Marrow Transplant Research. Median age was 48 years (range 18–65), 9% ≥ 60 years, 77 males and 55 females. The histology was: 98 (74%) B NHL, Follicular Lymphoma (FL) 26 (20%), Diffuse large B Cell Lymphoma (DLBCL) 47 (35%), Primary Mediastinal Large B Cell Lymphoma 12 (9%), Mantle cell Lymphoma (MCL) 6(4.5%), Marginal Zone Lymphoma 4 (3%), Small Lymphoplasmocytic 2 (1.5%), precursor B Lymphoplasmoblastic 1 (1%), and 35 (26%) T NHL, Peripheral T Cell Lymphomas NOS 12 (9 %), Anaplastic LC, T/N Cell systemic 9 (6.5%), Anaplastic LC, T/N Cell cutaneous 1(1%) and T/NK Cell Lymphoma 7 (5%), Angioinmunoblastic T Cell Lymphoma 2 (1.5%), Mycosis Fungoides 2 (1.5%), other T Lymphoma 2 (1.5%). We emphasize that 59 % of the patients had advanced disease at the moment of the transplant: 41% CR1, 11% CR2, 5% REL1, 8% primary induction failure, other 33% (CR3+, PR, and REL2+), and 2% missing/unknown. Condition regimens were BEAC 88%, BEAM 10% and CBV 2%. Stem cells source: 74% peripheral blood stem cells (PBSC) and 26% received bone marrow (BM) and PBSC. Overall survival was 86% (95 CI, 80–92) at 1 year, 78% (95 CI, 70–85) at 3 years and 71% (95 CI, 62–79) at 5 years. Median follow up of survivors was 96 months (3–181). Primary cause of death was relapsed or progression. We concluded that high dose therapy and Autologous Stem Cell Transplantation is an effective and feasible therapy for patients with high risk NHL. However relapse continues to be the most common cause of treatment failure. Newer strategies such monoclonal antibodody, require further investigation but early reports appear promising in reducing relapses in ASCT. Disclosures: No relevant conflicts of interest to declare.

Between 1995 and 2005, we performed 329 hematopoietic stem cell transplantation (HSCT), 286 autoulogous and 43 allogeneic. Long term results of treatment and outcome of ASCT in 100 Non Hodgkin Lymphoma (NHL) were analyzed. Median age was 47 years (range18 – 64) and the histology was: Follicular Lymphoma 15%, diffuse large B cell lymphoma (DLBCL) 47%, T lymphoma 27% and 11% others. At diagnosis 66% had advanced stage (III/IV), 40% had B symptoms, and 34% had extranodal involvement. Disease status at HSCT was: 5 % primary induction failure, 41% CR1, 20% CR2 +, 7% CRU, 12% relapsed. Number of prior chemotherapy regimens was 47% 2 lines, 20% 3 lines and 3% 4 lines; 27% had received prior induction or consolidation radiotherapy. Condition regimens consisted of BEAC (81%), BEAM (15%), others (4%). Stem cell source: 39% received BM + PBSC and 61% PBSC. Sixty nine are alive with a median survival of 3448 days (9.5 years). Median overall survival was similar in DLBCL (59%) and peripheral T lymphoma (60%). The best overall survival was observed in CR1 (77%) versus 52% in CR2 and 66% in PR1. Primary cause of death was relapsed or progression (24/31). We concluded that high dose therapy and autologous HSCT is an effective therapy for patients with poor risk NHL however relapse continues to be the most common cause of treatment failure. Newer strategies such as monoclonal antibody, require further investigation but early reports appear promising in reducing relapses in autologous HSCT.