ALBERT

Description: Key Points Posttransplantation cyclophosphamide is effective as sole GVHD prophylaxis for myeloablative HLA-matched–related or –unrelated BMT. Despite low chronic GVHD with PTCy, relapse and survival are comparable with outcomes reported using other GVHD prophylactic approaches.

Description: Abstract 840 Significance of Missing Inhibitory KIR Ligands in Nonmyeloablative, HLA-Haploidentical (Haplo) BMT with Posttransplantation High-Dose Cyclophosphamide (PT/Cy). Yvette L. Kasamon 1, Leo Luznik1, Mary S. Leffell1, Hua-Ling Tsai1, Heather J. Symons1, Javier Bolaños-Meade1, Gary Rosner1, Lawrence E. Morris2, Pamela A. Crilley3, Richard J. Jones1 and Ephraim J. Fuchs1, (1)Johns Hopkins University, Baltimore, MD, (2)Northside Blood and Marrow Transplant Program, Atlanta, GA, (3)Hahnemann University Hospital, Philadelphia, PA Introduction: NK cells can influence haplo BMT outcomes including risks of relapse and GVHD. Our group previously reported that, in allogeneic BMT for hematologic malignancies that incorporates PT/Cy, donor-recipient iKIR (inhibitory killer-cell immunoglobulin-like receptor) gene mismatches and having a KIR haplotype B donor were associated with improved outcomes (BBMT 2010;16:533). Because the reported impact of NK cell alloreactivity models in haplo BMT has been variable and some models are relevant to donor selection, we expanded our analysis of iKIR ligand status in this transplantation platform. Patients and methods: Outcomes of 212 uniformly treated patients (pts) enrolled on two similar clinical trials of related-donor, haplo BMT were retrospectively analyzed. Planned treatment consisted of fludarabine (30 mg/m2 IV on days −6 to −2), Cy (14.5 mg/kg IV on days −6 and −5), total body irradiation (200 cGy on day −1), and non-T-cell depleted bone marrow infusion. GVHD prophylaxis consisted of high-dose Cy (50 mg/kg IV on days 3 and 4), mycophenolate mofetil on days 5–35, and tacrolimus on days 5–180 without taper, with filgrastim begun on day 5. All pts (median age 51, range 1–73) had poor-risk hematologic malignancies; 60 (28%) had prior BMT. Diagnoses were Hodgkin lymphoma (31 pts), NHL (69), CLL (21), multiple myeloma (6), acute leukemia or lymphoblastic lymphoma (62), MDS (9), CML (9), CMML (4), PV (1). Missing ligands (ML; defined as absence in the recipient of one or more HLA ligands for iKIRs) and donor/recipient iKIR ligand incompatibility (LI; defined as presence of an iKIR ligand in the donor that is absent in the recipient) were determined using high-resolution HLA typing of class I alleles. For study purposes, HLA-A*2301, A*2402, and A*3201 were included in the Bw4 serologic group and effects attributable to HLA-A3 and A11 ligand groups were excluded. Results: With a median 2.9 year follow-up (range, 0.3–7 years) in pts without events, the actuarial 2-year progression-free survival (PFS) was 34%. On competing-risk analysis, cumulative incidences of grade II–IV acute GVHD and chronic GVHD were 28% and 14%, respectively; 1-year cumulative incidences of relapse and nonrelapse mortality (NRM) were 42% and 14%. Baseline characteristics in pts with ML (157 pts, of whom 76 had LI) and without ML were similar. On univariate analysis, pts with LI had no significant difference in PFS (figure A), grade II–IV acute GVHD, relapse or NRM compared to those without LI. In contrast, as compared to no ML, the presence of ML was associated with a statistically significantly improved PFS on univariate analysis (hazard ratio [HR] = 0.68, p = 0.03; figure B). This association was not identified in our previous analysis, potentially due to underpowering or inclusion of pts receiving one dose of PT/Cy. No statistically significant difference was detected according to the presence or absence of ML in the cumulative incidences of acute GVHD, relapse, or NRM, although presence of ML was associated with a tendency toward lower NRM risk (HR = 0.61, p = 0.17). On multivariate analysis, the presence of ML was found to be independently associated with a significant improvement in PFS (HR = 0.66, p = 0.03). This multivariate model also confirmed our previous observation (BBMT 2010;16:482) that greater donor-recipient HLA disparity was not detrimental to PFS (HR = 0.57, p = 0.04 for 3–4 antigen mismatches versus fewer at HLA-A, B, C, and DRB1 combined). We are currently investigating the impact of KIR haplotypes in this setting with the goal of optimizing donor selection. Conclusion: The presence of ML may be beneficial in haplo BMT with postgrafting immunosuppression that includes high-dose Cy. Further studies are needed to confirm and define the mechanisms of this effect. Our findings do not support selection of donors on the basis of LI in this transplantation platform. Disclosures: No relevant conflicts of interest to declare.

Description: Background: Although a lower relapse risk has been reported after allogeneic BMT with increasing HLA disparity, this potential benefit has been offset by higher rates of acute graft-versus-host disease (GVHD) and non-relapse mortality (NRM). However, it is possible that the type of GVHD prophylaxis could influence the balance between GVHD toxicity and relapse. Patients and methods: We retrospectively analyzed the outcomes of 185 patients with poor-risk hematologic malignancies enrolled on three similar clinical trials of related-donor, haploidentical BMT incorporating high-dose post-transplantation cyclophosphamide (Cy) for GVHD and graft rejection prophylaxis (as published in BBMT2008;14:641–50). Molecular typing was at an allele level for HLA-A, -B, -Cw, and -DRB1 and at an allele group level for -DQB1. All received Cy (14.5 mg/kg IV on days −6, −5), fludarabine (30 mg/m2 IV on days −6 to −2), total body irradiation (200 cGy on day −1), and non-T-cell depleted bone marrow infusion. GVHD prophylaxis consisted of Cy (50 mg/kg IV) either once (on day 3; n = 48) or twice (on days 3, 4; n = 137), mycophenolate mofetil for 35 days, and tacrolimus for up to 6 months, with filgrastim begun after the last dose of Cy. Most patients (median age 50, range 1–71) had advanced disease and 49 (26%) had failed autologous BMT. Diagnoses were MDS (22), CMML (3), acute leukemia or lymphoblastic lymphoma (58), CML (11), CLL (15), multiple myeloma (9), non-Hodgkin lymphoma (42), and Hodgkin lymphoma (25). Results: Median follow-up after BMT is 20 months (range, 2–71 months) in those without events. Nonengraftment attributed to primary graft failure or to residual bone marrow malignancy occurred in 29 of 177 evaluable patients (16%). Cumulative incidences of grade II–IV acute GVHD and chronic GVHD were 31% and 15%, respectively. Cumulative incidences of NRM and relapse or progression at one year were 15% and 50%, respectively. Actuarial event-free survival (EFS) at one year was 35%, with grade II–IV acute GVHD by day 100 associated with a trend toward lower cumulative incidence of relapse (p = 0.08) but a significantly higher cumulative incidence of NRM (p = 0.002) on subgroup analysis. Notably, increasing degrees of HLA mismatch at either class I or class II loci had no significant effect on cumulative incidence of acute or chronic GVHD or NRM. In contrast, the presence of a DRB1 antigen mismatch in the GVH, but not host-versus-graft (HVG), direction was associated with a significantly lower cumulative incidence of relapse (Figure a; p = 0.04) and improved EFS (Figure c; p = 0.009), whereas DQB1 antigen and class II allele mismatch status had no effect. Additionally, the presence of two or more class I allele mismatches (composite of A, B, and Cw) in either direction was associated with a significantly lower cumulative incidence of relapse (Figure b; p = 0.045 for GVH direction, p = 0.01 for HVG direction) and improved EFS (Figure d; p = 0.07 for GVH direction, p = 0.001 for HVG direction). Conclusion: Greater HLA disparity appears to be beneficial after nonmyeloablative, HLA-haploidentical BMT that incorporates high-dose post-transplantation Cy. These results suggest an anti-tumor effect of partially HLA-mismatched BMT that is irrespective of clinically significant GVHD. Potential effectors of anti-tumor immunity include HLA-DRB1 reactive CD4+ T-cells, class I reactive CD8+ T-cells, and/or natural killer cells recognizing missing self. Since most patients have several potential HLA-haploidentical related donors, the results support a strategy of choosing a donor who is incompatible for both HLA-DRB1 antigen and multiple HLA class I alleles. Figure Figure

Description: Abstract 4347 Background: Chronic myeloid leukemia (CML) is a disease that is responsive to T-cell-mediated immunity. K562/granulocyte macrophage-colony stimulating factor (GM-CSF) is a vaccine derived from a CML cell line that produces GM-CSF and expresses several CML-associated antigens. An initial pilot study was performed in 19 patients in chronic phase CML who had achieved at least a major cytogenetic response on imatinib mesylate (IM) but had measurable molecular disease. The results suggested that immunotherapy resulted in a lowering tumor burden in the majority of patients (n = 13) with a total of 7 patients achieving undetectable bcr-abl levels by QT-PCR. (Smith, Clinical Cancer Research, 2010). This extension study evaluated the biologic impact of K562/GM-CSF given as a “booster” in subjects who completed the pilot study's scheduled 4 vaccinations and continued to have have persistent measurable disease or who lost their best response to the original therapy. Methods: This is a single-institution pilot study using open-label K562/GM-CSF vaccination as a “booster” in chronic phase CML patients who were previously treated with a full 4-vaccination course of therapy and continued to have measurable CML disease. Patients were stratified as having either responded to the initial set of vaccines and had subsequent loss of response or as having had no measurable response to therapy. None experienced significant adverse events in the first set of vaccinations. “Booster” treatment consisted of 4 doses of 1 × 108 irradiated K562/GM-CSF given every 3 weeks. Imatinib was continued through the study at the patients’ starting doses. Disease burden was measured using peripheral blood RT-PCR and FISH was every 3 months throughout the course of planned booster vaccinations for up to a year following the vaccination boost. Patients with evidence of advancing disease requiring adjustments to their IM dosing or those progressing to accelerated or blast phase were taken off study. Results: 11 patients met the eligibility to receive the booster vaccinations. Mean age was 54 (range 38–78) years. Median dose of IM therapy was 600 mg daily (range 400–800 mg). The median time from final vaccination in the pilot study to first booster vaccination was 24 (range 18–24) months. Duration of follow up was a median of 36 months (range 6–42 months). In general, the trend for lower disease burden following booster vaccines was significant by Generalize Estimating Equation using all study measures (p pre-vaccination samples. Of these, 15 antigens were recognized in 2 or more subjects. The influence of the vaccine boost series on antibody titer and on the induction of antibodies to antigens not previously recognized is under study. K562/GM-CSF immunotherapy given as a “booster” vaccination was associated with the lowering tumor burdens in 7 of 11 treated patients. Ongoing efforts to identify tumor-associated antigens that may be serving as immunologic targets is ongoing. Disclosures: Levitsky: HL vaccine: Patents & Royalties.

Description: Abstract 2172 AML patients with FLT3/ITD mutations have an inferior survival compared to AML patients with wild-type (WT) FLT3, primarily due to an increased relapse rate. Allogeneic transplant represents a post-remission therapy that is effective at reducing the risk of relapse for many cases of poor-risk AML. Whether or not allogeneic transplant in first complete remission (CR) can improve outcomes for patients with FLT3/ITD AML remains controversial. Our institution has adopted a policy of pursuing allogeneic transplant, including the use of alternate donors, for FLT3/ITD AML patients in remission. As part of an IRB-approved study, we performed a review of the clinical data from November 1, 2004 to October 31, 2008 on all adult patients under the age of 60 presenting in consecutive fashion to the Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins with newly diagnosed non-M3 AML. We followed their outcomes through August 1, 2010. During the study period, 133 previously untreated AML patients between the ages of 20 and 59 were diagnosed and received induction and consolidation therapy at our institution. Of these 133 patients, 31 (23%) harbored a FLT3/ITD mutation at diagnosis. Fourteen of the total 133 patients were deemed unfit for intensive therapy, all WT patients. Of these, 6 (5%) received investigational agents on protocol while the other 8 (6%) were treated with combinations of supportive care and cytotoxic agents off protocol. Of the remaining patients, 119/133 (89%) received timed- sequential intensive induction therapy (TST) with infusional cytarabine, an anthracycline or anthracenedione, and a third drug. The majority, 95/133 (71%), received the three drug TST regimen of cytarabine, daunorubicin, and etoposide delivered in a timed sequential fashion, while 24/133 (18%) were treated with TST containing cytarabine, mitoxantrone, and the investigational agent flavopiridol on an institutional protocol. 72/119 (61%) achieved a CR with induction therapy (55 patients in AcDVP16 group and 17 patients in FLAM group). The OS (overall survival) from the time of diagnosis for the FLT3/ITD AML patients was compared to the OS of the entire cohort (n=133) (Figure 1). The median OS for the FLT3/ITD group was 19.3 (range 0.0–69.9) months and the median OS for the WT patients was 15.5 (range 0.7 to 64.6) months (p=0.56). Of the FLT3/ITD patients, 20/31 (65%) achieved a complete remission with intensive induction therapy. Of these 20 patients in CR1, 11 (55%) underwent an allogeneic transplant in first remission (4 HLA-matched myeloablative sibling, 5 HLA-matched myeloablative unrelated donor, and 2 nonmyeloablative haplo-identical related donor) compared to only 18/102 (17%) WT patients were transplanted in first CR, a statistically different proportion compared to the FLT3/ITD patients (p

Description: Background: High-dose PTCy has been shown to effectively reduce acute (a) and chronic (c) GVHD after MRD and MUD BMT and to enable the safe implementation of haplo BMT. However, GVHD-related risk factors and survival outcomes, the impact of donor type, and novel composite endpoints, such as cGVHD-free relapse-free survival (cGFRFS), have not been fully characterized in BMT with PTCy. Methods: We retrospectively analyzed 582 consecutive adult pts with advanced or poor-risk hematologic malignancies who received allogeneic BMT with PTCy at Johns Hopkins from 2002-2012. All pts received a T-cell replete bone marrow graft and PTCy (50 mg/kg/d IV) on D+3 and +4. Platforms consisted of: 1) myeloablative conditioning (MAC) with Busulfan/Fludarabine or Busulfan/Cy followed by MRD (n = 193; 33%) or MUD (n=119; 20%) allografting and PTCy as sole GVHD prophylaxis; or 2) nonmyeloablative (NMA) conditioning with Fludarabine/Cy/TBI followed by related haplo (n = 270; 46%) allografting and PTCy, mycophenolate mofetil D5-35, and tacrolimus D5-180. Results: The median follow up was 4 (range 0.3-11.4) years (y). The median pt age at time of BMT was 49 (range 18-66) in the MAC cohort and 54 (range 18-73) in the NMA cohort. On competing risk analysis, the D200 probability of grade II-IV aGVHD was 27% after haplo, 37% after MRD, and 50% after MUD BMT, and grade III-IV aGVHD was 4%, 11%, and 14% respectively. The 3-y probability of cGVHD was 12% after haplo, 8% after MRD, and 19% after MUD BMT. On multivariate analysis adjusted for age and original disease risk index (DRI), MRD and MUD BMT were associated with a statistically significantly higher risk of grade II-IV and grade III-IV aGVHD compared to haplo BMT (each p ≤ 0.001). Compared to haplo BMT, MUD, but not MRD, BMT was also associated with a significantly higher risk of cGVHD (p = 0.009). On multivariate analysis, female into male allografting was independently associated with a higher risk of cGVHD (p = 0.007), whereas age and CMV serostatus of the pt and donor were not statistically significantly associated with risks of acute or chronic GVHD. Pts with grade II-IV aGVHD or cGVHD had a lower probability of relapse, but a higher probability of nonrelapse mortality (NRM) at 3 y compared to pts without GVHD. Among pts with GVHD, an HCT-CI score ≥ 5 was associated with significantly inferior overall survival compared to lower HCT-CI scores. Although MAC matched BMT was associated with less relapse risk than NMA haplo BMT, the 3-y probabilities of NRM, DFS, and overall survival were comparable between the transplant platforms (Table). On multivariate analysis adjusted for pt age and DRI, there were no statistically significant differences in DFS, OS, or cGFRFS in MAC related or unrelated BMT compared to NMA haplo BMT. Conclusions: High-dose PTCy safely modulates acute and chronic GVHD across multiple BMT platforms. The apparently lower risk of aGVHD after NMA haplo BMT with PTCy likely reflects the reduced conditioning intensity and longer duration of immunosuppression utilized. Despite the limitations inherent to a retrospective analysis, these data suggest that key outcomes after BMT with PTCy are comparable across donor types and conditioning intensities. Notably, in all these settings, 3-y estimates of cGFRFS appeared to approach those of DFS. Thus, PTCy may minimize the late morbidity and mortality of cGVHD and allow earlier implementation of novel posttransplantation strategies for relapse prevention. TableOutcomes of BMT with PTCy3-y probabilitiesNMA HaploMAC MRD*MAC MUD*NRM141717DFS384144OS495856cGFRFS313533 * p = NS for all comparisons to haplo BMT on multivariate analysis Disclosures Off Label Use: High-dose posttransplantation cyclophosphamide.

Description: Background: Recent advances in NMA haplo BMT, including high-dose PTCy for GVHD prophylaxis, have expanded potentially curative treatment options for patients (pts) without a matched donor. The DRI (Blood 2012;120:905), based on disease type and status, was developed to stratify pt risk across histologies and conditioning regimens. The current study evaluated the newly refined DRI (Blood 2014;123:3664) in the largest series of NMA haplo BMT to date. Methods: We retrospectively analyzed the outcomes of 374 consecutive adult hematologic malignancy pts who received NMA related haplo BMT with PTCy at Johns Hopkins. Eligibility included ECOG PS ≤ 2, LVEF ≥ 35%, adequate pulmonary and renal function and absence of uncontrolled infection. All pts received fludarabine (30 mg/m2IV D -6 to -2), Cy (14.5 mg/kg IV D -6 and -5), TBI (200 cGy D -1) and T-cell replete bone marrow. GVHD prophylaxis consisted of high-dose PTCy (50 mg/kg IV D 3 and 4), mycophenolate mofetil and tacrolimus. Maintenance therapy (e.g., imatinib) after engraftment was permitted. The median age was 55 (range 18-75) at BMT, 132 (35%) pts were aged ≥ 60 and 71 (19%) had prior autologous BMT. Diagnoses were acute leukemia or lymphoblastic lymphoma (115 pts; 31%), MDS or MPN (36 pts; 10%), aggressive NHL (95 pts; 25%), Hodgkin lymphoma (36 pts; 10%), mantle cell lymphoma (29 pts; 8%) and indolent lymphoid cancers (63 pts; 17%). By the new DRI, disease risk was low in 72 pts (19%), intermediate (int) in 242 (65%), high in 50 (13%) and very (v) high in 10 (3%). Overall results: With a median follow-up of 3.4 (range 0.5-11.4) years (y) in surviving pts, 3-y probabilities of PFS and OS were 40 (95% CI 35-45)% and 50 (45-56)%, respectively. The probability of neutrophil recovery was 89% by D30 (median 17 d). By competing-risk analyses, the D180 probability of nonrelapse mortality (NRM) was 8 (95% CI 5-10)%, grade 2-4 acute GVHD was 32 (27-37)%, and grade 3-4 acute GVHD was 4 (2-6)%. The 2-y probability of chronic GVHD was 13 (10-17)%. Results by DRI: Among the 3 DRI risk groups (low, int, high/v high), there were no statistically significant differences in histology (lymphoid vs myeloid), HCT-CI risk category, median CD34+ graft dose or pt CMV serostatus. Median pt age was greater in the higher risk groups (P = 0.01). On unadjusted analyses of the new DRI, the probability of relapse by competing-risk differed clearly between the groups (P 〈 0.0001; Fig. A), with no statistically significant difference in NRM (P = 0.53). This was coupled with statistically significant differences in both PFS and OS. In low, int and high/v high risk groups, 3-y PFS estimates were 64%, 37% and 22%, respectively (P 〈 0.0001; Fig. B), and 3-y OS estimates were 69%, 49% and 34% (P = 0.0001). Furthermore, on multivariate analyses adjusted for age and year of BMT, the new DRI was independently associated with overall outcomes. Compared to low-risk pts, the HR for relapse was 3.0 (95% CI 1.8-5.2) for int risk pts (P = 0.0001) and 4.7 (2.6-8.5) for high/ v high risk pts (P 〈 0.0001). HRs for both PFS and OS were ≥ 2-fold greater for int and high/v high risk pts compared to low risk pts (each P ≤ 0.0002). On multivariate analyses, the original DRI (13% low risk, 68% int, 19% high/v high) was also independently associated with relapse, PFS and OS (each P ≤ 0.003). When stratified by DRI, survival outcomes with reduced-intensity, matched related or unrelated BMT (based on 614 pts from the original DRI study cohort; personal communication, P. Armand) and haplo BMT with PTCy appeared similar (Table). Conclusion: The DRI appears to effectively stratify and prognosticate pts undergoing NMA haplo BMT. When stratified by DRI, the efficacy and survival outcomes with NMA haplo BMT with PTCy appear comparable to those reported with matched BMT. Within this transplant platform, the results support the use of the DRI in outcome analyses and randomized clinical trials involving heterogeneous groups of pts. Figure 1 Figure 1. Table Survival Estimates by DRI 3-y PFS (%) 3-y OS (%) Original DRI Matched Haplo Matched Haplo Low 66 63 70 71 Intermediate 31 39 47 49 High / very high 15 25 25 38 Figure 2 Figure 2. Disclosures Off Label Use: High-dose posttransplantation cyclophosphamide.

Description: Abstract 3084 Peripheral T-cell lymphoma (PTCL) is characterized by high rates of chemoresistance and relapse. The role of allogeneic (allo) BMT remains to be defined. Treatment-associated toxicities and donor availability remain key concerns. We reviewed the outcomes of 44 consecutive, related donor allo BMTs for PTCL performed at Johns Hopkins Hospital from 1994–2011. Nodal (n=23), extranodal (n=14), leukemic/disseminated (n=3), and cutaneous (n=4) histologies were represented. This was a poor-risk cohort, with 60% receiving 〉 2 prior chemotherapy regimens, 50% having history of chemorefractory disease, and 25% having active disease at BMT. Patients receiving reduced-intensity conditioning (RIC) were significantly older (median 59 years, range 24–70) than patients receiving myeloablative conditioning (MAC; median 46 years, range 18–64), p=0.01; median age at RIC/haplo BMT was 60. Thirty patients received post-transplantation cyclophosphamide (PT/Cy) as part of their GVHD prophylaxis, including all RIC/HLA-haploidentical (haplo) BMTs (n=18), all RIC/HLA-matched BMTs (n=6), 3 of the 4 myeloablative conditioning (MAC)/haplo BMTs, and 3 of the 16 MAC/HLA-matched BMTs (where PT/Cy was the sole GVHD prophylaxis). With 3.9 years median follow-up for survivors (range 0.5–13.7 years), the estimated 3-year progression-free survival (PFS) and overall survival (OS) were both 37% (95% confidence interval (CI) 24–56% and 24–57%). In older patients (〉 60, n=14), the estimated 2-year PFS and OS were 38% (CI 13–63%) and 45% (CI 20–73%); in patients 〈 60 (n=30), 2-year PFS and OS were 41% (95% CI 24–59%) and 43% (95% CI 25–61%). On unadjusted analysis, there was a tendency towards superior PFS for allo BMT in first remission versus beyond first remission, with an estimated 3-year PFS of 53% (95% CI 34–82%) versus 23% (95% CI 10–51%), p=0.08. Of the 15 patients who remain alive in sustained remission, ten received allo BMT in first remission; represented among these ten are especially poor-risk histologies, including adult T-cell leukemia/lymphoma, hepatosplenic gamma-delta T-cell lymphoma, and subcutaneous panniculitis-like gamma-delta T-cell lymphoma. With a median time to relapse of 3.2 months (interquartile range 1.8–8.8 months), the estimated 3-year cumulative incidence of relapse was 46% after MAC, 56% after RIC, and 50% after RIC/haplo BMT by competing risk analysis. Estimated 1-year non-relapse mortality was 10% for MAC, 8% for RIC, and 11% for RIC/haplo BMT. On competing risk analysis, cumulative incidences of acute grade II-IV GVHD and chronic GVHD were 16% and 19%, with no differences between matched and haplo donors. On unadjusted analysis, patients with acute grade II-IV or chronic GVHD had a 17% probability of relapse, compared to 66% in patients without GVHD, p=0.02. Allo BMT affords long-term survival for a subset of PTCL patients. This RIC/haplo platform substantially expands allo BMT options to most patients with PTCL, including those who are older and unable to tolerate high-dose conditioning. Allo-BMT may be appropriate in first remission in select high-risk cases. Disclosures: Symons: Busulfex: Research Funding.

Description: Key Points Nonmyeloablative, related HLA-haploidentical BMT utilizing high-dose posttransplantation cyclophosphamide has a favorable safety profile. Risk-stratified relapse and survival outcomes with this approach are comparable to those of HLA-matched BMT.