ALBERT

Description: The optimal source of donor hematopoietic stem cells (HSC) is controversial. Granulocyte colony stimulating factor (G-CSF) mobilized peripheral blood (G-PB) has replaced bone marrow (BM) as the most common allograft source in adults but is associated with donor morbidity and higher rates of chronic graft versus host disease (GVHD) compared to BM. The CXCR4 antagonist plerixafor (Px) mobilizes HSC into the PB (Px-PB) faster than G-CSF and preliminary data suggest both quantitative and qualitative differences in allograft content that may impact clinical outcomes. We sought to assess the efficacy and safety of transplanted allografts collected following mobilization with Px alone in HLA-identical sibling transplantation. This was a Phase II, two-strata, multi-center prospective trial (NCT01696461) to evaluate Px-PB allografts prior to reduced intensity conditioning (RIC) and myeloablative conditioning (MAC) based hematopoietic cell transplantation (HCT). Patients aged 18-65 years with an HLA-ID sibling donor and a hematological malignancy suitable for HCT were eligible. The primary objective was to determine the proportion of donors whose cells could be successfully mobilized and collected with a sufficient CD34+ cell dose using Px as the sole mobilizing agent. Px mobilization was considered successful if ≥ 2.0x10^6 CD34+ cells/kg recipient weight were collected in no more than two leukapheresis (LP) collections. All donors receiving Px were included in the analysis of the primary objective based on the intention-to-treat principle. Secondary objectives included the incidence of acute and chronic adverse events in donors, rates of hematopoietic engraftment, donor chimerism, rates of acute and chronic GVHD, non-relapse mortality (NRM), progression free survival (PFS) and overall survival (OS) for the recipients. From July 2013 to December 2014, 64 donor/recipient pairs were enrolled at 12 centers. Donors received Px at 240μg/kg subcutaneously 4 hours prior to LP. LP was performed processing at least 4X blood volume for up to two consecutive days (a third day was allowed for low CD34+ cell yields after 2 LP procedures) to achieve a target CD34+ cell dose of ≥ 4.0 x 10^6/kg recipient weight with a minimum goal of ≥ 2.0 x 10^6/kg. All allografts were cryopreserved. GVHD prophylaxis included cyclosporine or tacrolimus in combination with methotrexate, mycophenolate mofetil, or sirolimus. G-CSF was given routinely post HCT only to MAC recipients. Patient demographics are provided in Table 1. The median donor age was 56 years (18-65). 64% of the donors were male. Donors underwent one (23%), two (72%), or three (5%) LP procedures. 63 of 64 (98%) donors achieved the primary objective. The median total CD34+ cell dose/kg recipient weight collected within 2 days was 4.6 (0.9-9.6). Maximal donor toxicity following Px injection and LP was grades 0 (30%), 1 (52%), 2 (17%), and 3 (2%). Bloating, flatulence, abdominal pain, headache, paresthesisas, injection site reaction, and dizziness were the most commonly observed toxicities. Bone pain was not observed. The one grade 3 toxicity was a vasovagal episode felt related to LP and unlikely to Px. Toxicities typically resolved within a week of LP. The median follow up is 6.3 months. Median days to ANC (〉0.5 x10^9/L) and Platelet count (〉20 x 10^9/L) recovery were 13.5 (10-148) and 19 (1-76) after MAC and 14.5 (0-25) and 18 (0-141) after RIC, respectively. The cumulative incidence of acute GVHD grades 2-4 and 3-4 at day 100 were 47% (95% CI: 30-64) and 9% (95% CI: 2-22) after MAC and 19% (95% CI: 6-38) and 5% (95% CI: 0-18) after RIC. Probability of NRM at day 100 was 4% (95% CI: 0-13) and 0% after MAC and RIC, respectively. The probability of OS at day 100 was 97% (95% CI: 88-100) and 90% (95% CI: 78-98) after MAC and RIC, respectively. In conclusion, this is the first multi-center trial to demonstrate that as an alternative to G-CSF, Plerixafor rapidly, safely, and effectively mobilizes sufficient numbers of CD34+ cells from HLA-ID sibling donors for HCT following both RIC and MAC regimens. Engraftment was generally prompt and early results of secondary endpoints in recipients are encouraging. Longer follow-up and more extensive analysis of donor allografts and recipient outcomes will be presented at the time of the meeting. Research support was provided in part by Genzyme, a Sanofi Company. Table 1. Characteristics of recipients Table 1. Characteristics of recipients Disclosures Chen: Bayer: Consultancy, Research Funding. Devine:Genzyme: Research Funding.

Description: Key Points Serum 2HG analysis by LC-MS can accurately identify patients with AML with and without IDH mutations. Oncometabolite testing of serum 2HG is indicated as a diagnostic, prognostic, and therapeutic monitoring tool in AML.

Description: Background: Lower total CD34+ cell dose and increased HLA-mismatch are known predictors of engraftment failure and higher transplant related mortality (TRM) in cord blood (CB) recipients. To compensate for cell dose, double unit grafts (DUCBT) are commonly used in adult. However, in the majority of patients (pts), only one of the two CB units engrafts. Identification of the factors that predict which unit will engraft remains elusive, although increased recipient-donor HLA-matching and larger CD3+ cell dose have been associated with the predominating unit in a single center retrospective analysis (Ramirez et al, 2012). Historically, CB units are selected by maximizing matching at the HLA-A and -B antigen and -DRB1 allelic level. Evidence supports that matching at HLA-C appears to decrease TRM, and many clinicians incorporate HLA-C antigen matching into unit selection. It is unclear, however, if HLA-C matching predicts the engrafting unit in DUCBT. This study retrospective study evaluates whether HLA-C matching is associated with the winning CB unit. Design: Clinical data was reviewed from all pts with a hematologic malignancy receiving a DUCBT at Moffitt Cancer Center between November 13, 2009 and August 29, 2013. Chimerism studies identified the predominating unit (〉 65% single unit) between day 21 and day 28. Subsequent chimerism analyses performed at a median of day 100 confirmed unit predominance. Unit selection required intermediate resolution antigen match at HLA-A, -B, -C, and high resolution allele match at -DRB1. Units were a minimum of 4/8 matched to the patient and each other with a minimum cell dose of 1.5 x 107 total nucleated cell dose (TNC) /kg. Serology for donor specific antibodies against both units was negative. Results: Excluding 6 pts who were missing HLA-C typing on one or both CB units, 54 pts with hematologic malignancies (ALL=6, MDS/AML=29, Other=19) received chemotherapy and total body irradiation as part of a myeloablative conditioning (MAC) or reduced intensity conditioning (RIC) with or without thymoglobulin (ATG) followed by a DUCBT (MAC=14, RIC=23, RIC+ATG=17). Median age was 52 (range 22-69) years. Seven pts demonstrated persistent mixed chimerism in the myeloid and/or lymphoid cell lines beyond day 100. A total of 20 pts with available chimerism data received at least one CB unit matched to the recipient at HLA-C, with one patient excluded due to persistent mixed chimerism. Six pts received both CB units matched at HLA-C, but of the 13 pts receiving one matched and one mismatched unit, the HLA-C matched unit was the engrafting unit 69% (9/13) of the time. Comparing similar HLA mispairings, a matched unit engrafted over a mis-matched unit at HLA-A 50% (5/10) of the time, at HLA-B 38% (5/13) of the time, and at HLA-DRB1 50% (3/6) of the time. TNC dose (larger vs smaller with a required difference of at least 0.03 x 107 TNC/kg), order of infusion (first vs second unit), and overall CB unit HLA matching (4/8-8/8), were assessed as potential predictors for engraftment. Of evaluable patients, the CB unit with the larger TNC engrafted 44% (16/36) of the time, and the first unit infused was the engrafting unit 54% (21/39) of the time. In patients with an unequal overall match grade between the CB units, the better HLA-matched CB unit engrafted 64% (14/22) of the time. Survival analysis of all pts revealed that those who received at least one CB unit antigen matched at HLA-C (n=20) had a 100 day and 1 year overall survival (OS) of 85% (95% Confidence Interval(CI): 67–97%) and 55% (95% CI: 33–75), respectively, whereas pts receiving two HLA-C mismatched CB units (n=34), 100 day OS was 62% (95% CI: 45–77) with 1 year OS 44% (95% CI: 28–61) (Fig 1). Conclusion: HLA-C antigen matching appears to help predict the winning unit in settings of HLA-match disparity and DUCBT. Confirmation in a larger population of DUCBT recipients is necessary. To date, the effects of HLA matching and other variables influencing engraftment have been predominately evaluated in recipients of single unit transplants and studies in DUCBT have been limited. Further investigation assessing HLA matching as well as donor-donor interactions is best served through a multicenter data resource. Figure 1 Figure 1. Disclosures No relevant conflicts of interest to declare.

Description: Graft-versus-host disease (GVHD) remains the principal obstacle to achieve successful outcomes in allogeneic hematopoietic stem cell transplant (HCT). Glucocorticoids are the current standard initial treatment for acute GVHD with complete responses of 25% to 41%. New immunosuppressive strategies are required to improve management of acute GVHD and decrease toxicities of immunosuppressive agents. We conclude that more effective acute GVHD therapy might improve remission rates that will result in better survival after allogeneic HCT. Vorinostast, a histone deacetylase inhibitor (HDACi) have shown efficacy for acute GVHD prevention. This protocol was design to test the safety and potential efficacy of a novel HDACi, panobinostat (LBH589), administered to patients with acute GVHD within 72 hours of initiation of glucocorticoid therapy (methylprednisolone 0.8 mg/Kg/day IV or equivalent for at least 14 days) as first line therapy. Panobinostat is a potent inhibitor of deacetylases and HSP90 belonging to a structurally novel class of the cinnamic hydroxamic acid class of compounds and is one of most potent HDAC inhibitors. We have enrolled n=13 subjects, median age 52 (range, 39-63) years, male n=8/female n=5, median day of GVHD development day + 37 post HCT (26 -528 days) with overall grade GVHD II (n=8) or III (n=5). The first three patients were treated with 2.5MG/M2 intravenously (IV) weekly x 4 and subsequent subject was treated with 5MG/M2 IV weekly x 4 achieving all GVHD CR by day +15. Patients were treated with azole for fungal prophylaxis. Due to manufacturer discontinuation of IV formulation production we were obliged to amend the protocol to use PO Panobinostat. Using 10MG PO TIW 3 doses q week x 4 weeks, we treated 2 subjects which were both discontinued from study drug as evidence of GHVD progression within 7 days of Panobinostat. Due to safety concerns, the next group was treated with a reduce dose of 5 MG PO TIW q week x 4 (Level -1). So far we have accrued 7 subjects whom by day 15 achieved GVHD CR (n:4) and PR (n:3) majority being in CR (n:6/7) on day +28 and PR (n:1). Toxicities by CTCAE 4.0 criteria included reversible thrombocytopenia and neutropenia grade 1-2 possible related to study drug. We are encouraged with a GVHD CR rate of 57% on day +15 and 86% CR at study drug completion on day+36. These results suggest a role HDACi Panobinostat as a tool to improve success of glucocorticoids for GVHD treatment. Correlative studies are planned to address pharmacodynamics of Panobinostat on inflammatory cytokines, to correlate DAC enzymatic activity inhibition and clinical response and to proteins/histones acetylation in T-cell subsets. Disclosures: No relevant conflicts of interest to declare.

Description: Introduction: Gastro-intestinal GVHD (GI GVHD) is a common and severe complication of allogeneic hematopoietic cell transplantation (HCT). Systemic glucocorticoids remain the standard of care for GI GVHD, despite their incomplete efficacy and toxicity. Steroid-sparing activity and improved survival were reported with oral administration of poorly absorbed beclomethasone dipropionate (BDP) in combination with systemic glucocorticoids for upper GI GVHD, and promising results were described with the adjunct of budesonide (BUD) for lower GI GVHD. No data have been reported on BDP or BUD without systemic glucocorticoids. Our team has adopted the practice of administering BDP/BUD without systemic glucocorticoids as fist-line therapy. Here we assess safety and efficacy of our practice in the treatment of isolated GI GVHD. Methods: We analyzed retrospective data from 297 consecutive patients (pts) with isolated GI GVHD after hematopoietic peripheral blood stem cell transplantation performed at the Moffitt Cancer Center between July 2004 and June 2013. At discretion of the treating physician, patients with upper with or without lower GI GVHD were treated with BDP (5 mg BID or TID orally), BDP plus prednisone (PRED 0.5-2 mg/kg or equivalent glucocorticoid dose), BDP+BUD (3 mg BID or TID orally) or BDP+BUD+PRED. The primary study endpoint was response of GI GVHD after 28 days, defined as complete resolution of all GI symptoms without addition of other immune suppressive (IS) agent(s) or partial reduction of GI symptoms, without resolution and without addition of other IS agent(s). Secondary endpoints were response to treatment after 200 days, chronic GVHD (CGVHD), CMV infection, relapse free survival (RFS), and overall survival (OS). All endpoints were analyzed according to treatment arm (Figure 1). A multivariable model was used to test the association between response after 28 days and treatment arm, after adjusting for primary diagnosis, conditioning regimen, disease status at HCT, pts/donor characteristics, GI GVHD overall grade, GI GVHD site, and albumin level. Results: BDP vs. BDP+PRED. Baseline characteristics were well balanced among the BDP (n=90) and BDP+PRED (n=24) groups, including treatment for isolated upper GI GVHD (84% vs. 67%, p=0.08), with the remainder affected by both upper and lower GI GVHD. BDP+PRED showed a significantly higher response of GI GVHD after 28 days compared to BDP (88% vs. 56%, multivariate OR 23, 95% CI 3-161, p=0.002); however there was no significant difference in response after 200 days (50% vs. 33%, univariate p=0.5). There were no significant differences in terms of treatment duration, requirement of additional IS agents, CMV reactivation, CGVHD development, RFS and OS between the two treatment cohorts. BDP+BUD vs. BDP+BUD+PRED. BDP+BUD+PRED pts (n=53) had more rapid onset of GI GVHD (median 20 vs. 26 days after HCT, p=0.001), higher incidence of lower GI involvement (61% vs. 38%, p=0.008) and higher incidence lower GI stage II-III GVHD (p=0.0004) compared to BDP+BUD pts (n=130). Despite adjusting for these higher risk features by multivariable analyses, BDP+BUD+PRED was associated with a significantly higher response after 28 (90% vs. 75%, multivariate OR 15, 95% CI 3-62, p=0.0003) and 200 days (70% vs. 45%, univariate p=0.0003). There were no significant differences in treatment duration, CMV reactivation, CGVHD development, RFS and OS between the two treatment cohorts. Conclusions: This retrospective analysis suggests that the addition of systemic PRED to topical BDP/BUD therapy for isolated GI GVHD was associated with a better response after 28 days of treatment. Despite the inferiority in GI GVHD response, there were no differences in secondary endpoints including treatment duration, CMV reactivation, RFS and OS. Figure 1 Figure 1. Disclosures No relevant conflicts of interest to declare.

Description: Relapse of malignancy is frequent in patients transplanted with advanced diseases. There is a relationship between higher Bu exposure and lower risk of relapse, but also higher transplant-related mortality, and data indicated the maximum tolerated daily Bu AUC is 〈 6000 microMol/min when Bu is used in combination with cyclophosphamide (Cy). To reduce transplant-related mortality, Flu has been substituted for Cy in many transplant centers. We hypothesized that pharmacokinetics-targeting of IV Bu, which results in a predictable systemic exposure, would produce values of tolerable Bu AUC that are higher for BuFlu than for BuCy. Our standard HCT regimen since July 2004 consists of once daily IV BuFlu where fludarabine 40 mg/m2 is given intravenously daily for four days and each infusion is followed immediately by an initial IV Bu dose of 130 mg/m2. Pharmacokinetic analysis is performed after the first infusion of busulfan; the goal is to adjust the busulfan doses for days 3 and 4 to achieve an average exposure targeted to an AUC of 4500–5600 microMol/min. Outcomes for the first sixty-nine patients were analyzed. Thirty-nine of 63 (62%) evaluable patients had their Bu doses adjusted, 30 increased [median adjustment 50% (8 – 175%)], and 9 decreased [median 30% (11 – 60%)], while 24 (38%) pts had an AUC within the desired range without adjustment. Most of the patients (98%) had hematological malignancies and 73% had high CIBMTR risk, median age was 48 (22–68) years, donors were HLA-identical siblings (33), matched (23) or mismatched unrelated donors (13). With a median patient follow-up of 392 (248 – 707) days, the non-relapse mortality was 4% at 100 days and 17% at one year. The K-M estimates of survival and event-free survival are 88%±4% and 83%±5% at 100 days, and 61%±6% and 51%±6% at 1 year, respectively. Subsequently, as part of a prospective, targeted AUC-dose finding trial, 20 patients received an initial Bu dose of 170 mg/m2 with subsequent doses targeted to achieve a 4-day average AUC of 5400–6600 microMol/min. Pharmacokinetic analysis was performed after the first and fourth infusion of busulfan. All patients had hematologic malignancies, 65% had high CIBMTR risk, median age was 48 (22 – 61) years, donors were HLA-A, B, C, DRB1, DQB1 matched siblings (11) or matched unrelated donors (9). Thirteen (65%) patients had their doses adjusted, six had it increased [median 37.1% (35.6 – 61.9 %)] and seven decreased [median 41.6% (18.3 – 55.2%)], while seven patients had an AUC within the desired range without adjustment. With a median follow-up of 111 (range 21–312) days, the 100-day K-M estimates of survival are 88%±8% and event-free survival 83%±9%. The complete observation of 100-day safety, relapse and survival will be presented at the meeting and data will determine further AUC escalation.

Description: Rituximab is a chimeric murine/human IgG1 kappa anti-CD20 monoclonal antibody that has revolutionized treatment of patients with CD20+ malignancies because of its non-cross resistance with chemotherapy and favorable toxicity profile. There is limited data evaluating the feasibility of combining rituximab with conditioning chemotherapy (or chemo-radiotherapy) for patients undergoing allogeneic hematopoietic cell transplantation (allo-HCT) for advanced CD20+ expressing malignancies. Twelve patients (M= 7; F=5), with a median age of 54.5 (41–66) years, underwent allo-HCT for the following diagnoses (disease status at time of transplantation) [chronic lymphocytic leukemia (CLL)= 7 (CR2=2; PR2= 3; ≥PR3=2); mantle cell lymphoma (MCL)= 3 (CR1=1; ≥PR2= 2); follicular NHL=1 (CR3=1), diffuse large B-cell (DLBC)=1 (〉PR3=1)]. Donors were as follows: matched-related donors (MRD) = 7; matched-unrelated donors (MUD) =3; mismatched unrelated donor (MMUD)= 2. Fludarabine-based conditioning regimens comprised fludarabine plus targeted doses of intravenous busulfan (FLU-BU=8), or total-body irradiation (FLU-TBI=3), or cyclophosphamide (FLU-CY=1). Anti-thymocyte globulin (ATG) was administered in two cases of MMUDs. GVHD prophylaxis consisted of tacrolimus plus mycophenolate mofetil= 8, or methotrexate = 4. Nine (75%) of 12 patients received rituximab 375 mg/m2 on day +1 (±3 days) and all (100%) patients received rituximab 375 mg/m2 on day +8 (± 3 days) without serious infusion reactions. All patients engrafted. Median time to neutrophil engraftment for the entire cohort was 15.5 (12–27) days. Median time to platelet engraftment in nine patients was 14.5 (10–17) days. Three patients never dropped their platelet counts below 20,000/uL. Median donor chimerism at day +90 (±10 days) for unsorted BM, CD3 and CD33 by PCR/STR method were 94% (70–100%), 86% (59–100%) and 100%, respectively. At a median follow up of 5 (0.6–30.3) months, the 100-day non-relapse mortality (NRM) in 11 evaluable patients was 10%. Acute GVHD, grades II, III, and IV, developed in 50%, 8.3% and 8.3%, respectively, at a median time of 27 (16–77) days. These findings demonstrate that administration of rituximab as part of conditioning chemotherapy is feasible and does not affect timely hematopoietic engraftment of allograft recipients with advanced CD20+ malignancies.

Description: Purpose: To report our experience with large volume leukapheresis (LVL) for allogeneic hematopoietic progenitor cell (HPC) transplantation, evaluating its safety and efficacy in 69 consecutive healthy donors. Methods: Donor medical records from 1995–2004 were reviewed. These consisted of 38 males, 31 females, age range 16–65 (median: 37). All were mobilized with G-CSF, based on a dose of 7.5 mcg/kg/day (median: 600 mcg, range 300–960 mcg) for four days prior to outpatient LVL (Cobe spectra). Vascular access was femoral vein in 59 and antecubital veins in 10 donors. Pre- and post-LVL determinations included: WBC count, hemoglobin, hematocrit, platelet count, serum potassium, and calcium (Ca++). Oral KCL and oral/intravenous Ca++ were given as indicated by laboratory values and symptoms. Catheter-related complications and blood product requirements associated with collection were assessed. Final CD34/kg recipient body weight (rec. BW) and recipient engraftment data was evaluated. Results: LVL was well tolerated by all donors undergoing a total of 74 procedures. Data/LVL Procedure Mean Range Procedures per patient 1 1–2 Blood volume processed (L) 24.2 15.0–34.4 Time (minutes) 273 180–386 Flow rate (ml/min) 92 65–100 ACD–A used (ml) 1008 636–1449 Heparin used (units) 3000 Not applicable CD34/kg rec. BW 8.2 1.36–33.9 Adverse reactions were minor and occurred in 40% of the donors. Local parasthesias accounted for majority (86%) of the adverse events. Bone pain secondary to G-CSF accounted for the remainder of the cases and was well controlled with analgesics. Oral electrolyte supplements were administered in 61% of the donors. Eleven (15.9%) required intravenous Ca++ during collection. There were no catheter-related complications and no requirement for blood products during or after collection. Target values of 2 x 106 CD34/kg rec. BW was obtained in 68 cases (98.6%). Engraftment was achieved in 92% of the cases (6 died prior to engraftment). There were no early or late graft failures. Median time to ANC recovery was 10 days (range 8–25 days). Self-sustained platelet count was achieved in a median of 13 days. Conclusion: LVL was a safe and efficacious method of allogeneic HPC collection. The use of a lower G-CSF dose for mobilization is more economical and well tolerated. This dose allows for adequate collection of CD34 positive cells. These cells support the sustained recovery from high-dose chemotherapy for allogeneic transplantation.

Description: Background: Although busulfan (Bu) in combination with cyclosphosphamide (Cy) is a commonly used conditioning regimen for the treatment of patients with hematologic diseases, its toxicity profile when administered intravenously (IV) as well as efficacy remains unclear, especially in the setting of autologous transplant for lymphoma. Objective: To determine toxicity and the efficacy of the IV Bu/Cy conditioning regimen in patients who underwent autologous peripheral stem cell transplantation (APSCT) for the treatment of lymphoma. Methods: A retrospective analysis was performed in 37 patients (21 male; 16 female) who underwent APSCT and received IV Bu/Cy regimen between January 2000 and May 2004. Results: The median age was 50 years old (range: 20–68). Forty-seven percent of the patients were heavily pretreated (≥ 3 previous treatment, range 2–5). The distribution of lymphoma was: diffuse large B-cell lymphoma (DLBCL, 23), follicular lymphoma (8), mantle cell lymphoma (MCL, 5), and T-cell lymphoma (1). All patients received IV busulfan 3.2 mg/kg and cyclophosphamide 120 mg/kg, and were evaluable for toxicity. The patients engrafted (ANC ≥ 500 μ/l) at a median of 11 days (range: 9–14), and sustained platelet count (≥ 20,000 μ/l) at a median of 11 days (range: 8–42). The most common toxicities encountered were grade 1–2 including nausea, vomiting, stomatitis, esophagitis, and diarrhea. Grade 3–4 toxicities included hepatic veno-occlusive disease (HVOD, n=2), SIADH (n=1), and atrial fibrillation (n=2). Treatment related mortality (TRM) was seen in 3 patients due to HVOD (n=2) and septic shock (n=1). Twenty patients are still alive and 18 have no evidence of disease progression, with a median follow up of 17 months (range: 2–54 months). Kaplan-Meir actuarial OS at 24 months was 55.3% with a 47.3% DFS. Median event-free survival was 24 months (range 2–52). Conclusions: IV Bu/Cy is a well-tolerated conditioning regimen with acceptable TRM, when compared with other regimens in heavily pretreated patients. The risk for HVOD is low. Further prospective trials are necessary to evaluate the role of Bu/Cy regimen in autologous stem cell transplant for lymphoma.

Description: We evaluated the safety of adding rituximab 375 mg/m2 only on days +1 and +8 following allo-HCT in 18 patients (M=12, F=6), median age 56 (41–66) years, with advanced CD20+ lymphoid malignancies [CLL=9 (CR2=3, PR2=3; ≥PR3=3); Mantle cell lymphoma (MCL)= 5 (CR1=1, PR2=2, ≥PR3=2); follicular (FL)=3 (CR3=2, ≥PR3=1); DLBC NHL=1 (≥PR3=1). Source of stem cells consisted of matched-related (MRD)=11 (61%), matched-unrelated (MUD)=5 (28%), or mismatched-unrelated (MMUD)=2 (11%) donors. Conditioning regimens consisted of fludarabine plus targeted doses of IV busulfan (FLU-BU) (N=11) or 200 cGy TBI (N=4), or cyclophosphamide (FLU-CY) (N=1). ATG was administered on days −3 and −1 in 2 MMUD cases (FLU-BU-ATG). Fifteen patients received rituximab on day +1 (±3) and all on day +8 (±3). GVHD prophylaxis was tacrolimus plus mycophenolate mofetil (N=11) or methotrexate (N=7). Non-relapse mortality at 100 days was 6%. Median time to neutrophils and platelets engraftment was 15 (6–27) days and 12.5 (9–18) days, respectively. Eight patients never dropped platelets below 20,000/uL. Median CD3 and CD33 chimerisms at day +90 (±10) were 89% (50%–100%) and 100% (15%–100%), respectively. DLI was required in 2 patients (FLU-BU=1, FLU-TBI=1) due to poor CD3 engraftment. Response rates after 90 days post allo-HCT, according to diagnosis, were as follows: CLL (evaluable=8/9; CR=7/8; PR=1/8); MCL (evaluable=4/5; CR=4/4); FL (CR=3/3); DLBC (PD=1/1). Twelve (67%) patients remain alive in remission at a median follow up of 9.4 (2.3–42.3) months. The incidence of grade 0,I, II, and III–IV acute GVHD (aGVHD) was 6%, 33%, 50%, and 11%, respectively. Time to onset of aGVHD was 29 (16–77) days. The incidence of chronic GVHD (cGVHD), per NIH consensus criteria, was as follows in 15 evaluable patients: no cGVHD= 27%, mild= 33%, moderate= 13%, and severe=27%. These findings suggest that administration of rituximab 375 mg/m2 only on days +1 and +8 is safe. Response rates are encouraging; but controlled studies will be needed to conclusively determine the effect of post-transplant rituximab on efficacy.