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  • 1
    In: Human Immunology, Elsevier BV, Vol. 71 ( 2010-9), p. S88-
    Type of Medium: Online Resource
    ISSN: 0198-8859
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2010
    detail.hit.zdb_id: 2006465-2
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  • 2
    In: Blood, American Society of Hematology, Vol. 110, No. 11 ( 2007-11-16), p. 3051-3051
    Abstract: It is unclear how related donor transplants in which the donor-recipient pair is mismatched in one locus (1AgMM) compare to transplants performed using a fully matched unrelated donor (MUD), matching at HLA-A, B, C, DRB1 and DQB1. Here, we performed such a comparison. Methods: We studied 83 consecutive patients (pts) with acute leukemias and myeloproliferative/myelodysplasia syndromes receiving grafts considered to be “1-antigen mismatched related” (1AgMM) and compared their outcomes to that of 134 MUD HSCT performed from 1992 to 2006. Among 83 1AgMM transplants, 40 had prospectively or retrospectively performed high-resolution HLA typing (Hires), of which 6 pts were 8/10 matched, and 43 had only low resolution (Lowres) typing. 8/10 Hires pts were excluded from this analysis. All MUD donor-recipient pairs were typed by Hires. Median age, gender, cytogenetic risk, disease status at transplant and stem cell source were similar. Diagnosis were ALL in 5% of the Hires group, 28% of the Lowres and 0 in the MUD group; AML/MDS cases were 76%, 60% and 87%, respectively; and CML cases were 19%, 12% and 13%, respectively(p 〈 0.001). Preparative regimens were of reduced intensity for 22% of Hires, 21% of Lowres patients and 40% of MUD patients (p=0.02). High-resolution typing was performed for HLA-A, B, DRB1, DQB1 and DPB1, and SBT/SSOP for HLA-C. Cumulative incidence of NRM, acute and chronic GVHD was estimated accounting for death in the absence of event as a competing risk. The Cox’s proportional hazards model was used to compare outcomes beteween groups. Results: With a median follow-up of 15 mo for MUD pts, 27 mo for Hires patients and 33 mo for Lowres pts, OS at 18 mo is 52%, 46% and 22% (p= 0.002 for the comparison of MUD vs Lowres; P=NS for the comparison of MUD vs Hires); NRM is 23%, 26% and 54%(p=0.001 for the comparison of MUD vs Lowres; P=NS for the comparison of MUD vs Hires). Primary graft failure occurred in 1% of MUD, 5% of MOL and 12% of SER (p=0.003). Cumulative incidence of grade II-IV aGVHD is 34% for MUD pts, 48% for Hires and 49% for Lowres(p= 0.07); cGVHD: 34%, 40% and 54%(p=0.01 for the comparison of MUD vs Lowres). We divided the Hires related group according to presence of Class I or Class II mismatches, and compared their outcomes to the MUD group (Table). 23 pts had Class I and 11 pts had Class II mismatches; median follow-up is 26 and 62 mo, respectively. Distribution of gender, diagnosis, cytogenetic risk, dis. status at transplant, ablative/RIC regimens and stem cell source was similar between the 2 groups. Pts with class I mismatches had the worse survival. Conclusion: Cumulative incidence of grade II-IV aGVHD and cGVHD, non-relapse mortality and overall survival of 1AgMM (allele level typing) patients was similar to that observed in a cohort of recipients of molecularly matched, HLA 10/10 MUD transplants. OS at 18 mo HR (95%CI) P C. Incid. gd II-IV aGVHD HR (95% CI) P C. Incid. chronic GVHD HR (95% CI) P C. Incid= cumulative incidence MUD n=134 52% Reference 34% Reference 34% Reference Class I n=23 34% 1.8 (1–3.1) P=0.05 40% 1.3 (0.6–2.9) P=0.4 35% 1.1 (0.5–2.5) P=0.7 Class II n=11 73% 0.6 (0.2–1.9) P=0.4 64% 2.8 (1.3–6.3) P=0.01 48% 2.3 (0.9–5.7) P=0.08
    Type of Medium: Online Resource
    ISSN: 0006-4971 , 1528-0020
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    Language: English
    Publisher: American Society of Hematology
    Publication Date: 2007
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  • 3
    In: Blood, American Society of Hematology, Vol. 114, No. 22 ( 2009-11-20), p. 3394-3394
    Abstract: Abstract 3394 Poster Board III-282 CB transplantation (CBT) is often complicated by delayed or failed engraftment. We conducted a study of ex vivo co-culture of CB mononuclear cells with either third party family member ≥ 2/6 HLA matched marrow derived MSCs (N=8) or off-the-shelf mesenchymal progenitor cells (MPCs) from Angioblast Systems Ltd. (N=9). MSCs provide a microenvironment for the generation of complex molecular cues that direct proliferation and regulate the differentiation and maturation of hematopoietic progeny. Patients had two CB units matched in at least 4/6 HLA antigens, with a minimum of 1×107 TNC/Kg per unit. Methods: Diagnoses were AML/MDS (N=10), ALL (N=3), NHL (n=1), MM (n=1), and CLL (N=2). Five patients (29%) were in CR (CR1, n=1) and 12 (71%) had active disease at CBT. Preparative regimen: myeloablative fludarabine, melphalan, thiotepa and ATG (n=17), with rituximab in the 3 ALL pts. GVHD prophylaxis: tacrolimus and MMF. Median weight was 79.7 Kg (range, 15-102) and median age was 36 years (2-55 years). Donor-recipient HLA matching was 5 of 6 in 29% of the cases and 4 of 6 in 71%. Ex-vivo EXP: 100 ml of marrow was aspirated from the family donor and MSCs generated in ten T175 flasks, which took ∼21 days (n=8) or one vial of Angioblast MPCs was thawed and expanded to confluence in 10 flasks within 4 days (n=9). The CB unit with the lowest TNC dose was then thawed, divided into 10 fractions, and each placed into 1 flask containing the confluent layers of MSCs/MPCs in expansion media with SCF, FLT3, G-CSF and TPO. After 7 days at 37°C, the non-adherent cells were removed from each flask, placed into each of ten one-liter Teflon-coated culture bags (American Fluoroseal) and cultured for an additional 7 days (14 days total), while 50 ml of media/growth factors was added to the flasks to culture the remaining adherent layer during that time period. On day 14 the cells from the bags and the flasks were combined, washed and infused along with a second unmanipulated CB unit. Results: The median number of infused total nucleated cell (TNC) and CD34+ cells per kg in unmanipulated CB was 2.3 × 107 (range, 1.9-8.2) and 1.6 × 105 (range, 0.3-1.26). There were no toxicities attributable to the EXP cells. The median TNC fold-EXP for recipients of family-MSCs was 11.7 (0.7-28) and for Angioblast-MPCs was 15.5 (3.1-22.5); Fold-EXP of CD34+ cells was 11.7 (1.7-50.1) for family-MSCs and 46.6 (3.85-71.9) for Angioblast-MPCs. The median number of infused TNC and CD34+ cells per kg after EXP for all pts was 5.8 × 107 (range, 0.1-1.43) and 6.05 × 105 (range, 0.18-30). Median time to neutrophil and platelet engraftment was 15 days (9-25 days) and 37.5 days (13-56). Sixteen (94%) and 14 (82%) of all patients engrafted neutrophils and platelets, respectively. One patient died before engraftment. All evaluable patients became complete donor(s) chimeras. One CB unit dominated in all patients; on transplant day +21, EXP unit contributed with a mean of 10% of T cell and 24% of myeloid chimerism; on day +40, corresponding proportions were 2% and 4%, and on day +70, 0% and 3%, respectively. Acute grade II-IV and III-IV GVHD rate was 38% and 12%, while 50% of at-risk patients developed chronic GVHD. Ten patients (59%) are alive (3-14 months after CBT), while 7 patients have died due to infections (n=4), relapse (n=2) and GVHD (n=1). Actuarial 6 and 12 month survival is 70% and 50%, respectively. Conclusion: The decreased logistical demands and expansion results demonstrate that off-the-shelf Angioblast-MPCs are the preferred stroma for this CB EXP procedure. MSC/MPC-CB EXP is feasible and may provide rapid engraftment of neutrophils and platelets. Platelet engraftment occurred in a high proportion of patients (80%) in this cohort of high-risk patients with a median weight of 80 Kg. Disclosures: No relevant conflicts of interest to declare.
    Type of Medium: Online Resource
    ISSN: 0006-4971 , 1528-0020
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    Language: English
    Publisher: American Society of Hematology
    Publication Date: 2009
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  • 4
    In: Blood, American Society of Hematology, Vol. 108, No. 11 ( 2006-11-16), p. 3125-3125
    Abstract: The HLA class II DP locus encode for both subunits of DPB1 heterodimers, which have low levels of expression on the cell surface of antigen presenting cells. We hypothesized that donor-recipient HLA-DP mismatch would lead to an increased incidence of acute (a) graft-versus-host disease (GVHD), and that 2 mismatches would likely be even more significant. Methods: We studied 84 consecutive patients (pts) with myeloid leukemias in complete remission (CR) transplanted from 01/02 to 02/06. Preparative regimens were ablative IV Busulfan-based (n=58) or Cy/TBI (n=2), and reduced intensity (Fludarabine (Flu)/Bu 130 mg/m2/2 doses plus Gleevec (n=8), and Flu/Melphalan 140 mg/m2 (n=16). Stem cell (SC) source was bone marrow (n=70) or peripheral blood (n=14). ATG was given in 78 cases. GVHD prophylaxis was tacrolimus and mini-methotrexate in all cases, with additional pentostatin in 31 pts. High-resolution typing was sequence-based for HLA-A, B, DRB1; SSP was used for DRB3/4/5, DQB1 and DPB1, and SBT/SSOP for HLA-C. A Cox proportional hazards regression model was used to study aGVHD-free and relapse-free (RFS) survival. Variables with a p-value 〈 0.25 by univariate analysis were included in the multiple regression analysis (MV). Variables were age, gender, weight, conditioning regimen, GVHD prophylaxis, diagnosis, cytogenetics, SC source, ABO group, infused CD34 and CD3 cell dose, and HLA matching. AGVHD-free survival was calculated from transplant date to date of development of grade II–IV GVHD or completion of 100 days of follow-up. Results: Median age was 48 yrs (range, 14–72). Diagnoses were MDS (n=5), AML (n=58), and CML (n=21). 54 pts (64%) were beyond 1st CR; all CML pts were in 〉 1st chronic phase (CP). Sixty-one pts were 10/10 HLA match (A, B, C, DRB1, DQB1), and 23 had one or more mismatches. All but one pt engrafted neutrophils at a median of 13 days. 33 pts (39%) and 13 pts (15%) developed grade II–IV and III–IV aGVHD, respectively. Chronic GVHD incidence was 51%. With a median follow-up of 18 mo. (range,1.3–52) 60 pts are alive; 40 pts have relapsed or died. Median survival has not been reached. Number of DP mismatches and incidence of aGVHD is shown in the table. The following covariates influenced aGVHD-free survival by MV analysis: Flu-based regimen (P=0.005; HR 0.25 (95%CI 0.1–0.66), reduced intensity regimens (p=0.02; HR 0.35 (95%CI 0.15–0.83) and presence of 2 DPB1 mismatches (p=0.02; HR 3.07 (95%CI 1.19–7.95). Presence of 1 DPB1 mismatch was not significantly associated with aGVHD. There was no statistically significant correlation between presence of 2 DP mismatches and RFS (P=0.17;HR 0.3 (95%CI 0.06–1.65);HR 0.75 for 1 mismatch) or with cGVHD. Actuarial 2-yr survival for 10/10 matched pts without DP mismatches (12/12) versus those with DP mismatches is 82% versus 71%(P=0.6). In the 10/10 matched group, GVHD was the cause of death only among recipients of 2 DP mismatches transplants (n=4). Conclusion: Mismatching at HLA-DPB1 may increase the risk of aGVHD following UDT. The role of DP in the development of GVHD and GVL effects merits future study. Incidence of acute GVHD 10 of 10 matches number of DP mismatches grade II–IV grade III–IV 0 8% 0% 1 23% 8% 2 45% 18% 〈 10 of 10 matches number of DP mismatches grade II–IV grade III–IV 0 45% 15% 1 82% 36% 2 80% 40%
    Type of Medium: Online Resource
    ISSN: 0006-4971 , 1528-0020
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    Language: English
    Publisher: American Society of Hematology
    Publication Date: 2006
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  • 5
    In: Biology of Blood and Marrow Transplantation, Elsevier BV, Vol. 17, No. 6 ( 2011-06), p. 923-929
    Type of Medium: Online Resource
    ISSN: 1083-8791
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2011
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  • 6
    In: Leukemia & Lymphoma, Informa UK Limited, Vol. 53, No. 5 ( 2012-05), p. 901-906
    Type of Medium: Online Resource
    ISSN: 1042-8194 , 1029-2403
    Language: English
    Publisher: Informa UK Limited
    Publication Date: 2012
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  • 7
    In: Blood, American Society of Hematology, Vol. 114, No. 14 ( 2009-10-01), p. 2884-2887
    Abstract: The polymorphic products of major histocompatibility complex class I–related chain A (MICA) genes are important in solid organ transplantation rejection. MICA expression is limited to gut epithelium and may play a role in triggering acute graft-versus-host disease (aGVHD). A total of 236 recipients of unrelated donor transplantation were studied. Donor-recipient human leukocyte antigen (HLA) match was 10/10 human leukocyte antigen (HLA-A, -B, -C, -DRB1, -DQB1) in 73% and MICA mismatch in 8.4%. Because of physical vicinity of the loci, MICA mismatch was significantly associated with mismatch at HLA-B and HLA-C. A higher rate of grade II-IV aGVHD was seen in MICA-mismatched patients (80% vs 40%, P = .003) irrespective of degree of HLA matching (HLA 10/10 match: 75% vs 39%, P = .02) and HLA any mismatch (83% vs 46%, P = .003). The rate of grade II-IV gastrointestinal aGVHD was also higher in MICA-mismatched patients (35% vs 17%, P = .05). We conclude that MICA may represent novel a transplantation antigen recognized by human allogeneic T cells. This study was registered at ClinicalTrials.gov (Identifier NCT00506922).
    Type of Medium: Online Resource
    ISSN: 0006-4971 , 1528-0020
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    Language: English
    Publisher: American Society of Hematology
    Publication Date: 2009
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  • 8
    In: Blood, American Society of Hematology, Vol. 112, No. 11 ( 2008-11-16), p. 58-58
    Abstract: MICA is a highly polymorphic locus located in the Class III region of the HLA system in the short arm of chromosome 6. The products of MICA can elicit humoral allo-recognition and are the ligands of the NKG2-D receptors of natural killer cells. MICA is involved in chronic and possibly acute graft rejection in kidney transplantation. The impact of mismatches in MICA has not been examined systematically in bone marrow transplantation. We hypothesized that donor-recipient MICA mismatches may influence graft-versus-host disease (GVHD) and relapse rates after UD hematopoietic stem cell transplantation (HSCT), and tested this hypothesis in a cohort comprised of all patients with myeloid leukemias transplanted in our institution from January, 2002 to December, 2007 (n=238). Methods: Typing of each of the classical human leukocyte antigen (HLA) and MICA loci was performed by amplification with locus-specific primers of genomic DNA by PCR followed by nucleotide sequencing. For the assignment of MICA alleles, the polymorphisms in exons 2, 3, 4, and 5 were evaluated. Matching grade is described in the GVH direction. Outcomes were acute (a) GVHD incidence, and aGVHD-free survival (time dependent variable, with development of aGVHD as the event), and relapse-free survival (RFS), both estimated by the Kaplan Meier method. Cox proportional hazards regression model was used to estimate the influence of HLA match degree, patient, disease, and transplant-related characteristics on outcomes. Median age was 50 years (range, 18–74; 24% over age 59). Diagnosis were AML/high-risk MDS in 82% (n=195) and CML in 18% (n=43). 42% (n=100) of the patients were in remission (CR) at HSCT. Preparative regimens were ablative in 59% (n=141), and contained ATG, fludarabine and IV busulfan in respectively 96%, 90% and 70% of the HSCT. GVHD prophylaxis was tacrolimus and mini-methotrexate-based in all HSCT. Stem cell source was bone marrow (BM) in 72% (n=172) and peripheral blood (PB) in 28% (n=66) of HSCT. 78 patients have relapsed (34%) and 133 have died (56%). Results. 169 pairs were matched in HLA A, B, C, DRB1, and DQB1 (10/10; 71%); 69 (29%) were & lt;10/10 matches, of which 60 were 9/10 (78% of the mismatches were in HLA class I). One or two HLA-DPB1 mismatches were present in 48% and 25% of the patients, respectively. MICA one or two mismatches were present in 22 pairs (9%). Grade (gd) II–IV and III–IV aGVHD rates for patients with MICA mismatches were 80% and 30%, respectively, versus 40% and 14% for those with no MICA mismatches. Effect of MICA on aGVHD was similar among 10/10 and & lt;10/10 patients. RFS at 52 weeks post HSCT was 0.58 (95%CI 0.5–0.66) versus 0.77 (95%CI 0.59–1) for patients without and with MICA mismatches (P=0.5). Multivariate models are shown in the table. Conclusion: MICA mismatches independently increased the incidence of grade II–IV aGVHD. Multivariate Models for grade II-IV acute GVHD and relapse-free survival (RFS) Variable Incidence Univariate P value Multivariate P, HR and 95% CI Grade II-IV aGVHD Fludarabine-based regimen(yes vs no) 39% vs 72% P=0.0009 0.02; HR 0.51 (0.29–0.9) DPB1 mismatches (0/1 vs 2) 38% vs 52% P=0.06 0.03; HR 0.59 (0.37–0.94) Ablative conditioning (no vs yes) 31% vs 48% P=0.001 0.05; HR 0.65 (0.43–0.99) MICA mismatches (yes vs no) 80% vs 38% P=0.0002 0.002; HR 2.33 (1.37–3.98) RFS Rate at 52 weeks 95%CI Univariate P Multivariate P, HR and 95% CI DPB1 (0 vs 1 vs 2) 0.54(0.42, 0.68) P=0.09 0.03; HR 1.65 (1.051–2.6) 0.55(0.45, 0.67) 0.7(0.58, 0.84) CR at HSCT (yes vs no) 0.78(0.69, 0.87) P & lt;0.0001 & lt;0.0001; HR 0.308 (0.18–0.52) 0.44(0.36, 0.55) (P and HR for aGVHD-free survival) HR: hazard ratio; CI: confidence interval
    Type of Medium: Online Resource
    ISSN: 0006-4971 , 1528-0020
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    Language: English
    Publisher: American Society of Hematology
    Publication Date: 2008
    detail.hit.zdb_id: 1468538-3
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  • 9
    In: Blood, American Society of Hematology, Vol. 112, No. 11 ( 2008-11-16), p. 976-976
    Abstract: Introduction/Methods: A key component of improving the success rate of allogeneic HSCT for AML in CR1 is to reduce non-relapse mortality (NRM), which, if excessive, will deny the benefit of the graft-versus-leukemia effect. UD HSCT has traditionally been associated with high NRM rates. We reported previously on the significant reduction of NRM using the conditioning regimen of fludarabine 40mg/m2, IV busulfan 130 mg/m2 for 4 days and thymoglobulin. Here we analyze the outcomes of all patients (n=37) with AML in CR1 treated with this regimen and UD HSCT in our institution from January 2002 to December 2007. High-resolution allele level HLA typing was performed for all donorrecipient pairs for HLA-A, -B, -C, DRB1 and DQB1; up to one mismatch was allowed (9/10). Median follow up is 30 months (range, 9–72). Results: Median age was 48 years (range, 13–68); 30% (n=11) were older than 54 years and 51% (n=19) were male. Eleven patients (30%) had secondary AML. Prognostic cytogenetics classification was poor and intermediate in 53% and 47% of the cases, respectively. Stem cell source was bone marrow (BM) in 68% (n=25) and peripheral blood (PB) in 32% (n=12). Graft-versus-host disease (GVHD) prophylaxis was tacrolimus and mini-methotrexate with and without pentostatin (1 or 1.5 mg/m2 on days 8, 15, 22 and 30) in 46% (n=17) and 54% of the cases (n=20), respectively. Donor-recipient HLA match was 9/10 and 10/10 in 14% and 86% of the cases. Median infused total nucleated and CD34+ cells was 3.72 x 108 (range, 0.57 – 11.78) and 3.77 x 106 (range, 0.45 – 12.4), respectively. Median time to neutrophil and platelet engraftment was 12 days (range, 8–18) and 14 days (range, 8–101), respectively. All but one patient engrafted. Grade II–IV acute (a) GVHD rate was 13% (n=2) and 50% (n=10) for patients that received and not received pentostatin-based prophylaxis. Grade III–IV aGVHD rate was 0% versus 15% (n=3) for patients receiving and not receiving pentostatin. Chronic GVHD was diagnosed in 55% (n=18) of all patients (extensive in 10). 100-day and 3-year NRM rate was 11% (n=4) and 20% (n=4), respectively, and was due to engraftment failure (n=1) and aGVHD (n=3). Eight patients (22%) have relapsed, and 8 (22%) have died (4 of relapse, and 4 of NRM causes). Relapse rate was 18% (3/17) and 25% (5/20) for patients that received and not received pentostatin as part of GVHD prophylaxis. Actuarial 3-year event-free and overall survival (figure) is 68% and 78%, respectively. Actuarial 3-year overall survival for patients receiving BM and PB is 80% and 75%, respectively. Conclusion: Long-term disease control can be achieved in a significant fraction of high-risk AML patients undergoing UD transplants as described in this abstract. Use of pentostatin in this context deserves further prospective evaluation. Figure Figure
    Type of Medium: Online Resource
    ISSN: 0006-4971 , 1528-0020
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    Language: English
    Publisher: American Society of Hematology
    Publication Date: 2008
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  • 10
    In: Blood, American Society of Hematology, Vol. 116, No. 21 ( 2010-11-19), p. 489-489
    Abstract: Abstract 489 Relapse remains the major cause of treatment failure after allogeneic hematopoietic transplantation for AML and MDS. Alloreactive NK cells mediate a potent antileukemic effect and may also enhance engraftment and reduce GVHD. We performed a phase I study infusing “third party” alloreactive NK cells from a haploidentical related donor as a component of the preparative regimen for allotransplantation from a separate HLA identical donor. The goal was to augment the antileukemia cytotoxicity of the preparative regimen by infusion of alloreactive NK cells and improve the overall outcome of hematopoietic transplantation. Patients with advanced AML or high risk MDS in relapse or beyond first remission were eligible. They received the busulfan-fludarabine preparative regimen, followed by infusion of NK cells predicted to be alloreactive by KIR:KIR ligand incompatibility. The NK cell enriched product was produced from a steady state apheresis product by depleting CD3+ cells using the CliniMACS device (Miltenyi Corp). A second step positively selecting CD56+ cells was performed for the first dose level, but discontinued thereafter in order to increase the cell yield. The NK cell product was then cultured in complete media containing rIL-2 for 16 hours and infused intravenously following completion of the busulfan-fludarabine chemotherapy. After 5 days, ATG was administered followed by PBSC infusion from the HLA identical sibling or unrelated donor. Patients received tacrolimus and methotrexate for GVHD prophylaxis. Patients were treated in 4 dose levels of the NK cell enriched product; 1) 106 cells/kg, 2) 5 × 106/kg, 3) 3 × 107/kg, and 4) 3 × 107/kg followed by systemic interleukin-2 0.5 million units/m2 SQ daily for 5 days. CD3+ cells in the NK cell product were required to be 〈 105/kg (median infused 1.1 x104/kg). Median CD56+ cells infused (x106/kg) were from 0.9 (level 1), 1.5 (level 2), and 4.9 (levels 3 and 4). 13 patients were entered. Median age was 51 years (range 2–60). 11 had active disease and 2 were in a second remission. Only mild infusion toxicity occurred with the NK cell infusion. Other toxicities were similar to that experienced with the preparative regimen without NK cells. The 2 patients at dose level 4 tolerated interleukin-2 systemic treatment without fever or increased toxicity. The haploidentical NK cells were transiently detected in the blood by chimerism studies in one patient. Rapid engraftment and hematologic recovery uniformly occurred from the HLA matched PBPC donor in all patients. None had graft failure. Grade 2 acute GVHD developed in 3 patients; all responded to corticosteroid treatment. None developed grade 3 or 4 acute GVHD. 9 of 11 patients with active disease achieved a complete remission. Only one patient died of nonrelapse mortality; she died in remission from infection 2 months post transplant. This trial confirms the feasibility of producing the haploidentical NK cell product, and the lack of major toxicity attributable to the NK cell infusion in combination with an HLA compatible allogeneic transplantation. Infusion of haploidentical alloreactive NK cells was well tolerated and did not interfere with engraftment or increase the rate of GVHD after allogeneic hematopoietic transplantation. This approach merits further phase II and III study designed to reduce relapse and improve the outcome of allogeneic hematopoietic transplantation for AML/MDS. N NK cell doseCells/kg grade 2 GVHD Relapse NRM Alive in CR 4 106 1 4 0 0 4 5 × 106 0 3 0 1 (27+ m) 3 3 × 107 2 1 1 1 (11+ m) 2 3 × 107 + IL-2 0 0 0 2 (9+ m, 4+ m) Disclosures: No relevant conflicts of interest to declare.
    Type of Medium: Online Resource
    ISSN: 0006-4971 , 1528-0020
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    Language: English
    Publisher: American Society of Hematology
    Publication Date: 2010
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