ALBERT

Description: Abstract 4986 Background. Splenic marginal zone lymphoma (SMZL) is an uncommon indolent B-cell non-Hodgkin's lymphoma usually presenting with marked splenomegaly and bone marrow (BM) and/or peripheral blood (PB) involvement. Although splenectomy has traditionally been the treatment of choice in symptomatic patients, systemic treatment is required in cases of widespread disease, high risk from surgery, or relapse after splenectomy. There is no standard first line treatment in SMZL, but the anti-CD20 monoclonal antibody Rituximab has shown encouraging results in SMZL, with sustained responses. Aims. To assess, retrospectively, response to treatment, toxicity profile, progression-free survival (PFS) and overall survival (OS) after treatment with rituximab in SMZL. Methods. Twenty-nine patients from two different centers, diagnosed with SMZL between 1982 and 2011, received one or more treatments with rituximab. Eighteen patients (62%) received rituximab alone and 20 (69%) combined with chemotherapy; thus 9 patients received each of these treatments sequentially, to improve response, with or without interim relapse. The median age at diagnosis was 62 years (range 37–89 years); the male:female ratio was 2:3; B symptoms were present in 12 patients; ECOG performance status was 0–2 in 28/29 patients. All presented with splenomegaly, with involvement of the BM in 27 patients, PB in 24, lymph nodes in 11 and extranodal involvement in 7 patients. Diagnosis was made according to the WHO 2008 classification by spleen histology (n=12), BM histology (n=19), PB morphology (n=12) and immunophenotype (n=13). Rituximab monotherapy was administered at 375 mg/m2/weekly x4 weeks. In combination with fludarabine-based regimens (n=14), or other regimens including CHOP (n= 6), rituximab was administered on day 1 of each cycle. Responses were assessed according to the Response Criteria Guidelines for SMZL (Matutes, Leukemia 2008). Toxicity was graded according to the CTCAE v3.0. The Fisher exact test was used to compare best responses between groups. Survival was estimated using the Kaplan-Meier method. Results. All patients responded to rituximab monotherapy and/or to a combination treatment. At least one complete response (CR) was achieved in 20/29 patients (69%). This compares with a CR in only 4/17 (24%) of these same patients after any prior therapy (p=0.005): 11 patients had received splenectomy, with or without chemotherapy and 6 had received chemotherapy only. There was no difference in the CR rate between rituximab monotherapy (71%) versus rituximab combinations (68%). The most common adverse event was grade 3–4 neutropenia (n=7, 24%). Two patients had grade 3–4 infections. Anemia (n=3) and thrombocytopenia (n=2) were grade 1–2 only. Four cases presented with histological transformation prior to rituximab, all achieving CR with rituximab combination therapy. After a median follow-up of 24 months from rituximab treatment (range 4–102 months), progression-free survival (PFS) has been evaluated in 28/29 patients (1 patient not assessed yet at the time of presenting these data). PFS was longer after rituximab (n=32 evaluable treatments), either alone or in combination, than it had been in these same patients after prior therapy (n=17 prior treatments in total) (p=0.002) (Fig 1). When we compared PFS between rituximab monotherapy (n=17) and rituximab combined with chemotherapy (n=15 combined treatments), single agent rituximab was superior to rituximab in combination (p=0.02) (Fig 2). The median overall survival was not yet reached. Survival at 2 years after rituximab was 100%. Only one death, due to lung cancer, occurred at 48 months follow-up. Conclusions. In patients with SMZL, the CR rate after rituximab, either alone or in combination with chemotherapy, was significantly better than the CR rate after other prior treatments in the same patients, with manageable toxicity. Although we observed no difference in the CR rate between rituximab monotherapy or combination therapy, PFS was longer in patients receiving rituximab as single agent. Therefore, the addition of chemotherapy did not appear to add any advantage over rituximab alone in our cohort. Rituximab, with or without splenectomy, should be considered in the therapeutic scenario of SMZL. Disclosures: No relevant conflicts of interest to declare.

Description: Introduction Graft versus host disease (GvHD) is the main cause of morbimortality after allogeneic stem cell transplantation (allo-SCT). Several single-nucleotide polymorphisms (SNPs) in in the promoter region of cytokine genes have shown to alter their expression and are therefore associated with donor-recipient alloreactivity and, ultimately, with SCT outcome. Interleukin 17 (IL-17) is secreted by CD4+ T-cells and has been implicated in the pathogenesis of various autoimmune diseases but its importance in SCT is not well-known. Objective To analyse the influence of IL-17A SNP genotypes on the risk and severity of GvHD and other complications after HLA-identical allo-SCT. Patients and Methods Genomic DNA obtained from peripheral blood samples belonging to 546 patients and their HLA-identical sibling donors (Table 1) included in the DNA Bank of the Spanish Group for Hematopoietic Stem Cell Transplantation (GETH). Genotyping of the polymorphisms of interest, rs8193036 (-737C〉T), rs2275913 (-197G〉A), rs3819024 (-444A〉G), rs4711998 (-877A〉G), were performed by multiplex primer extension followed by mass spectrometry (MALDI-TOF; Sequenom MassArray). Results Genotype frequencies are shown in Table 2 and the association between IL-17A genotypes and complications after allo-SCT are shown in Table 3. Patients transplanted from donors harboring genotype CC for the SNP rs8193036 show increased risk of grade III-IV acute GvHD (7/26 vs 47/397, p=0.035) and of grade II-IV acute GvHD (13/26 vs 133/409, p=0.048). Patients transplanted from donors harboring allele A in the SNP rs4711998 show increased risk of extensive chronic GvHD (53/161 vs 43/177, p=0.045). Relapse rate was not related with IL-17A SNP genotypes. Finally a higher risk of toxicity-related mortality (TRM) was observed in patients transplanted from donors harboring allele A for SNP rs2275913 (78/293 vs 46/227, p=0.048), donors harboring allele G for SNP rs3819024 (78/279 vs 46/242, p=0.011) and donors harboring allele A for SNP rs4711998 (68/250 vs 55/229, p=0.044). Conclusions IL-17A SNP genotyping might be useful to anticipate complications after sibling HLA-identical allo-SCT and, therefore, to improve the clinical management of transplanted patients. This results further support the idea of a genetic predisposition to certain complications after allo-SCT. Paper presented on behalf of the GvHD/Immunotherapy committee of the Spanish Group for Hematopoietic Transplantation (GETH). Disclosures: No relevant conflicts of interest to declare.

Description: Several authors have reported ASCT as a feasible, safe and effective treatment in HIV associated lymphoma patients (pts) receiving Highly Active Antiretroviral Therapy (HAART), particularly when being autografted with chemosensitive disease. To gain a better understanding of the usefulness of ASCT in HIV+ Lymphoma pts a retrospective comparative study (HIV+ vs HIV- lymphoma pts with ASCT) has been performed using the EBMT-LWP Registry. Methodology: Registry-based, retrospective, individually matched case-control analysis. Within the participating centres one or two HIV- controls for each HIV+ pt were selected from the registry with the following inclusion criteria: Known HIV serological status at ASCT, lymphoma (HL or NHL), ASCT performed between 1999 and 2006 and pts over 18 years of age. Two cohorts (HIV+ vs HIV-) were matched for histology, IPI at diagnosis (NHL), stage at diagnosis, disease status at ASCT, age at ASCT, year and country of ASCT. Results: 40 HIV+ lymphoma pts undergoing an ASCT were matched with 46 HIV- pts. Pts and transplant features are shown in table 1. With a median follow up of 36 mo, the differences regarding OS and PFS were not significant: 62% for HIV+ vs 69% for controls, and 56.5 vs 58%, respectively. No differences were seen regarding HL and NHL pts. An overall TRM of 10% was observed in the HIV cohort, mainly related to infections, while no cases of TRM were seen within the control arm. Since survival rates between the HIV+ and the matched HIV- lymphoma populations remained comparable, the HIV condition should not preclude these pts from being treated according to the same criteria as the HIV negative lymphoma population. Nevertheless, infectious complications should be cautiously followed within the HIV+ lymphoma pts undergoing an ASCT. Patients and transplant features HIV+ HIV- n=40 % n=46 % Age [Median (range)] in years 41.4 (29.2–62.5) 44 (16–62.4) p= NS Male sex 35 87.5 25 54.3 p=0.001 Histology     DLBCL 24 60 25 54.3 p= NS     Burkitt lymphoma 2 5 2 4.3 p= NS     T-cell NHL 2 5 3 6.6 p= NS     HL 12 30 16 34.8 p= NS Disease status at ASCT     Complete remission (CR) 21 (12 in CR1) 52.5 (30 in CR1) 20 (11 in CR1) 43.5 (24 in CR1) p= NS     Chemosensitive disease 16 40 25 54.3 p= NS     Chemorefractory disease 3 7.5 1 2.2 p= NS CD34+ cells infused mill/kg [median (range)] 4.9 (1.6–21.2) 4.8 (0.9–21.2) p= NS     G-CSF prior to engraftment 36 90 21 46 p= 0.0001     Neutrophil engraftment 39 98% 46 100 p= NS Cause of Death     Relapse/progression 9 60% 10 84% p=0.08     Secondary malignancy 1 6.7% 1 8% p= NS     Transplant-related deaths 4 26.7% 0 0% p=0.06     Other 1 6.7% 1 8% p= NS

Description: Abstract 4547 Background Fungal infections remain a vital threat to the immunocompromised patient. Due to the high mortality rate of invasive mycoses, antifungal prophylaxis and prevention appear appropriate in some settings. Patients (pts) with prolonged and severe neutropenia or recipients of allogeneic hematopoietic stem cell transplantation (HSCT) appear to be at high risk for filamentous fungal infections, which are associated with low survival rates. However, there is no consensus on the optimal prophylaxis, eligible patients or its effectiveness and clinical impact. Objective To analyze the need for antifungal prophylaxis in Acute Leukemia patients receiving chemotherapy and the effectiveness of fluconazol, followed by posaconazol if GVHD developed, in recipients of allo-HSCT as antifungal prophylaxis. Methods and patients Period: from june’07 through june’09. Acute leukemia adult patients receiving chemotherapy as induction or re-induction therapy did not received primary antifungal prophylaxis. Recipientes of Allo-HSCT received 400 mg/d of fluconazole until discharge followed by 200 mg/8h of posaconazole if graft-versus-host disease (GVHD) developed, until its resolution. Patients received secondary antifungal prophylaxis according to their IFI. There were 77 pts who presented 218 episodes of post-chemotherapy neutropenia (80 in ALL and 138 in AML), 207 received no antifungal prophylaxis. On the other hand, we analyzed 40 consecutive Allo-HSCT adult recipients with an average age of 39 years (15-65) followed as in-patient and out-patient basis during a mean period of 18 months (3-24). Standard myeloablative or reduced intensity conditioning schemes were used and donors were HLA-identical sibling (27), unrelated donor (8) and umbilical cord blood (5). Diagnoses: AML (21), ALL (10), NHL (3), MDS (2), CML (2), HL (1) and AAS (1). The GVHD prophylaxis was according to standard protocols with MTX and CsP/MMF or standard umbilical cord blood protocols. Non-normal distribution data were expressed as median values (range). Chi-square test or Fisher exact test were used to compare differences between groups of categorical data. Differences were considered statistically significant for p-values 〈 0.05. All statistical analyses were performed using SPSS 16.0 software (Chicago, IL). Results Acute leukemia patients: There were 8 proved or probable fungal infections (EORTC/MSG consensus), with an incidence of 3.6%. The incidence of IFI in the whole induction AML group was 2.4%, (6.9% in the consolidation AML group, 25% in the re-induction AML group) and 5.2% in induction LLA and no case (0%) in the re-induction ALL group. As etiology, Aspergillus Fumigatus (1), Aspergillus spp (4), Candida tropicalis (1) and Candida spp (2). There were 3 deaths caused by IFI (37.5% of IFI); two of them in the re-induction AML group. Allogenic hematopoietic stem cell transplantation recipients: 33 patients received fluconazole (82.5%) and 4 pts (10%) fluconazole followed by posaconazole. Other 3 received posaconazole (2) or voriconazole 200 mg/12 hours (1) as secondary prophylaxis since the conditioning. There were 7 cases of IFI (incidence of 17.5%), 3 proved IFIs and 4 probable IFIs. As etiology, Aspergillus Fumigatus (2), Aspergillus spp (4) and Candida albicans (1). Six patients had received fluconazole and one (candidiasis), fluconazole and posaconazole. The mortality attributable to IFI were 4 cases (57% of IFI). There was no IFI in the group of 9 pts without GVHD and all IFIs occurred in patients treated for GVHD. Conclusions 1) Patients in re-induction of AML may require an effective prophylaxis against fungal infections, but not AML during induction or ALL in any situation. 2) The prophylaxis regimen studied in allogenic HSCT recipients was effective in preventing IFIs in patients without GVHD but not in patients with GVHD, particularly in the case of filamentous fungi. 3) The overall incidence of IFI in allo-HSCT was similar to that reported in other series of high risk and mortality from IFI similar to that described in recent years. 4) Patients with GVHD require more effective antifungal prophylaxis regimens and are candidates for clinical trials. Disclosures: No relevant conflicts of interest to declare.

Description: Abstract 4539 BACKGROUND: Cytomegalovirus (CMV) end-organ disease is a serious complication after allogeneic stem cell transplantation (Allo-SCT). Described risk factors for CMV infection are pretransplant CMV seropositive status of the recipient, non related donor or umbilical cord transplant, depleted lymphocyte graft, high intensity conditioning regimen, severe graft versus host disease (GVHD), CD34+ selection of the graft and delayed CMV specific immune reconstitution. OBJETIVES: To identify different profiles of allogeneic stem cell recipients based on their previously described risk factors for CMV infection and its association with their clinical outcomes. PATIENTS AND METHODS: A prospective study of consecutive recipients of Allo-SCT was performed from June 2008 through December 2009 at a single institution. Patients were sequentially monitored both clinically and analytically. CMV viral load was determined by real time PCR and CMV-specific T cell response was determined by flow cytometry. Non-normal distribution data were expressed as median values (range). Chi-square test or Fisher exact test were used to compare differences between groups of categorical data. Differences were considered statistically significant for p-values 〈 0.05. All statistical analyses were performed using SPSS 16.0 software (Chicago, IL). RESULTS: Twenty-six patients were included with a median age of 33 years (range:15-61). The donor was an identical sibling in 42.3%, unrelated donor in 53.8% and a mismatched family member in 3.8%. The source was peripheral blood 76.9%, cord blood 15.4% and bone marrow in 7.7%. Previous positive serostatus for CMV was 76.9% in recipients, and 53.8% in donors. The conditioning regimen was myeloablative in 57.7% and reduced-intensity in 42.3%. Graf versus host disease (GvHD) prophylaxis was cyclosporine (CsA) plus methotrexate (MTX) in 57.7% and CsA plus mycophenolate mofetil (MMF) in 42.3%. The incidence of acute GvHD was 76.9% and chronic GvHD was 53.8%. Treatment of GVHD was steroids plus CsA or tacrolimus and/or MMF in 76.9% of acute and 46.2% of chronic GvHD. Previously described risk factors for developing CMV infection were compared between patients developing (n=18) and non-developing (n=8) CMV infection. A higher risk for developing CMV infection was associated with previous CMV positive serostatus of the recipient (84% in viremic patients vs. 16% in non-viremic patients; p=0.01) and CsA plus MMF as GvHD prophylaxis (90.9% vs. 9.1%; p=0.04). We analyzed whether having several risk factors for developing CMV infection has an effect on the risk for developing CMV replication after the transplant. Patients that presented four or more risk factors, developed viral replication more frequently than patients having less than four risk factors (91.6% vs. 8.3%; p=0.02). Patients who acquired an earlier specific CMV immune reconstitution did not developed CMV replication, opposite to those with later immune reconstitution (week 2 vs. week 8, p= 0.01). Overall survival at one year was of 44.4% in the group with viral replication, and 100% in the group with no viral replication, p=0.014 (Figure 1). CONCLUSIONS: Patients that did not developed episodes of CMV replication after the transplant presented less than four risk factors for developing CMV infection, developed an early T-cell mediated CMV immune response and had better overall survival. The development of CMV specific immunity able to control CMV replication may be considered as a paradigm of post-transplant immune reconstitution with potential influence on overall survival. Disclosures: No relevant conflicts of interest to declare.

Description: Following the widespread use of Highly Active Antiretroviral Therapy (HAART), ASCT has been reported as a feasible and effective treatment in the setting of HIV-Ly patients (pts). Nevertheless just series including up to 20 patients have been published so far. We present a preliminary analysis of the outcomes regarding the experience within the EBMT-LWP. Methodology: A retrospective analysis including HIV-Ly patients undergoing peripheral blood ASCT from 1999 to 2005 and reported to the EBMT was performed. Main endpoints: OS, EFS and TRM. Results: 44 pts from 14 institutions/7 countries were included: 39 males, median age 43 (29–62) years old. One pt underwent more than 1 ASCT (follow up censored at time of 2nd ASCT). In addition to HIV infection, 11 pts were co-infected by HBV, 8/43 by HCV and 16/36 pt met AIDS criteria (other than lymphoma) at the time of lymphoma diagnosis. Histology: 34 NHL (20 DLBCL; 7 Burkitt/Burkitt-like; 4 plasmablastic; 3 other), 59% of them with IPI〉2 at diagnosis; 10 HL (50% with Ann-Arbor stage〉IIB at diagnosis). Patients received a median of 2 (1–5) treatment lines pre-ASCT. Status at ASCT: 22 CR (13 in CR1); 18 in PR/chemo-sensitive relapse and 4 in primary induction failure/chemo-resistant relapse. Conditioning: 41 pts received BEAM/variants and 3 TBI-based regimens. Post-ASCT anti-tumour pre-emptive treatment was used in 10 pts (8 radiotherapy; 2 Rituximab). The median count of T-CD4+ cells/μl was 162 (8–702) at the time of ASCT; 26/38 had undetectable HIV viral loads. HAART was given in 39/42 pts during conditioning but was withdrawn in 9 of them. The median number of CD34+ cells infused was 5 (1,6–21,2) x106/kg. G-CSF was used until engraftment in 39/43 pt during a median of 8 (2–29) days. All pts but one who died on day +15 reached neutrophils〉500/μl at a median time of 11 (8–36) days. Platelet count 〉20.000/μl was reached in 39/44 pt at a median time of 14 (6–455) days. The pt engrafting platelets on day +455 was transfusion independent since day +49. Three new post-ASCT malignancies were reported: in situ epitelioma and myelodysplasia (+4 years) in 1 pt, and kidney adenocarcinoma (+3 years) in another one. Relapse occurred in 13 (29,5%) pts which status at SCT was CR in 4, PR/chemosensitive relapse in 5 and chemo-resistant disease in 4. The median time to relapse/progression was 5,2 (0,6–32,1) mo. Seventeen pts died (38,6%): disease relapse/progression (n=11), ASCT-related complication (n=4) -bacterial infection (n=3), secondary myelodysplasia (n=1)-, 1 pt died from an HIV-related complication and 1 pt died on day +15 of multi-organ failure within the context of a bacterial sepsis and pre-transplant renal dysfunction. With a median follow up time of 36,3 (3,2–72,3) mo, the OS and DFS probability at this point were 60,2% (67,5% when chemo-resistant pts were excluded from analysis) and 55% respectively. For those pts in CR1 at ASCT, OS at 36,3 mo was 85% vs 60% for those in CR〉1/PR/chemosensitive relapse. Conclusion: The results from the EBMT-LWP experience, the largest reported so far, show that ASCT remains a useful treatment in terms of TRM, long-term OS, and DFS for high risk HIV-Ly patients. These outcomes are comparable to those observed in HIV negative lymphoma patients.

Description: Abstract 1457 Background Factors such as hypoxia, angiogenesis and increased cell proliferation have been described to the pathogenesis of myeloid neoplasms. In the current study we have analyzed the expression of different genes involved in such pathways and its correlation with clinical and biological parameters in myelodysplastic syndromes (MDS) and acute myeloid leukemia (AML). Methods and patients: A total of 83 bone marrow (BM) samples were analysed including: Lower-risk MDS (LR-MDS; defined as IPSS low/Int-1; n=37), higher-risk MDS (HR-MDS; IPSS Int-2/high risk; n=13) and AML (blasts 〉20%; n=33). All samples were collected at the time of diagnosis. Bone marrow samples from healthy controls were used as control group (n=11). Baseline characteristics are shown in table 1. Total RNA from BM was treated with DNase, and cDNA was synthesized using a cDNA Sinthesis kit. Gene expression was quantified by qRT-PCR in triplicate using §-actin gene as control. Relative gene expression was determined by 2 (ΔΔCt) method. Cells populations of blasts (CD45+,CD34+,CD117+) were sorted with MoFlo Cell Sorting and separated by positive selection. No differences in gene expression were noticed by sorting as compared to total RNA from whole BM samples. Genes analysed were: vascular endothelial growth factor (VEGF) for angiogenesis, cMYC, macrophage migration inhibitory factor (MIF) and glycogen synthase (GYS) for metabolism and cell-proliferation. Clinical and biological parameters evaluated were: peripheral counts, BM blast percentage, karyotype (good, int and poor by IPSS in MDS and favourable, Int-I, Int-II and adverse by the European Leukemia Net Prognostic System in AML), transfusion dependency, response to intensive chemotherapy (IC) and survival. Statistical significance was determined by t-test, Wilcoxon test and Kaplan Meier with SPSS software (v.16). P values

Description: Abstract 2323 Graft-versus-host disease (GVHD) remains a major complication after allogenic hematopoietic stem-cell transplantation (alloHSCT) from HLA-identical donor. It is due to donor T-cell responses against minor histocompatibility antigens (mHags) of the recipient. Nevertheless, there is a complete lack of studies addressing the B-cell response to mHags in GVHD. Glutathione S-transferase T1 (GSTT1) is a drug metabolizing enzyme that is involved in detoxification processes. It is highly expressed in liver, kidney and erythrocytes. The GSTT1 gene is absent in 20% of the Caucasian population. In liver and renal transplantation, we have reported that some GSTT1-negative patients who received a GSTT1-positive graft produce anti-GSTT1 antibodies (abs) and present signs of chronic rejection. The aims of this study were to analyze the effects of GSTT1 donor/recipient mismatches in the development of hepatic GVHD and to detect production of anti-GSTT1 abs after alloHSCT. For that purpose, we have studied a group of 40 patients that received an alloHSCT from HLA-identical donors between January 2004 and July 2009 in HU Virgen del Rocío, whose DNA samples and their corresponding donor samples were available. All patients and their donors gave written informed consent. GSTT1 genotyping was performed by PCR and a commercially available ELISA test with the GSTT1 human recombinant protein was used to detect anti-GSTT1 abs. We studied abs in serum samples corresponding to different pre and post transplant phases. The distribution of the four possible GSTT1 genetic combinations was as follows: 25 donor+/recipient+, 6 donor+/recipient-, 5 donor-/recipient+ and 4 donor-/recipient-. Anti-GSTT1 antibodies were detected in 5 patients all of them with a donor that carries the null genotype. Four of the 5 patients included in the donor-/recipient+ group developed anti-GSTT1 abs (of the IgG class) after the infusion and were diagnosed with acute hepatic GVHD. In all of these cases the donor was a multiparous female. The presence of anti-GSTT1 abs is significantly associated with hepatic GVHD (p=0,01, Table 1). The fifth recipient within this group had a non-transfused male donor and did not produce abs. In all the cases, anti-GSTT1 abs were found in post-transplant serum samples of the recipient (never in pre-transplant samples) under a condition of 100% chimerism. Our hypothesis is that the immune system of the null donors has encountered the GSTT1 antigen during pregnancy of a positive-fetous and memory B-cells would be in the peripheral blood stem-cell infusion. These cells, once in a positive recipient, would be activated when contacted with the antigen present in the recipientxs liver. In the patients, the B-cells produced high levels of anti-GSTT1 abs that were associated with GVHD episodes. In conclusion, we describe that the presence of anti-GSTT1 abs is associated with the development of hepatic graft-versus-host-disease and that the null genotype of the donor is a necessary condition for antibody-production. These results confirm the GSTT1 gene as new minor histocompatibility antigen. With Hepatic GVHD Without Hepatic GVHD With 4 1 5 anti-GSTT1 abs Without anti-GSTT1 abs 6 29 35 10 30 n = 40 Disclosures: No relevant conflicts of interest to declare.

Description: Abstract 1141 Poster Board I-163 Hepatitis C virus (HCV) infection has been reported to be an important cause for serious liver disease including cirrhosis and liver failure after hematopoietic stem cell transplantation (HSCT). This study was initiated by the EBMT in 1993 and recruited patients to 1996 with the aims to prospectively follow a cohort of HCV infected patients and study late effects and responses to antiviral therapy. The requirements for participation were for a center to report all HCV infected HSCT patients having survived for at least 6 months and to be willing to report baseline and follow-up data approximately every five years. Initially, 236 patients were registered. However, no follow-up information was reported on 41 patients. Thus, 195 patients from 12 centers were included in this analysis. The diagnosis, clinical follow-up, and antiviral therapy were made according to each center's routines. Kaplan-Meier curves were calculated for overall survival. Cumulative incidences were calculated for death from liver failure with death from other causes as the competing risk and for development of severe liver complications including death from liver failure, liver transplantation, and biopsy verified cirrhosis with death occurring without the diagnosis of severe liver complication as the competing event. Uni- and multivariable logistic regression was performed with the aim to determine risk factors for severe liver complications. 134 patients had undergone allogeneic and 61 autologous HSCT. The median follow-up from HSCT is currently 16.3 years and the maximum 27.1 years. 33 of 195 patients have died of which seven died from liver complications. The survival probability at 20 years after HSCT was 81.4% and the cumulative incidence for death in liver complications was 4.1% (3.3% in allogeneic and 6.5% in autologous HSCT recipients). 120/195 patients had a least one liver biopsy performed during follow-up. The cumulative incidence of severe liver complications (death from liver failure, liver transplantation, cirrhosis) was 7.6% at 15 years and 11.3% at 20 years after HSCT. 85 patients have been treated with interferon based therapy; 43 in combination with ribavirin. 16 patients have been treated more than once. At last follow-up, 42 patients had become PCR negative of whom seven had relapsed, 25 did not respond, two were not yet evaluated, and for 16 the PCR status was unknown. The sustained virological response rate among all treated patients was 40%. The rates of severe side effects were comparable to other patient populations and no patient developed exacerbations of GVHD. Patients who received antiviral therapy had a trend towards a decreased risk of severe liver complications (p=.058). HCV infection is associated with morbidity and mortality in long-term survivors after HSCT. Antiviral therapy might reduce the risk for severe complications and can be given safely with similar rates of side effects and antiviral response as in non-HSCT patients. Disclosures No relevant conflicts of interest to declare.

Description: Introduction Burkitt lymphoma (BL) is a highly aggressive and chemosensitive B cell non-Hodgkin lymphoma derived from germinal or post-germinal center B cells, which affects commonly extranodal sites. Although studies have described 100% of 18F-FDG avidity in BL, PET/CT is not routinely used in those patients being only recommended in the context of a clinical trial. The aim of the present study is to evaluate retrospectively, the role of PET/CT instead of CT scan alone both to stage newly diagnosed BL patients as well as to evaluate disease response after chemotherapy. Patients and Methods 53 PET/CT (20 PET/CT at diagnosis, 28 after first line treatment and 5 to monitor residual disease detected in response assessment PET/CT) were performed in 32 patients, between 2006 y 2012. Locations of involved areas were registered comparing staging CT and PET/CT and were classified as discrepancy or not. Results Patientxs baseline characteristics are summarized in table 1. At diagnosis, abdominal adenopathies had the highest SUVmax with a mean of 14,83 (3,5-35). Discrepancies were found in 64,7% of patients who had both imaging test available at diagnosis (n=17), almost all of them in extranodal sites. These findings upstaged 12% patients from localized to advanced disease. Sensitivity of PET/CT and CT was 100% and 53%, respectively. Regarding the response assessment, in 5 patients out of 13 (38%) who had both imaging test, the PET/CT after first-line treatment was negative whereas the CT demonstrated residual masses. No relapses were observed in those patients. Among 28 patients with a PET/CT available after first-line treatment, CR was attained in 22 patients; one true-positive and 5 false-positive lesions (FP) (1 nodal and 4 extranodal) were detected after completing treatment. SUVmax of FP single nodal site was 2,6 as compared to a mean of 14,9 for the positive lesions at diagnosis while the mean SUVmax of false-positive extranodal sites was 4,4 as compared to 12,1 at diagnosis. NPV was 100% and PPV 16%. SUVmax value of FP lesion was