ALBERT

Description: Conventional chromosome analysis (CCA) and interphase fluorescence in situ hybridization (FISH) was performed in 42 patients with mantle-cell lymphoma (MCL), with BCL1 rearrangement. The t(11;14)(q13;q32) or 11q abnormalities were detected by CCA in 34 cases, 20 of which had additional aberrations. A normal karyotype was observed in 8 cases. Probes detecting the chromosome aberrations that were observed in at least 3 cases by CCA, ie, +12, 13q14 deletion, and 17p deletion, were used for interphase FISH analysis. FISH detected total or partial +12, 13q14 deletion and 17p- in 28.5%, 52.4%, and 26% of the cases, respectively. The presence of these anomalies was not a function of karyotype complexity. Based on the results of CCA/FISH, three groups of increasing karyotype complexity were recognized: group 1, including 11 patients without detectable aberrations in addition to BCL1 rearrangement; group 2, including 14 patients with 1 to 2 additional anomalies; and group 3, including 17 patients with three or more additional anomalies. Clinical parameters associated with shorter survival were male sex (P= .006) and primary lymph-node involvement compared with primary bone marrow involvement (P = .015). Trisomy 12 was the only single cytogenetic parameter predictive of a poor prognosis (P = .006) and the best prognostic indicator was the derived measure of karyotype complexity (P 〈 .0001), which maintained statistical significance in multivariate analysis (P〈 .0001). We arrived at the following conclusions: 13q14 deletion occurs at a high incidence in MCL; 17p deletion and total/partial +12 are relatively frequent events in MCL, the latter aberration being associated with a shorter survival; and the degree of karyotype complexity has a strong impact on prognosis in this neoplasia.

Description: Several studies have shown that therapy-related MDS (tMDS) and AML (tAML) have a poor outcome with very few long-term survivors. Curative treatment strategies are not yet standardized and the role of hematopoietic stem cell transplantation (SCT) is still not fully elucidated in standard care treatment. We performed a retrospective outcome research with the aim of looking at the survival curves of tMDS and tAML patients treated at 7 different Institutions. According to the presence of comorbidities or a matched donor, 71 patients (pts) received the best treatment option based on attending physician opinion: 24 pts (group A) with tAML (n=13, FAB M0, M1, M2, M4) and tMDS (n=7 RAEB-2. n=4 RAEB-1) received allogeneic transplantation, 28 pts (group B) with tAML (n=20, FAB M0, M1, M2, M4, M5) and tMDS (n=3 RAEB-2, n=4 RAEB-1, n=1 RA) received chemotherapy and 19 pts (group C) received supportive care only (n=1 tAML, n=18 low-risk MDS or RAEB-1 (n=5)). Median age was 55 years (range 23–67) in group A, 61 years (range 27–73) in group B and 55 years (range 22–70) in group C. Conventional karyotype analysis was available in 12 pts of group A (n=7 complex, n=1 normal, n=2 isolated del(7q) or monosomy 7, n=1 isolated del(5q), n=1 trisomy 21) and in 15 pts of group B (n=3 complex, n=8 normal, n=1 isolated del(Y), n=1 isolated del(11), n=1 isolated trisomy 11, n=1 isolated trisomy 8). In the group A, all pts, because of age and/or comorbidities, received a fludarabine-based reduced-intensity conditioning followed by allogeneic peripheral blood SCT. Disease status at transplant was categorized as low risk (n=9 CR1 or CR2), high risk (n=3 PR, n=6 PD, n=2 refractory) and 4 pts were treated up-front. The median time from diagnosis to allografting was 6 months (range: 1–80 months). Pts received allogeneic stem cells from HLA-matched siblings (n=16), or HLA-matched unrelated donors (n=6), or haploidentical related donors (n=2). All pts engrafted. Acute GVHD grade II–IV occurred in 6 pts (n=1 post-DLIs), chronic GVHD developed in 6 pts (n=1 post-DLIs). OS at 5 years was 5.5%, the 4-year EFS was 0%, TRM at 100 days and at 1 year were 28%. No statistical differences were observed in TRM, EFS, and OS according to disease status at transplant and diagnosis of tMDS or tAML. DFS for pts in CR at transplant was 23% at 1 year. In the group B, pts received chemotherapy and 11 of them an autologous stem cell transplantation. OS at 5 years was 16%, EFS at 5 years was 10%, DFS at 1 year was 31%. TRM at 5 years was 30%. In the group C, OS was 28% at 5 years. Our data show that, in daily clinical practice, the outcome of patients receiving chemotherapy followed by allogeneic SCT is not improved compared to the patients not having a suitable donor. At the present time, considering the very low chance of cure, in therapy-related disorders the main goal for clinicians should be prevention.

Description: Haploidentical stem cell transplantation (SCT) can be used in relapsed haematological malignancies for patients lacking a matched sibling or unrelated donor. Major barriers of this strategy are the poor immune reconstitution and the high risk of relapse. Here, we report results of a phase I–II trial evaluating early add-backs of CD8-depleted donor lymphocytes (DLIs) (from 1x10^4 up to 1x10^5 cells/kg starting at day+45 up to day +105 at monthly intervals) after a reduced intensity conditioning (RIC) regimen [thiotepa (10 mg/kg), fludarabine (120 mg/sqm), cyclophosphamide (60 mg/kg) and TBI (2 Gy)]. Ex-vivo and in-vivo TCD were carried out by CD34+ cell selection using the CliniMACS device and alemtuzumab (15mg/m2, day-2), respectively. Twenty-one patients [n= 10 NHL (n=5 CLL, n=5 high-grade NHL), n=7 HL, n=1 MM, n=1 ALL, n=2 AML] were transplanted with advanced disease: 16 (76%) failed a previous autograft and 13 (62%) had refractory disease. A median of 10.4x10^6/Kg CD34+, 1x10^4/kg CD3+, 10x10^4/kg CD19+, 0.9 x10^4/kg NK+ were infused. All patients engrafted with full donor chimerism from day +90. At a median follow-up of 12 months (range, 4–41 months), 12 of 21 pts are alive (7 CR, 2 PR and 3 PD) and 9 died [n=3 infection with GVHD (+610, +187, +253), n=6 disease]. The estimated 2-year overall survival was 49%: pts transplanted in remission had better outcome (83% versus 31%, p=0.13). The estimated 2-year cumulative incidence of TRM and relapse were 27% and 58%, respectively. CMV reactivation and hospital readmissions for opportunistic infections occurred in 76% and 57% of patients, respectively. For CD8 depletion of donor leukaphereses, a new depletion protocol using clinical grade CD8 microbeads (Miltenyi) was applied. This procedure is efficient to reduce the content of CD8 T cells by 3 logs while the median cell recovery of CD3+, CD4+, CD56+/CD3+, CD 20+ was 60%, 86%, 54%, 72%, respectively. Before DLIs, only 2 of 21 patients (10%) developed acute GVHD (no grade III–IV). A total of 36 CD8-depleted DLIs were administered to 17 pts without any acute toxicity. Following DLIs, 6 pts (35%) developed acute GVHD (grade II) and 5 (30%) chronic GVHD (n=2 limited, n=3 extensive). Overall, the incidence of acute GVHD is higher (50% vs 22%, p=0.33) in pts receving larger numbers of donor cells (10–15x10^4/kg versus 3–5x10^4/kg CD8-depleted DLIs). The median values of CD4+/uL, CD8+/uL and NK+ were 100, 280 and 680 at 4 months and 220, 200, 500 at 6 months after SCT in patients receiving CD8-depleted DLIs. Measurable TREC/ucg DNA (mean value 316; mean value donors 3740) and polyclonal T cell repertoire, evaluated by spectratyping, were observed at 9 months in patients younger than 40 years and/or without GVHD. Our results suggest that: haploidentical SCT with RIC regimen provides high engraftment rate T-cell addback allows the achievement of more than 100/uL CD4+ at 4 months after SCT in the majority of patients Survival rate is promising in patients who had transplantation in remission suggesting that this strategy should be evaluated earlier in high risk haematological diseases.

Description: Placental growth factor (PlGF) is a member of the vascular endothelial growth factor (VEGF) family which signals through VEGF receptor-1. In mice, administration of an adenoviral vector expressing human PlGF accelerates bone marrow recovery following myelosuppression and mobilizes PBPCs. By injecting either murine or human PlGF alone, we failed to detect any PBPC mobilization in mice, whereas the combined injection of PlGF plus G-CSF resulted in a 2- to 4-fold increase of PBPCs. Due to the relevant clinical impact of any procedure capable of improving PBPC mobilization, we tested the mobilizing activity of PlGF (Geymonat S.p.A., Anagni, Italy) as an adjunct to G-CSF in a nonhuman primate model. A cohort of Rhesus Monkeys (n = 4) was initially mobilized with G-CSF alone (100 μg/kg/day, SC, for 5 days) (cycle 1), and after a 6-week wash-out period, received a second mobilization therapy consisting of PlGF (130 μg/kg, IV, for 5 days) plus G-CSF (cycle 2). After an additional 6-week wash-out period, a third mobilization cycle consisting of PlGF (260 μg/kg, IV, for 5 days) plus G-CSF (cycle 3) was administered. Hematopoietic mobilization was evaluated by white blood cell counts (WBCs), committed colony-forming cells (CFCs), high-proliferative potential CFCs (HPP-CFCs), and long-term culture-initiating cells (LTC-ICs). Mobilization parameters were analyzed daily during treatment (days 1 to 5), and 3 and 5 days post-cessation of therapy. As compared to baseline values, a 5-day administration of G-CSF alone induced an average 5-fold increment of the mean (±SD) WBC counts (8,708±2,458 vs 43,523±13,790, P ≤.005). As compared to G-CSF alone, the peak values of WBCs were slightly increased by adding PlGF at 130 μg/kg (60,040±9,508) or 260 μg/kg (49,048±7,120). As compared to pretreatment values, the absolute numbers of circulating CFCs per ml blood were increased on average by 85-, 335-, and 358-fold under G-CSF (11,406±4,093, P ≤.005), G-CSF/PlGF 130 μg/kg (46,283±8,287, P ≤.005), and G-CSF/PlGF 260 μg/kg (60,777±8,563, P ≤.005), respectively. At cycles 2 and 3, the peak levels of CFCs were increased by 4- and 5-fold over cycle 1 (G-CSF alone). As compared to pretreatment values, the absolute numbers of circulating HPP-CFCs per ml blood were increase on average by 17-, 158, and 284-fold after under G-CSF (1,593±405, P ≤.005), G-CSF/PlGF 130 μg/kg (8,557±1,142, P ≤.005), and G-CSF/PlGF 260 μg/kg (12,205±2,172, P ≤.005), respectively. At cycles 2 and 3, the levels of day-5 HPP-CFCs were increased by 5- and 8-fold over cycle 1. Under G-CSF alone, the absolute numbers of circulating LTC-ICs were increased by 53-fold as compared to baseline values (211±41 vs 4±7, P≤.005). The combined G-CSF/PlGF (130 μg/kg) treatment increased LTC-ICs by 389-fold as compared to pretreatment values (3,115±988 vs 8±5, P≤.005), with a 15-fold increase over G-CSF alone. In conclusion, our data demonstrate that in nonhuman primates PlGF strongly synergizes with G-CSF for the mobilization of primitive and committed PBPCs.

Description: Positron emission tomography (PET) scan using 18-fluorodeoxyglucose [18F-FDG] has a prognostic value in patients (pts) with Hodgkin Lymphoma (HL) or aggressive Non-Hodgkin lymphoma (NHL) receiving chemotherapy. Chemosensitive disease is a critical prognostic factor for the success of both autologous and allogeneic stem cell transplantation (allo-SCT). We have recently shown a lower risk of death or progression for pts in CR versus those in PR before reduced-intensity conditioning (RIC) allo-SCT (Corradini P, Leukemia 2007). Thus, to better assess the value of pre-transplant disease response, we retrospectively assessed the prognostic role of PET scan before allotransplant. Between 2000 and 2007, 64 consecutive patients with a histologically proven diagnosis of aggressive NHL [n=30: diffuse large B cell lymphoma (n=18), peripheral T-cell lymphomas (n=11), Burkitt lymphoma (n=1)] or HL [n=34], responding to salvage therapy, were evaluated with a PET scan before and after allo-SCT. PET scans were performed at 3 different Nuclear Medicine Units. Presence (PET-positive) or absence (PET-negative) of abnormal 18F-FDG uptake was correlated to progression-free survival (PFS) and overall survival (OS) curves. Patients’ median age was 37 years (range, 17–65 years). Thirty-three pts (52%) were allografted from a HLA-identical sibling donor, 14 from a haploidentical donor and 17 from an unrelated donor. Pts had relapsed disease: 52 pts (81%) had failed autologous SCT, the median number of prior chemotherapy regimens was 3 (range, 1–6). All pts received a RIC regimen followed by allo-SCT. PET scans were performed at a median of 30 days prior to allograft (range, 3–90 days): 34 out of 64 pts showed an abnormal 18F-FDG uptake [NHL (n=16), HL (n=18)] whereas 30 were completely negative [NHL (n=14), HL (n=16)]. Patients with PET-positive or PET-negative scans were balanced in terms of diagnosis, previous treatments, and type of donor. At a median follow-up of 24 months (range, 6–86 months), 41 pts are alive and 23 died [toxicity n=10 (n= 5 NHL, n=5 HL), disease n=13 (n=8 NHL, n=5 HL)]. Overall, the estimated 3-year PFS in pts with negative or positive PET scans were 64% (95% CI, 42%–86%) versus 28% (95% CI, 8%–48%), respectively (p

Description: BACKGROUND: The WHO and iwCLL diagnostic criteria for CLL rely on morphology and immunophenotype based on the co-expression of CD19/CD5/CD23 on B-cells with weak CD20 and monoclonal sIg expression. These diagnostic criteria are likely to persist in the near future because there is no specific diagnostic molecular abnormality for CLL. The current criteria have some limitations affecting reproducibility, particularly flexibility in marker expression with many centres using a scoring system that permits absence of CD5 or CD23. Potentially informative new markers have been identified but there is no consensus yet on which should be routinely assessed. AIM: To identify reproducible criteria and to achieve a consensus on markers recommended for the diagnosis of CLL METHODS: ERIC/ESCCA members were invited to classify 35 flow-cytometry markers as being required or recommended for the diagnosis of CLL. Consensus was considered to be achieved if 〉75% of participants agreed on the marker classification. A diagnostic panel was identified by the steering committee and characteristics of component markers that could be reproducibly validated within an individual laboratory were identified. The proposed panel was assessed in 13 different centres. RESULTS: Responses were received from 154 members (100 laboratory staff, 14 clinicians and 36 from both laboratory and clinic) with a diagnostic workload 〉20 cases per week in 23/154 (15%), 5-20 in 82/154 (53%) and

Description: Allogeneic hematopoietic stem cell transplantation (allo-HSCT) is the only cure for several patients with high-risk hematological malignancies. Recent advances in supportive therapies have significantly reduced the treatment-related mortality over the last decades. Nevertheless graft-versus-host disease (GvHD) still represents a major complication, and research is needed to achieve further progress in this area of transplantation. Moreover, although initial studies suggested relative equivalence, recent and large prospective studies showed higher rates of acute and chronic GvHD, and worse survival in allo-HSCT from unrelated donors (URD) compared with HLA-identical sibling donors. Following our encouraging results in haplodentical setting with the more recently post-transplantation cyclophosphamide (PTCy) and sirolimus as GvHD prophylaxis (Cieri et al, 2015), in this study we investigated whether the incorporation of low dose anti-thymocyte globulin (ATG) to PTCy and sirolimus GvHD prophylactic approach, may alleviate some of the increased alloreactivity associated with URD transplants. We retrospectively evaluated a cohort of 21 haematological patients receiving URD allo-HSCT in the San Raffaele Haematology and BMT Unit, from 2013 to 2015. All subjects had high-risk hematologic malignancies, with the most common diagnosis being myeloid diseases (52%). A total of 11 patients had active disease at HSCT, while 9 were in hematologic remission. Nine patients scored high according to disease risk index defined by Armand et al, 10 scored intermediate, while only 2 had a low disease score. Myeloablative conditioning consisted of treosulfan (14 g/m2/day) on days -6 to -4, fludarabine (30 mg/m2/day) on days -6 to -2, and melphalan (70 mg/m2/day) on days -2 and -1, followed by T-replete G-CSF-mobilized PBSCs (n=19) or BM grafts (n=2). Whether 12 patients received stem cells from HLA- matched URD (fully 10/10 HLA matched), the remaining 9 had one-locus HLA-mismatched from their donors. During conditioning patients received ATG-Fresenius 5 mg/kg per day IV on day -4 to -2. In vivo B-cell depletion was obtained by rituximab (i.v. 375mg/m2 given as a single dose on day -1). Postgrafting immunosuppression consisted of PTCy (50 mg/kg/day) on days 3 and 4. Sirolimus was given orally from day 5, and monitored to maintain a target therapeutic plasma level of 5-14 ng/ml. According to chimeric status and evidence of GVHD, the dosage of sirolimus was tapered during the second month post-transplantation, ending in complete withdrawal within the sixth month after HSCT. Mycophenolate mofetil (MMF) was initiated orally at 10 mg/kg t.i.d. on day 5 after HSCT, and withdrawn on day 30. Median follow up was 247 days (range 29-486) from HSCT. All patients were engrafted in a median time of 17 days (range, 14-51 days), with full donor chimerism achieved by day 30. Poor graft function was observed in 11 patients. Post-HSCT recovery of lymphocyte subsets was lengthy as compared to other unmanipulated HSCT, with a median time to CD3〉100/ml of 41 days (range, 22-389 days) by flow-cytometry, while 5 patients never reached immune reconstitution. All except one developed febrile neutropenia during aplasia. We observed a high rate of serious infections: severe pneumonia in 7 cases (5 required NIV, 4 were admitted to ICU), CMV reactivation in 13 (3 CMV disease), HHV6 reactivation in 10, BK virus haemorrhagic cystitis in 2 patients. Although the overall mortality associated with these complications was limited, as evidenced by a favourable NRM, it caused significant morbidity in patients and often required aggressive therapies, potentially contributing to poor graft function. The incidences of acute and chronic GVHD were low. A grade II-IV acute GvHD was reported in 10% patients, while five patients developed chronic GvHD (mild in 4 cases, only one moderate). Non-relapse mortality (NRM) at 100 days and 1 year was 4.8% and 20.7%, respectively. The estimated 1-year overall survival (OS) and relapse incidence were 51% and 22.5% respectively. Although limited by a small number of patients with relatively short follow-up, our study suggests that URD allo-HSCT with ATG, PTCy and sirolimus-based GvHD prophylaxis, can be very effective in preventing GvHD, but at the expense of delayed immune reconstitution and high rate of infectious complications, while warranting acceptable NRM and relapse incidence. Disclosures Bonini: MolMed S.p.A: Consultancy.

Description: Abstract 4577 Patients with therapy-related acute myeloid leukemia (tAML) and myelodysplastic syndromes (tMDS) have a bad prognosis. Allogeneic stem cell transplantation (alloSCT) is potentially curative, but the majority of these patients die because of the high incidence of relapse (RI) and non relapse mortality (NRM). Since it is critical to understand which patients should receive alloSCT, we designed this retrospective study to assess which patients’ characteristics may predict the alloSCT outcome in tAML/tMDS. All the patients affected by tAML or tMDS and allografted in 4 Italian hematology units between 1998 and 2009 were included. Total patients were 28: 24 (86%) had tAML, 4 (14%) had tMDS. Patients had a median age of 49 years (range 21–65) at transplant; 15 patients were female (54%). Previous neoplasia was lymphoma in 23 patients (82%, 15 Hodgkin and 8 non-Hodgkin), or non-hematologic cancer (5, 18%) like breast carcinoma (2), seminoma (1), testicular embryonal carcinoma (1), and osteosarcoma (1). Previous cancer had been treated with chemotherapy (CT, 7 patients, 25%), radiotherapy (RT, 4 patients, 14%), or both (17, 61%). Fourteen patients (50%) had received 〉=2 therapy lines, 6 (21%) had received autologous stem cell transplant. tAML/tMDS occurred after a median time of 86 months (range 13–253) after the previous cancer treatment. Cytogenetic analysis was performed in 24 patients (86%): 8 patients (33%) had intermediate risk and 16 (57%) high risk cytogenetics according to Medical Research Council AML10 Trial definitions. Twenty-three patients (82%) received induction CT for tAML/tMDS, 19 (68%) received consolidation; 5 patients (18%) received upfront alloSCT. Induction consisted of idarubicin+cytarabine+/−etoposide (12 patients, 43%) or fludarabine+cytarabine+/−idarubicin (11 patients, 39%); 15 patients (54%) had an infection after induction. Median time from tAML/tMDS diagnosis to alloSCT was 5.7 months (range 0–25). At transplant, 10 patients (36%) had a Karnofsky Performance Status (KPS)1. Donor was identical sibling for 9 patients (32%), and alternative for 19 patients (68%): mismatched related (1, 3%), matched unrelated (15, 54%) or haploidentical (3, 11%). Disease status of patients at transplant was as following: 12 patients (43%) were in CR (11 in CR1), 4 (14%) in PR and 7 (25%) in PD; 5 patients (18%) received alloSCT at diagnosis. Patients underwent reduced intensity (11 RIC, 39%) or myeloablative (17, 61%) alloSCT. Myeloablative conditioning was mainly busulfan-based (15 patients, 54%); the majority of RIC patients received thiotepa+cyclophosphamide-based conditioning (9, 32%). Twelve patients (43%) are alive at last follow-up, 7 patients (25%) died of disease, 9 (32%) died of NRM. The main reason of death by NRM was infection (8 patients, 29%). Median follow-up of surviving patients was 528 days (55-1704). One- and 2-years overall survival (OS) was 50% and 36%, progression free survival (PFS) was 42% and 38%. RI was 28% at both 1 and 2 years, NRM was 18% at 100 days, 30% at 1 year and 35% at 2 years. Nine (32%) patients had acute GVHD of grade 〉=2, 8 patients had chronic GVHD (cGVHD, 29%), 3 patients (11%) had extensive cGVHD. OS and PFS were reduced in patients with high-risk cytogenetics (p=0.03 and p=0.01, respectively) and KPS

Description: Abstract 3542 Patients affected by Hodgkin's lymphoma (HL) who are chemorecfractory or relapsed after an autologous transplantation (autoSCT) may be eligible to a reduced intensity allogeneic stem cell transplantation (RIC alloSCT). Patients in progressive (PD) or stable disease (SD) at transplant seem to do worse than those in complete (CR) or partial remission (PR). We reviewed 43 cases of HL patients treated with a RIC alloSCT in our Institute from 2001 to 2010, focusing on the outcome based on disease status, disease characteristics, and treatment used to induce remission before transplant. Thirty patients (70%) were affected by nodular sclerosis HL. Median age at transplant was 31 (range, 53-19), 22 patients (51%) were female. The median number of previous chemotherapy was 4 (range, 2–10). Seven patients (16%) underwent autoSCT followed by alloSCT and 3/7 of them (43%) were in CR before allografting. All but one of the other 36 patients (81%) relapsed after an autoSCT and before allografting, were treated as follows: 19 received hyperfractioned polichemotherapy (D-PACE n=16, HypercHidam n=2, EPOCH n=1), 8 patients received conventional chemotherapy (gemcytabin based-chemotherapy n=4, BEACOPP n=1, bendamustine n=2, mecloretamin n=1) and 12/27 (44%) of these patients achieved CR, 8 patients received non-chemotherapy drugs alone or combined with chemotherapy in the setting of phase I-II trials and 3/8 (37%) were in CR at transplant, only one patient was in untested relapse. Thirty two (74%) patients had previously received radiotherapy. Disease status at transplant was: CR n=18 (42%), PR n=16 (37%), PD/SD n=9 (21%). Sixteen patients (37%) had extranodal disease. C-reactive protein (PCR) value at admission was above the normal range in 14 patients (33%). In 40 patients HCT-CI was assessed and it was 0 in n= 5 (13%), 1–2 n= 11 (27%), and ≥3 n= 24 (60%), with almost all the patients having abnormal pulmonary function tests. The type of donor was: HLA identical sibling n= 15 (35%), haploidentical sibling, n= 16 (37%), matched unrelated (MUD) n= 12 (28%). The conditioning regimen was based on thiotepa, fludarabine and cyclophosphamide; 2Gy TBI and T-cell depletion with alemtuzumab or ATG were used in case of haploidentical donor. The median follow-up of living patients was 26 months (range, 2–70). All but one patients engrafted. The median PFS and OS were 10 months and 38 months, respectively. The estimated 3-year progression free survival (PFS) and 3-year overall survival (OS) were 37% and 52%, respectively. One year and 2-year transplant related mortality (TRM) was 7.6% and 10.8%, respectively. We performed an univariate analysis based on sex, histology, donor type (sibling versus MUD versus haploidentical), number of previous therapies (3), extranodal disease, disease status before transplant (CR versus PR versus SD/PD), treatment received at relapse before alloSCT (chemotherapy versus autoSCT versus experimental drugs), previous radiotherapy, HCT-CI (0 versus ≥1), PCR value (normal versus abnormal). OS was influenced by sex (p=0.008, female patients did worse), disease status before alloSCT (p=0.025, both PR and PD/SD patients did worse than CR patients), extranodal disease (p=0.001), and elevated PCR (p=0.002). PFS was adversely correlated to female sex (p= 0.009), PR/PD/SD (p=0.0001), HCT-CI 〉=1 (p=0.03), extranodal disease (p=0.01), and abnormal PCR (p〈 0.001). Haploidentical recipients showed a lower cumulative incidence of relapse (p=0.05), despite a higher NRM (0.02). Of note, the type of therapy received before transplant, either chemotherapy, autoSCT or experimental drugs, did not influence the outcome. In multivariate analysis including disease status, PCR value and extranodal disease, the latter was predictive of OS (p=0.04), disease status (CR versus PR/PD/SD) (p