Abstract: 7006 Background: AlloHCT has been regarded as risky in HIV pts, with concern about fatal infection. We set out to assess feasibility and safety of alloHCT in this first prospective multicenter trial. Methods: The primary endpoint was 100-day non-relapse mortality (NRM). Pts had drug-susceptible HIV; age ≥ 15 yr; adequate organ function; acute myeloid leukemia (AML) or acute lymphocytic leukemia (ALL), high risk myelodysplastic syndrome (MDS), or Hodgkin (HL) or non-Hodgkin lymphoma (NHL) beyond first CR; an 8/8 HLA-matched related or at least a 7/8 unrelated donor. Pts received myeloablative (MA) or reduced intensity (RI) regimens. HIV outgrowth assays (VOA) were performed with resting CD4+T-cells in pts who had clinically undetectable HIV plasma RNA at 1 yr. Results: Between 5/2012 and 12/2015, 17 pts underwent alloHCT. Pts were: male (17); white (11), African American (3), Other/Unknown (3); median age 47 yrs (25-64). Associated malignancies were AML (9), ALL (2), MDS (2), HL (1), NHL (3). Median CD4 was 224 (55-833). Conditioning was MA (8) and RI (9). At 100 days there was no NRM, 13 pts were in CR, 4 pts had relapsed/progressive disease; and 8 pts achieved complete chimerism. The cumulative incidence of Grades (Gr) II-IV acute Graft vs Host Disease (GvHD) was 41 % (95%CI: 18 %, 64%). At 6 mo, OS was 82 % (95% confidence interval [CI] : 55%, 94%); 9 pts achieved complete chimerism. At 1 year, OS was 57 % (CI: 31%, 77 %); 8 deaths were from relapsed/progressive disease (5), acute GvHD (1), adult respiratory distress syndrome (1) and liver failure (1). Infections were reported in 11 pts (3 Gr 2, 8 Gr 3). Infectious HIV was detected by VOA in 2 of 3 pts who were mixed chimeras but 0 of 2 who were 100% donor. Median follow up of survivors is 24 mo (7 to 27 ). Conclusions: HIV pts with heme malignancies underwent MA or RI alloHCT without any100-day NRM and there were no infectious deaths at 1 year. AlloHCT should be considered the standard of care for HIV pts who meet usual eligibility criteria. Clinical trial information: NCT01410344.

Abstract: Introduction. Our previous flow cytometry-based comparison of HIV(+) and HIV(-) autologous hematopoietic stem cell transplant (auto-HSCT) recipient immunomes at 56, 180 and 365 days post-transplant to each other and to healthy controls (HCs) showed that both sets of auto-HSCT recipient immunomes approached HCs over time, but retained significant differences. HIV(+), but not HIV(-), auto-AHCT recipients retained pro-inflammatory features consistent with chronic HIV infection. Here, we report the results of a quantitative and functional analysis of immune reconstitution in HIV(+) patients treated with allogeneic hematopoietic stem cell transplant (allo-HSCT), in comparison with HIV(+) auto-HSCT recipients and HCs. Methods. Blood samples were collected for analysis at days 56, 180 and 365 post-transplant from HIV(+) transplant recipients and at 1 time point from HCs. Whole blood analysis was performed by five-color flow cytometry across 100 immune marker combinations. Comparisons were made between HIV(+) allo-HSCT recipients (n=17, acute myeloid leukemia, acute lymphocytic leukemia, myelodysplastic syndrome, Hodgkin and non-Hodgkin lymphoma that received myeloablative or reduced intensity conditioning on the BMT-CTN-0903/AMC-080 trial), HIV(+) auto-HSCT recipients (n=36, aggressive B cell non-Hodgkin lymphoma or Hodgkin lymphoma that received myeloablative conditioning on the BMT-CTN-0803/AMC-071 trial) and 71 HCs. Unsupervised principal component analysis (PCA) examined differences in immune cell proportions, identified by flow cytometry across 100 cell subsets at each time point. Wilcoxon rank-sum tests compared median absolute counts and median proportions of cell subsets. An independent feature importance score analysis (FIS) identified contributions of immune cell populations expressing specific immune marker combinations to the differences between HIV(+) auto-HSCT recipients, HIV(+) allo-HSCT recipients and HCs. Functional responsiveness of HIV(+) allo-HSCT recipients' T cells to stimulation with CD3- and CD28-directed antibodies, NK cells to stimulation with IL-12 and IL-18 and monocytes to stimulation with lipopolysaccharide (LPS) was assessed in a preliminary mass cytometry on peripheral blood mononuclear cells isolated at the same time points (n=2) and compared to HCs (n=2). Results. PCA showed that immunomes of HIV(+) allo-HSCT recipients and HIV(+) auto-HSCT recipients clustered together with each other, but away from HCs at all time points throughout the post-transplant year. FIS identified: 1) 13 cell subsets that defined the difference between HIV(+) allo-HSCT recipients (all visits) and HCs, and 2) 11 immune cell subsets that defined the difference between HIV(+) auto-HSCT recipients (all visits) and HCs; in both of these comparisons, activated CD3+/HLA-DR+ T cells had the greatest impact on the difference between HIV(+) and HC immunomes. At 1 year, both HIV(+) transplant recipient cohorts had higher absolute numbers of activated T cells, effector T cells and CD8+ T cells than HCs (Wilcoxon rank-sum test, p 〈 0.0031). HIV(+) autologous and allogeneic HSCT recipients also had lower numbers of CD4+ T cells, naïve T cells and activated NK cells compared to HCs (p 〈 0.0031). FIS also identified 20 immune cell subsets that defined the difference between HIV(+) autologous and allogeneic HSCT recipients immunomes at 1 year, with CD8+/CD27- effector T cell subset exerting the highest impact on the difference. Preliminary functional mass cytometry analysis of 2 HIV(+) allo-HSCT recipients and 2 HCs showed that: 1) IFNʏ production by CD8+ T cells was increased above that of HCs at all time points. 2) Expanded populations of CD4+/T-bet+ cytotoxic cells expressing granzyme B and perforin, and CD8+ cytotoxic T cells expressing granzyme B and perforin, persisted in HIV(+) allo-HSCT recipients at all time points, but not in HCs. 3) NK cells retained an ability to produce IFNʏ in response to stimulation with IL-12 and IL-18 in HIV(+) allo-SCT recipients. 4) Monocytes showed an enhanced production of TNFα in response to stimulation with LPS in HIV(+) allo-HSCT recipients compared to HCs at 1 year post-HSCT. Conclusion. Chronic HIV infection confers the pro-inflammatory immune features on the phenotypic and functional profiling of the T lymphocyte immunome of stem cell transplant recipients, irrespective of allogeneic or autologous stem cell donor source. Disclosures Devine: Bristol Myers: Other: Grant for monitoring support & travel support; Kiadis Pharma: Other: Protocol development (via institution); Magenta Therapeutics: Other: Travel support for advisory board; My employer (National Marrow Donor Program) has equity interest in Magenta. Noy:Janssen: Consultancy; Medscape: Honoraria; Prime Oncology: Honoraria; NIH: Research Funding; Pharamcyclics: Research Funding; Raphael Pharma: Research Funding. Popat:Bayer: Research Funding; Incyte: Research Funding; Jazz: Consultancy. Hofmeister:Celgene: Honoraria; Janssen: Membership on an entity's Board of Directors or advisory committees; Nektar: Honoraria, Membership on an entity's Board of Directors or advisory committees; Karyopharm: Membership on an entity's Board of Directors or advisory committees; Imbrium: Membership on an entity's Board of Directors or advisory committees; Oncopeptides: Membership on an entity's Board of Directors or advisory committees. Navarro:Atara Biotherapeutics: Employment, Equity Ownership. Behbehani:Fluidigm corporation: Other: Travel funding. Lozanski:Boehringer Ingelheim: Research Funding; Beckman Coulter: Research Funding; Stemline Therapeutics Inc.: Research Funding; Genentec: Research Funding. Baiocchi:Prelude: Consultancy.

Abstract: Background: Clinical outcomes for patients with HIV-related lymphomas who have undergone autologous hematopoietic cell transplantation (AHCT) are similar to HIV-negative patients (Alvarnas et al., Blood 2016). Here we report a detailed, longitudinal immunophenotypic and functional evaluation of immune recovery of patients enrolled on the BMT CTN 0803/AMC 071 multicenter phase II study (clinicaltrials.gov NCT01141712). Methods: Comprehensive analysis of cellular immunome was performed using 5 color flow cytometry. Acquisition and analysis was performed via FC500 cytometry analyzers with CXP software and prism plot. Comparisons were made between HIV+ and HIV- cohorts of peripheral blood mononuclear cell (PBMC) subsets at 56, 180, and 360 days post AHCT. The HIV- cohort was collected from 30 multiple myeloma patients enrolled in a longitudinal immune recovery study after AHCT (median age 52.5 years (18-71); 57% male, no post AHCT exposure to IMID or other treatment). Control samples were collected from 72 healthy volunteers (median age of 49 (21-68); 53%, M). A Wilcoxon rank sum test was utilized to compare the HIV+ and HIV- groups to controls and to each other at each time point for 18 immune cell subsets common to all three panels. An unsupervised analysis was performed utilizing a principal component analysis (PCA) to look for overall differences in the cohorts. Similar methodologies were used to compare HIV+ to controls that analyzed 100 PBMC subsets. Functional immune recovery was evaluated by IFNg Elispot assay where 2x105 PBMC collected at each time point were pulsed with control, EBV (BZLF1) or HIV (GAG) pepmix preparations. As a control for TCR responsiveness, anti CD3/CD28 antibody-beads were used to immobilize TCR in ELISPOT assay. T cell responses from PBMCs of each of the three time points of HIV+ patients on trial were compared to PBMCs from HIV- donors (n=6). Results: Wilcoxon Rank sum tests show significant differences between transplant patients and controls and between HIV+ and HIV- patients at all visits. There are fewer cell subsets significantly different at day 365 compared to day 56 or 120 in all comparisons. The PCA showed group differences between HIV+, HIV- and control subjects. CD3+/HLA-DR+ (late activation), CD8+/CD25- (cytotoxic T cells) and CD3+/CD314+ (T cells with activating NKG2D) were found to be more prevalent in HIV+ transplant patients. These findings may be consistent with expanded populations of chronically activated cytotoxic T lymphocytes in HIV+ transplant patients. Subsets of NK, Th1 and Th2 cells showed statistically significant differences between HIV+ (low), HIV- (higher) and controls (higher). When the principal components are plotted by visit there is a pattern of both HIV+ and HIV- transplant patients clustering closer to controls as patients recover from AHCT. The PCA was also utilized to compare the HIV+ cohort to controls which had the same panel of cell subsets tested and allowed for the use of 100 cell subsets in the analysis. This analysis showed a similar group separation and pattern of clustering closer to controls in later visits. These findings demonstrate complex interactions between T and NK cell subsets. Functional assessment of antigen-specific T cell responsiveness was evaluated in Elispot assays with EBV (BZLF1) and HIV (GAG) recall antigens and anti-CD3/CD28 controls. Of 30 evaluable patients, 28 HIV+ patients demonstrated measurable IFNg production in response to GAG (spots/2x105 PBMC, range: 8-615), 21 showed measurable response to BZLF1 pepmix (range 12-450); and all patients demonstrated responsiveness to anti CD3/CD28 stimulation. Magnitude of IFNg production from HIV+ samples was generally higher than that observed healthy, HIV- controls. Assessment of NK cell responsiveness is currently underway. Conclusions: While clinical outcomes following AHCT between HIV+ and HIV- patients is comparable, clear distinctions were observed with immune recovery of specific PBMC subsets during the first year following AHCT with differences diminishing as patients recover post transplant. Longitudinal immune responsiveness of PBMC from HIV+ patients to EBV and HIV recall antigens and TCR stimulation generally showed more robust IFNg production compared to PBMCs from HIV- volunteer controls. These data provide further justification supporting AHCT as an option for HIV+ patients provided they meet standard transplant criteria. Disclosures Little: This study was coordinated by the ECOG-ACRIN Cancer Research Group (Robert L. Comis, MD and Mitchell D. Schnall, MD, PhD, Group Co-Chairs) and supported by the National Cancer Institute of the National Institutes of Health under the following award number: Employment. Noy:Pharmacyclics, LLC, an AbbVie Company: Other: travel, accommodations, expenses, Research Funding. Krishnan:celgene: Consultancy, Speakers Bureau; takeda: Consultancy, Speakers Bureau; janssen: Consultancy, Speakers Bureau; onyx: Speakers Bureau. Hofmeister:Signal Genetics, Inc.: Membership on an entity's Board of Directors or advisory committees; Celgene: Research Funding; Arno Therapeutics, Inc.: Research Funding; Incyte, Corp: Membership on an entity's Board of Directors or advisory committees; Janssen: Pharmaceutical Companies of Johnson & Johnson: Research Funding; Karyopharm Therapeutics: Research Funding; Takeda Pharmaceutical Company: Research Funding; Teva: Membership on an entity's Board of Directors or advisory committees. Forman:Mustang Therpapeutics: Other: Construct licensed by City of Hope. Lozanski:Boehringer Ingelheim: Research Funding; Beckman Coulter: Research Funding; Stemline Therapeutics Inc.: Research Funding; Genentech: Research Funding. Baiocchi:Essanex: Research Funding.

Abstract: Background: The benefit of allogeneic blood or marrow transplantation (alloBMT) following myeloablative conditioning (MAC) in first complete remission (CR1) compared to chemotherapy has been demonstrated in a randomized trial for adults with acute lymphoblastic leukemia (ALL). Persistence of measurable residual disease (MRD) prior to alloBMT confers an increased risk of relapse. Blinatumomab eradicates persistent or recurrent MRD at levels ≥10 -3 in 78% of B ALL. However, post-hoc analyses of patients who have undergone alloBMT following blinatumomab for MRD demonstrate non-relapse mortality (NRM) of 36.5%. NRM following nonmyeloablative (NMAC) alloBMT with high-dose post-transplantation cyclophosphamide (PTCy) is just 11%. Given broadly similar outcomes between HLA-matched MAC alloBMT and HLA-haploidentical NMAC alloBMT following PTCy, we have shifted to using exclusively NMAC alloBMT with PTCy and sought to explore outcomes depending on receipt of pre-transplant blinatumomab. Methods: The bone marrow transplant database at Johns Hopkins was queried for adult patients with Ph-negative B-ALL who received NMAC alloBMT in CR1 using PTCy between January 2008 and July 2020. Characteristics of patients were summarized and compared using the student's T test for continuous variables and Fisher's exact test for categorical variables. Estimators of OS and RFS were reported using the Kaplan-Meier method. Differences in time-to-event outcomes were estimated using Cox proportional hazards model for OS and RFS, and Fine and Gray's model for cumulative incidence of relapse (CIR)/NRM considering competing events. Results: Among the 50 identified patients undergoing 1 st transplant in CR1 with NMAC, all received conditioning with fludarabine and cyclophosphamide followed by total body irradiation (TBI). In addition to PTCy, all patients received mycophenolate mofetil and either tacrolimus or sirolimus as GVHD prophylaxis. Sixteen patients (32%) received blinatumomab in CR1 or achieved CR1 following blinatumomab and proceeded to transplant without intervening therapy, while 34 patients (68%) did not. At the time of treatment with blinatumomab; 3 patients had & gt;5% blasts after chemotherapy, 8 had persistent or recurrent MRD & gt;10 -4 after chemotherapy, and 5 had no evidence of MRD at a sensitivity of 10 -4. Among the 5 MRD- patients treated with blinatumomab; 1 had been refractory to their first course of chemotherapy (67% blasts), 3 had MRD & gt;10 -4 at the first MRD response assessment following chemotherapy, and 1 had CNS involvement at diagnosis. The demographics of these two groups are presented in Table 1 and separated by pre-transplant blinatumomab status. The groups were well balanced in terms of gender, age, WBC at diagnosis, CNS involvement at diagnosis, and donor type. Patients who received blinatumomab were more likely to have been refractory to their initial course of chemotherapy and were transplanted later after their initial diagnosis than those who did not. All patients who received blinatumomab were MRD-negative at a sensitivity of 10 -4 prior to their transplant, while 11.8% of patients who did not receive blinatumomab were MRD-positive. Relapse-free and overall survival, cumulative incidence of relapse, and non-relapse mortality by receipt of blinatumomab prior to transplant are shown in Figure 1. Non-relapse mortality was not increased among patients who received pre-transplant blinatumomab (HR=1.06, p=0.94). The causes of non-relapse mortality included GVHD (1) and secondary malignancy (1) in patients who received blinatumomab; and infection (1), bleeding (1), secondary malignancy (1), and other (1) in patients who did not receive blinatumomab. Receipt of pre-transplant blinatumomab was associated with a decreased cumulative incidence of relapse (HR=0.15, p=0.07) and improved relapse-free survival (HR=0.32, p=0.07). Overall survival (HR=0.63, p=0.5) between the two groups was similar, likely reflecting the efficacy of salvage therapies such as CD19 CAR T cells; blinatumomab; and inotuzumab in the relapsed, post-transplant population. Conclusions: Treatment with blinatumomab prior to NMAC alloBMT with PTCy in CR1 for Ph-negative B ALL did not increase NRM and produced a 3-year RFS of 81%. The low CIR and NRM of NMAC alloBMT in an MRD-negative CR1 following blinatumomab suggest it could be a viable alternative to MAC. Figure 1 Figure 1. Disclosures Webster: AmGen: Consultancy; Pfizer: Consultancy. DeZern: Takeda: Consultancy, Membership on an entity's Board of Directors or advisory committees; Taiho: Consultancy, Membership on an entity's Board of Directors or advisory committees; Novartis: Consultancy, Membership on an entity's Board of Directors or advisory committees; Bristol-Myers Squibb: Consultancy, Membership on an entity's Board of Directors or advisory committees. Levis: Takeda: Honoraria; BMS: Consultancy, Honoraria, Membership on an entity's Board of Directors or advisory committees; Pfizer: Consultancy, Honoraria; Jazz: Consultancy, Honoraria; Astellas and FujiFilm: Research Funding; Amgen, Astellas Pharma, Daiichi-Sankyo, FujiFilm, and Menarini: Honoraria; AbbVie: Consultancy, Honoraria, Membership on an entity's Board of Directors or advisory committees. Ghiaur: Syros Pharmaceuticals: Consultancy; Menarini Richerche: Research Funding. Hourigan: Sellas: Research Funding. Jain: Syneos Health: Research Funding; CTI Biopharma: Research Funding; CareDx: Other: for advisory board participation; Bristol Myers Squibb: Other: for advisory board participation; Targeted Healthcare Communications: Consultancy. Ali: Janssen: Consultancy; BMS: Consultancy; Oncopeptides: Consultancy; Sanofi: Consultancy; Amgen: Consultancy; Aduro: Consultancy; Poseida: Research Funding; Aduro: Research Funding; BMS: Research Funding.

Abstract: e19045 Background: Mismatched blood or marrow transplantation (BMT) using post-transplantation cyclophosphamide (PTCy) for graft-versus-host disease (GvHD) prophylaxis has not been well-studied in CTCL. Methods: We analyzed all patients above 18 years old with relapsed/refractory CTCL undergoing mismatched alloBMT. Primary endpoints included disease-free survival (DFS) and overall survival (OS). Secondary endpoints included time to neutrophil and platelet recovery, GvHD outcomes, and day +30 and day +60 donor chimerism. Results: From 2003-2020, 8 patients with relapsed CTCL underwent mismatched related (n=7) or mismatched unrelated (n=1) BMT. Mean age was 50 years (range 30-62); median time from diagnosis was 2 years (range 1.3-11.4). All had received prior treatment for their disease; two (25%) had received immune checkpoint inhibitors. Four (50%) were in partial response and 4 (50%) were in complete remission prior to BMT. Six received bone marrow grafts. Two received mobilized peripheral blood. Five (62.5%) achieved full donor chimerism by day 30 after BMT; 6 (75%) had achieved full donor chimerism by day 60 after BMT. One patient failed to engraft. Mean time to neutrophil recovery was 17.3 days (range 17-45); mean time to platelet recovery was 28.4 days (range 11-69). Median DFS was 11.3 months (95% confidence interval 2.6 months-not reached). Median OS was not reached. One patient developed grade 1 acute GvHD, and 2 patients developed mild chronic GvHD. There were no instances of transplantation-related mortality (TRM). At 1 year post-BMT, 4 patients had relapsed (50%), and no patients had died. At 3 years post-BMT, 7 patients had relapsed (87.5%), and 1 patient had died (12.5%). Conclusions: In our preliminary retrospective study, partially mismatched BMT with PTCy-based GVHD prophylaxis for advanced-stage CTCL was associated with minimal GvHD, no TRM, and good long-term survival. Investigation into relapse reduction is warranted.[Table: see text]

Abstract: To evaluate BMT outcomes in patients (pts) with newly diagnosed or relapsed mantle cell lymphoma, 58 consecutive pts were selected through the BMT registry at Johns Hopkins. Flow cytometric and immunohistochemical features were confirmed. Fifty-four pts (88%) had stage III or IV disease and 39 (67%) had documented bone marrow involvement at diagnosis. First-line therapy was CHOP +/− rituximab in 71% and was fludarabine-based in 17%. Thirty-seven pts (64%) were transplanted after first partial or complete remission, 14 pts (24%) after one or more relapses, and 12% after primary induction failure (PIF). Median age at BMT was 55 years. Thirty-eight pts (66%) received autologous (auto) BMT, 19 pts (33%) allogeneic (allo) BMT, and 1 pt syngeneic BMT. Preparative regimens in all but 1 case consisted of cyclophosphamide plus busulfan or total body irradiation. The estimated 3-year event-free survival (EFS) following BMT was 51% (95% CI, 35–65%), probability of relapse 31% (17–51%), and overall survival 59% (42–73%). Median follow-up is 16 months (range 〈 1 month to 79 months) for all pts and 23 months for surviving pts. Twelve relapses were documented, 8 after auto BMT. Four auto pts and 1 allo pt are alive with relapsed disease, and 3 auto pts developed MDS or AML. Actuarial EFS at 3 years was 57% (CI 35–74%) after auto BMT and 37% (17–57%) after allo BMT. Actuarial relapse rate at 3 years was 34% following auto BMT and 19% following allo BMT. On multiple regression analysis, BMT after one or more relapses (HR 3.0, CI 1.2–7.4, P = 0.02), PIF (HR 5.4, CI 1.9–15.4, P = 0.002), and allo BMT (HR 3.0, CI 1.3–6.8, P = 0.007) predicted an inferior EFS; Figure Figure whereas PIF and residual bone marrow involvement independently predicted relapse. Notably, however, EFS curves were not statistically different for auto and allo BMT performed in first remission, with the 3 year EFS approaching or equaling 70%. Figure Figure The benefit of BMT for mantle cell lymphoma is thus most apparent when performed in first remission. While the comparative efficacy of auto and allo BMT remains to be determined, allo BMT warrants continued study especially early in the disease course.

Abstract: Background: [18F] FDG-PET after only 2–3 cycles of chemotherapy is highly prognostic in newly diagnosed aggressive non-Hodgkin’s lymphoma (NHL), with reported relapse rates of 71–100% after standard therapy if midtreatment PET remains positive. We hypothesized that early treatment intensification, based on individualized risk assessment by PET, would improve outcome. Methods: A phase II, single center trial was activated in 2/2004 for patients (pts) with newly diagnosed aggressive NHL. PET-CT was performed between days 11 and 20 of cycle 2 or 3 of CHOP + rituximab (R). Pts whose PET scan was considered positive on semiquantitative visual interpretation, irrespective of stage or international prognostic index (IPI), received 2 cycles of (R)ESHAP or (R)ICE, followed by autologous stem cell transplantation (SCT) with busulfan-cyclophosphamide conditioning. Biopsies of FDG positive areas were not performed. Pts with negative midtreatment PET completed standard therapy. Tumor FDG uptake was graded on a 5-point scale: 0, no tumor activity (cold); 1+, minimal; 2+, equivocal (equal to mediastinal blood pool); 3+, moderately greater than blood pool; 4+, strong. Scores of 3+ or 4+ were considered positive. Results: As of 8/16/2007, 58 evaluable pts have been accrued, 55 with large B-cell lymphoma. Median age at diagnosis was 51 (20–78); 39 pts had stage III or IV disease. Thirty-two pts (55%) had positive midtreatment PET (17 with score of 3+, 15 with score of 4+). Twenty-six pts (45%) had negative midtreatment PET (10 with score of 0, 3 with score of 1+, 13 with score of 2+). PET was positive in 23 of 38 pts (61%) with IPI 0–2 and in 9 of 18 pts (50%) with IPI 3-5; 2 pts had undetermined IPI. Twenty-eight of 32 pts with positive midtreatment PET have completed SCT; 3 were ineligible because of early disease progression; 1 withdrew consent. At a median follow-up of 20.4 months, their actuarial 2-year event-free survival (EFS) after SCT is 67% (figure). Overall, 19 of 28 transplant recipients are alive and without evidence of relapse or secondary cancers: 6 relapsed at a median of 3.6 months ( & lt; 1–17 months) after SCT; 1 died of venoocclusive disease (1.4 months); 1 developed MDS (24.8 months); 1 had an unrelated death (9.9 months). On intent-to-treat analysis, the actuarial 2-year EFS from the time of midtreatment imaging is 60% if PET positive (including pts not eligible for transplant), 86% if PET negative. Of the PET negative pts, 2 have relapsed and 1 developed AML. Conclusion: These data confirm the strong prognostic value of negative midtreatment PET scans, with excellent outcomes in such pts treated with (R)CHOP alone. Early treatment intensification for poor-risk pts, as identified by midtreatment PET, results in a significantly better outcome than that achieved historically. Outcome for midtreatment PET positive pts Outcome for midtreatment PET positive pts