ALBERT

Description: Background. Measurement of serum M-spike is used to determine response to therapy and treatment free survival in Waldenstrom Macroglobulinemia (WM). However, there are many limitations to the use of IgM M-spike, and new sensitive markers are needed to determine early response or progression in these patients. We have previously shown that involved serum free light chain (sFLC) accurately diagnosed patients with WM, and correlated with markers of poor prognosis, specifically beta- 2 microglobulin (B2M). In this study, we sought to determine the role of levels of involved in the response to therapy in patients with WM treated on clinical trials, and compare it to the response observed using the traditional M-spike measurement. Methods. We prospectively studied involved sFLC in 61 WM patients enrolled on 2 clinical trials, at diagnosis (N=8) and with relapse/refractory disease (N=53). Patients were treated on one of two clinical trials: either perifosine (N=30; given 150mg oral daily) or combination of bortezomib and rituximab (N=30; given IV bortezomib 1.6mg/m2 at days 1, 8, 15 q 28 days × 6 cycles and rituxan 375 mg/m2 at days 1, 8, 15, 22 on cycles 1 and 4). Response was assessed after cycle 2, confirmed on 2 consecutive measurements, and included minor response (MR), partial response (PR) or complete remission (CR). Results. The baseline characteristics of the patients were as follows: the median age was 65 years (44–83), male/female ratio 2.38, serum B2M 3.0mg/L (1.00–7.30), hemoglobin 11.0g/dL (7.00–14.90), platelet count 216 ×109/mm3 (46–563), serum M-spike 2.24g/L (0.41–4.62), and involved sFLC 95.2mg/L (4.92–868). The WM International staging system (WM-ISS) showed that 28% of patients had low ISS, 31% intermediate, and 41% high ISS scores. The overall response rate for the entire cohort was 62.3%, assessed by M-spike measurement (MR=23, PR=13, nCR=2). The overall response rate using involved sFLC level was 72.1% (MR=14, PR=29, and CR=1), (p

Description: BACKGROUND: AML in elderly patients, secondary AML and/or AML with complex karyotype respond poorly to conventional intensive chemotherapy (CT) and have a poor prognosis. In those patients, however, AZA can bring some benefit, especially in the absence of adverse cytogenetics, if WBC 〈 15 × 10⁹/L and performance status (PS) 〈 2 (Thepot, Am J Hemat, 2014; Pleyer Ann Hematol, 2014). Whether molecular findings can predict outcome in AML receiving first line AZA (as they do in AML receiving CT) is however unknown. PATIENTS AND METHODS: 96 AML patients who received between 2007 and 2012 first line treatment with AZA (75mg/m2/d x 7 d/4 weeks SC for a median of 7 cycles, range 1-33) in 8 French centers were retrospectively analyzed. Initial response was evaluated based on blood and marrow examination after 4 -6 cycles of AZA. We analyzed the impact on overall survival (OS) of conventional clinico-biological parameters, and molecular biology parameters including EVI1 expression, MLL-PTD, and the mutational status of 16 genes analyzed by next-generation sequencing (NGS) and Sanger sequencing: ASXL1, CEBPA, DNMT3A, EZH2, FLT3, IDH1, IDH2, NPM1, NRAS, KRAS, RUNX1, SF3B1, SRSF2, U2AF1, TET2, and TP53. RESULTS: Median age was 73 (range, 44-88). Median PS was 1 (range, 0-3). 55% patients had secondary AML, including post MDS or MPN AML (N=39), and therapy related AML (N=14). 64% of patients had high risk cytogenetics and only 14 normal karyotype. Median WBC was 3.87 G/L and 28 patients had WBC 〉10 G/L. Median platelets and Hb were 61 G/L and 9.25 g/dL respectively. 41 and 55 patients had marrow blasts 〈 30% and ≥ 30% respectively, and median circulating blast % was 15% (range, 0-95). The median number of somatic mutations per patient was 2 (range, 0-5). The most frequently mutated genes were TP53 (40%), TET2 (22%) and SRSF2 (19%), then DNMT3A (14%), ASXL1 (13.5%), IDH2 (11%) and RUNX1 (11%). EVI1 overexpression (defined stringently in this study as DD CT ≤ 8 EVI1/ABL) was found in 12 patients. Overall response rate was 29% (14% CR, 8% PR and 7% Cri), and median response duration was 9.4 months. Median OS was 10.9 months. In univariate analysis, the following factors were significantly associated with shorter OS: platelets and Hb below median (p

Description: Key Points Patients with a history of acquired TTP and persistent severe ADAMTS13 deficiency during remission are at high risk of relapse and death. Preemptive infusions of rituximab in remission significantly decrease TTP relapse rate.

Description: Abstract 2964 Background. Lenalidomide is an oral IMiD®, immunomodulatory compound, approved for use in combination with dexamethasone (Len/Dex) in patients with RRMM who have received one prior therapy. Len/Dex is indicated until evidence of disease progression at the best-tolerated dose of both Len and Dex (Dimopoulos et al. Leukemia 2011). However, the tolerability profile of long term exposure to Len/Dex is not well described, and evidence that long term exposure to Len/Dex would improve on the response rate and survival has yet to be determined. We sought to determine the efficacy and safety profile of long term exposure to Len/Dex in RRMM pts in a multicentre study. Method. We retrospectively reviewed the medical records of 50 RRMM pts treated with Len/Dex and remaining on Len for ≥2 years with a special focus on pts receiving Len for ≥3 years. All pts included had complete follow up records. Results. The median (range min-max) age was 58 years (39–79) with 30% (n=15) 〉 65 years (elderly MM), the sex ratio M/F was 1.2, 49% (n=24) ISS 2 and 3, 12% (n=6) severe renal insufficiency (CrCl 〈 30mL/min), and 8% (n=4) adverse FISH [del17p and/or t(4;14)]. Overall, 25 pts (50%) had Len/Dex at first relapse, 19 pts (38%) at second relapse and 6 (9%) pts in subsequent relapses. Len/Dex was given at first relapse in 10 (66%) elderly patients. The median time from diagnosis to starting Len/Dex was 4.5 years (1–16) for overall cohort and 3 years (1–8) for elderly patients (p=0.05). 28 pts (56%) received Len/Dex for ≥3 years. The median duration on Len/Dex was 3 (2–7) years for the overall cohort, and was 4 (3;7) years for patients exposed to Len ≥3 years. Treatment duration was similar across age categories and across number of previous relapses. With a median follow up of 4 years, 19 patients had stopped Len/Dex. The response rate (ORR, ≥PR) was 96% (n=48), including 37 (74%) patients with ≥VGPR, similar across age categories. Interestingly, the ORR and ≥VGPR were similar irrespective of whether patients have stopped Len/Dex in our study. The ORR was also similar across number of previous relapses, but the ≥VGPR rate was lower in patients at third relapse and beyond, (50%; p=ns). The ORR and ≥VGPR rate was 93% and 77% in patients exposed to Len ≥3 years, similar to the whole cohort. The median time to first response and best response were 2 (1–5) months and 4.5 (2–9) months, respectively. Overall, 9 (18%) patients stopped treatment due to toxicity, 9 (18%) progression of MM, and 1 (0.5%) patient decision. With a median follow up of 4 years, the median (95%CI) TTP was not reached, the estimated 4-yr TTP was 51.5%. There was no imbalance in the incidence of toxicity based on age, number of previous relapses, and patients exposed to Len ≥3 years did not discontinue more often due to toxicity, 14% versus 19% for those receiving Len 〈 3 years. The hematological safety profile was similar across age categories, number of previous relapses, and patients exposed to Len ≥ 3 years; overall, 8 (16%) patients experienced grade 3–4 neutropenia, 6% thrombopenia, and 6% anemia. Ten (20%) patients experienced a thromboembolic event (VTE), all of them of venous type. Two patients had previous history of VTE, but none of them experienced VTE on Len/Dex, likely related to adequate VTE prophylaxis. The median time to first occurrence was 5 (1;28) months, although 4/10 occurred in patients with ≥3 years on Len. All VTE occurred while on VTE prophylaxis except for 1 patient, 5 on aspirin, 2 on prophylactic doses of LMWH, and 2 on VKA (target INR 2–3). The incidence rate of second primary malignancy (SPM) was 3 (6%) (larynx, lung, and MDS). The SPMs occurred at a median time of 4 years from start of Len, while Len was already stopped in 2/3 patients, the latter stopped len at time SPM was diagnosed. Interestingly, none of the patients with more than 3 years exposure on Len had SPM. Conclusions. The current study provides estimates of responses, TTP and safety in a series of MM pts with long-term exposure to Len-based regimen at relapse. 62% of patients remained on Len beyond 3 years reflecting the efficacy and good safety profile of Len in relapsed MM, irrespective of age and number of prior therapies. Furthermore, no excess of long term side effects, including SPM, was observed with a prolonged long follow-up in this study. Disclosures: Robinson: Celgene: Employment. Miljkovic:Celgene: Employment. Morel:Celgene: Employment. Boccacio:Celgene: Employment. Facon:millenium: Membership on an entity's Board of Directors or advisory committees; janssen: Membership on an entity's Board of Directors or advisory committees; celgene: Membership on an entity's Board of Directors or advisory committees; onyx: Membership on an entity's Board of Directors or advisory committees. Hulin:celgene: Honoraria, Membership on an entity's Board of Directors or advisory committees; janssen: Membership on an entity's Board of Directors or advisory committees. Leleu:Onyx: Honoraria, Speakers Bureau; Sanofi: Honoraria; Amgen: Honoraria, Research Funding; Novartis: Honoraria, Research Funding; Janssen: Honoraria, Research Funding, Speakers Bureau; Celgene: Honoraria, Research Funding, Speakers Bureau; LeoPharma: Honoraria, Speakers Bureau.

Description: Abstract 3970 Background: Measurement of serum M-spike is used to assess response to therapy and treatment-free survival in IgA myeloma. However, its resolution on SPEP and the presence of IgA-dymers can make accurate measurement difficult. The more the M-spike decreases on SPEP, the more imprecise the M-spike measurement is using SPEP. IgA M-spike often migrates in the betaglobines that renders the M-spike measurement often complicated to analyze. Furthermore, quantification of the clonal IgA chain by nephelometry (IgAneph), which inherently includes monoclonal and polyclonal immunoglobulins, does not accurately reflect the tumour burden. Currently, there is a need in myeloma with IgA isotype (approximately 30–40% of patients) to identify new markers that better reflect the disease burden and the response to treatment, and correlate to patients' outcome. Hevylite® measures IgAkappa and IgAlambda and might provide precise quantitative measurement of the IgA M-spike. We sought to determine whether Hevylite® can be used as a reliable marker for diagnosis and response to therapy in IgA myeloma as compared to the M-spike measurement on SPEP and nephelometry. Methods: We conducted a retrospective analysis on 113, smoldering or symptomatic, IgA myeloma patients at diagnosis referred to our department from 1997 to 2011. All serum samples were collected prior to treatment or at relapse (for sequential data) and were kept frozen since collection. Hevylite® measurements were made at The Binding Site Ltd, Birmingham, UK. A normal range was produced from normal (blood donor) sera (n=138), and were for IgA kappa 0.48–2.82g/L, IgA lambda 0.36–1.98g/L and IgA K/L ratio 0.80–2.04. For ease of comparison we have studied the IgA hevylite ratios expressed as IgA K/L ratio. Results: The median age at diagnosis was 65 years (range: 33–93) and the M/F sex ratio was 0,91. Forty-eight percent of patients had an ISS greater than 2 (n=86). On nephelometry the median IgA level was 22g/L (range min-max, 0–100). Fifty patients had M-spikes migrating among the betablobulines, 27 among the gammaglobulines, 10 migrated in both and 23 unspecified. Fourteen patients had oligosecretory disease (M-component 〈 10g/L). Forty-two patients had an IgA kappa clonal chain, 70 others an IgA lambda and for one patient the data was not available. Among IgA kappa patients the mean HCLratio was 616.6 (median 117.7 [0.021–4323.7]) whereas it was 0.61 (0.21 [0.004–0.455]) among the IgA lambda patients. Across the entire population, 58 patients were identified by SPEP and HCL ratios. Among the 55 patients whose M-component was not quantified on SPEP, HCL ratios were abnormal in 53/55 (96%) cases. In the subgroup of patients whose M-protein migrates in the beta-region 29 out of 50 are identified by HCL ratios and SPEP. Another 19 patients (38%) had abnormal HCL ratios while unquantified on SPEP. The same was seen in patients whose M-protein migrates among the gammaglobulins with 16/27 and 11/27 (40%), respectively. In the last subgroup of patients with beta and gamma migrating M-proteins, all (10/10) were identified by HLC and SPEP. More interestingly, among the oligosecretory MM patients identified by an M-component 〈 10g/L, all (14 patients) had an abnormal HCL ratio. In our series of IgA myeloma, 51% of patients were accurately quantified on SPEP. When using HCLratios, an extra 47% of patients became measurable, with an abnormal HLC ratios allowing IgA myeloma in up to 98% of cases. When considering IgA measurement using nephelometry, 102 patients had both high IgA levels (90%) and abnormal HCL ratios. Interestingly, 7 patients had normal IgA levels with IgAneph and abnormal HCL ratio offering a useful diagnostic tool for 96% of patients as compared to IgAneph. In our series, IgA myeloma was neither associated with a poor outcome (median [range] OS: 119 months [0,5–604]) nor a poor response to therapy (median [range] TTP: 16 months (1–92). HCL involved chain ROC analysis identified a 37g/L cut-off as prognostic in IgA myeloma(p=0.039). Conclusion: Hevylite® is a new and reliable marker for diagnostic and monitoring of IgA myeloma. It enables to quantify accurately up to 98% of IgA-MM patients. These preliminary data need confirmation in further prospective trials in order to monitor further the impact of this marker in IgA myeloma patients before it becomes the gold standard to monitor the IgA M-protein in years to come. Disclosures: Boyle: Chugai: Consultancy, Honoraria. Combat:The Binding Site: Employment. Pietrantuono:The Binding Site: Employment. Facon:onyx: Membership on an entity's Board of Directors or advisory committees; celgene: Membership on an entity's Board of Directors or advisory committees; janssen: Membership on an entity's Board of Directors or advisory committees; millenium: Membership on an entity's Board of Directors or advisory committees. Harding:The Binging Site: Employment. Leleu:Celgene: Honoraria, Research Funding, Speakers Bureau; Janssen: Honoraria, Research Funding, Speakers Bureau; Novartis: Honoraria, Research Funding; Amgen: Honoraria, Research Funding; Sanofi: Honoraria; Onyx: Honoraria, Speakers Bureau; LeoPharma: Honoraria, Speakers Bureau.

Description: Context Acquired thrombotic thrombocytopenic purpura (TTP) results from a severe, antibody-mediated, deficiency in the von Willebrand factor-cleaving protease ADAMTS13. Rituximab is increasingly used in this indication in patients with a suboptimal response to plasma exchange. When severe acquired ADAMTS13 deficiency persists during remission, the estimated incidence rate is of 0.4/year. So far, it is still controversial whether preemptive rituximab efficiently prevents relapses in these patients. Patients and methods We defined two groups of patients with a history of acquired TTP who displayed a persistent severe ADAMTS13 deficiency during remission. Patients of group 1 were treated with preemptive infusions of rituximab. Patients of group 2 were managed in centers in which preemptive rituximab infusions were not the standard of care. The relapse incidence was evaluated and compared between both groups. Patients were treated according to National recommendations and enrolled from 12 French centers during a 12-year period. Patients were explored for ADAMTS13 activity and peripheral B-cell count every 3 months. Only patients with a 〉 12-month follow-up after rituximab administration are reported here. Median (25th - 75th percentile) was determined for all continuous variables. Wilcoxon’s test was used to compare continuous variables and the chi-square test or Fisher’s exact test to compare binary data. Relapse-free survival was compared between both groups using the Kaplan-Meier estimator with the corresponding 95% confidence interval. Results Forty-eight patients (20.6%) with a history of acquired TTP displayed a persistent severe ADAMTS13 deficiency on remission or experienced a subsequent severe ADAMTS13 deficiency (24 cases each) after a median follow-up of 17 months (12-29 months). Anti-ADAMTS13 antibodies concentration was 44 U/mL (24-59 U/mL). Thirty patients received preemptive infusions of rituximab (group 1), whereas 18 others had no therapeutical intervention (group 2). In group 1, 16 patients experienced a past history of TTP with a median number of 2 (1-3) episodes, corresponding to a relapse incidence of 0.22 (0-0.57)/year. Rituximab infusions were performed 14.5 months (6.5-27.4 months) after the last TTP episode. A median number of 4 (1-4) rituximab infusions were performed. The median follow-up between the first preemptive infusion of rituximab and the last ADAMTS13 evaluation is of 36 months (24-65 months). After preemptive rituximab administration, only 3 patients experienced a clinical relapse (0 [0] episode/year), corresponding to a significant reduction in the relapse incidence (P 〈 .01). ADAMTS13 activity was 58.5% (30.5%-86.3%). Three months after the first rituximab infusion, ADAMTS13 activity was 46% (30-68); it further increased until the 12th month, and subsequently decreased. Accordingly, B-cell lymphocytes remained undetectable until the 6th month, and progressively increased at the 9th month to reach normal values at the 18th month. Nine patients (30%) required one (5 cases), two (2 cases), three (1 case) or ten (1 case) additional courses of rituximab for a further decrease or a persistent undetectable ADAMTS13 activity, which allowed to maintain a detectable ADAMTS13 activity in all but one patients. The time between two consecutive courses of rituximab was 26 months (5-59 months). At the end of follow-up, ADAMTS13 activity remained normal in 18 patients; 10 patients had a moderate ADAMTS13 deficiency, and 2 patients had a persistently undetectable ADAMTS13 activity. In four patients (13%), rituximab alone failed to increase durably ADAMTS13 activity, which required additional immunosuppressive drugs. In group 2, 14 patients relapsed after a 66-month follow-up (36-105 months), corresponding to a higher relapse incidence than in patients who received preemptive infusions of rituximab (0.23 [0.1-0.46] relapse/year, P

Description: Abstract 794 Introduction: Human herpes virus 6 (HHV6) is known to reactivate after allo-SCT. It has been suggested that HHV6 may be associated with severe clinical manifestations, but little is known about its exact role in patients' outcomes following allo-CST. Patients and methods: Here we report our findings in 225 consecutive patients who underwent allo-SCT in our unit between January 2004 and March 2009. The median age was 42 years (3-62). Donors were HLA-identical sibling (n=110), and unrelated (n=115). Source of stem cells was bone marrow (BM; n=124), peripheral blood stem cell (PBCS; n=69) and cord blood (CB; n=32). Conditioning regimen was myeloablative (n=151), or reduced intensity (RIC; n=74). HHV6 plasma loads were measured almost weekly by quantitative PCR. We treated symptomatic patients when no other cause than HHV6 reactivation could explain the symptoms. However, patients with associated CMV reactivation were also treated with anti-viral therapy. At the time of analysis on July 31st 2009, the median follow-up was 33 months (4-68). A total of 105 (46%) patients had early positive HHV6-PCR within the first 100 days following transplantation (group I). In this retrospective study we compared the outcome of patients in group I to those who did not reactivate HHV6 or those who had positive HHV6-PCR after day 100 (group II; n=120). Results: Patients with PBSC and those who received RIC showed evidence of HHV6 reactivation less often than the others (p=0.049 and p=0.076, respectively). When HHV6-PCR was positive, only 10 patients in group I were asymptomatic while 95 patients experienced either fever (n=55), skin rash (n=51), diarrhea (n=41), pulmonary complications (n=16), neurological disorders (n=12), liver dysfunction (n=8) and/or others (n=7). Of note, 73 patients (70%) experienced more than one symptom concomitant to HHV6 reactivation. Thirty-seven patients received anti-viral therapy for HHV6-reactivation alone (n=18) or associated with CMV reactivation (n=19) resulting in negative HHV6-PCR in 31 of them. Out of the 6 patients who failed to have negative HHV6-PCR, 2 died 25 and 90 days after anti-viral therapy initiation, respectively. Although, there was no significant difference in overall survival or relapse-free survival between the two groups, patients in group II had earlier platelet engraftment (〉 50 G/L) than those in group I with a median of 22 versus 28 days (p=0.003). In addition, patients in group I developed more often acute grade III-IV graft-versus-host disease (GvHD) than those in group II (34/105 versus 15/120, p=0.008). Of note, for 53% patients in group I with acute grade III-IV GvHD, HHV6 reactivation was observed before the development of acute GvHD. In multivariable analysis, the most important factors influencing acute grade III-IV GvHD were early HHV6 reactivation, [HR: 2.10; 95%CI, 1.20-3.66] (p=0.011) and unrelated donor, [HR: 1.17; 95%CI 1.04-1.32] (p=0.007). Conclusions: HHV6 reactivation is common after allo-SCT and is responsible for platelet engraftment delay and high-grade acute GvHD. Careful monitoring of HHV6-PCR is warranted during the early period of transplantation, as symptomatic patients require treatment. Disclosures: No relevant conflicts of interest to declare.

Description: Background Richter syndrome (RS) refers as to the onset of aggressive lymphoma, mostly diffuse large B cell lymphoma (DLBCL), in patients (pts) with chronic lymphocytic leukemia (CLL). The outcome of RS pts is usually very poor with both low response rates to chemoimmunotherapy and short survival, except for the minority of them whose tumor cells are clonally unrelated to the underlying CLL. While BCR and BCL2 inhibitors have transformed the management of CLL pts, these drugs do not prevent the onset of RS. Modulating anti-tumor immunity has recently been suggested as a promising approach in RS (Ding, 2017). Blinatumomab is a bi-specific T-cell engaging antibody construct that transiently links CD3-positive T cells to CD19-positive B-cells, inducing T-cell activation and subsequent lysis of tumor cells. It has been approved for the treatment of pts with relapsed or refractory B-ALL and has also been evaluated in the setting of persisting minimal residual disease. More recently, blinatumomab (stepwise dosing 9-28-112 μg/d) has been evaluated in pts with relapsed or refractory DLBCL and demonstrated promising results (ORR 43%) with acceptable safety (Viardot, 2016). We hypothesized that blinatumomab would improve response in RS pts failing to achieve CR after initial debulking with R-CHOP. Methods We report here the first results of a currently ongoing phase 2 multicenter study investigating the efficacy and safety of blinatumomab after R-CHOP debulking therapy for pts with untreated RS of DLBCL histology (NCT03931642). The pts achieving complete remission (CR) after 2 cycles of R-CHOP21 discontinued study while those with persisting (PR, SD) or progressive disease (PD) were eligible to receive an 8-week course of blinatumomab induction. An additional 4-week consolidation cycle was optional and might be proposed according to the treating-physician decision, especially in pts who were ineligible for stem-cell transplantation. Blinatumomab was administered at a stepwise dose of 9 μg/d in the first week, 28 μg/d in the second week, and 112 μg/d thereafter. The primary endpoint was CR rate according to the revised Lugano criteria after the 8-week induction course of blinatumomab. Interim analysis (Simon two-stage design) was planned after completion of blinatumomab induction in 10 pts. Results A total of 15 pts out of 35 has already been enrolled in the trial to date. Median age was 67 years (range, 38-80) andsex ratioM/F was 12/3. CLL features at baseline were as follows: 9/15 (60%) pts hadTP53alterations and 10/13 (77%) unmutated IGHV status. Median number of prior therapeutic lines for CLL was 2 (range, 0-4): 10 (67%) pts previously received chemo-immunotherapy, 10 (67%) pts were exposed to BCR inhibitors and 3 (20%) to venetoclax. As of the data cut-off of July 1st, 2020, the blinatumomab induction course has been completed for 5 pts while it is still on-going in 3 others. Three pts are still on R-CHOP debulking. Four pts discontinued study before receiving blinatumomab for the following reasons: 2 pts achieved CR after R-CHOP, 1 patient died because of febrile neutropenia after R-CHOP and 1 patient discontinued study before starting R-CHOP (no RS criteria after pathology review). Regarding toxicity during blinatumomab, data are available for the 5 pts having completed the blinatumomab induction to date. Four pts had at least one grade 1 adverse event (AE), 2 had grade ≥3 AE. The most common AE, regardless of relationship to blinatumomab, were grade 1 fever (2 pts) and grade 2 leukopenia (2 pts). Other grade 〉1 AE were observed in 1 pt only (grade 3 anxiety, grade 2 anemia, grade 2 neutropenia, grade 3 lymphopenia). In terms of neurologic event, 1 pt had grade 1 AE (paresthesia, myoclonus and muscle contraction) and another one presented grade 4 confusion while on first 9 μg/d dose leading to permanent discontinuation of blinatumomab. In terms of efficacy, after R-CHOP debulking therapy (n=10 evaluable pts), 2 pts achieved CR (and did not pursuit on study), 5 pts were in PR and 3 pts were progressive. At evaluation after the blinatumomab induction (n=5 evaluable pts), 2 pts achieved CR, 1 patient PR and 2 pts were progressive. Conclusions Our preliminary data suggest that blinatumomab shows encouraging anti-tumor activity and acceptable toxicity in pts with RS. Further analyses are warranted to validate these conclusions. Updated efficacy/safety in the remaining pts enrolled in the trial will be presented at the meeting. Disclosures Guieze: astrazanecka:Honoraria, Other: advisory board;gilead:Honoraria, Other: travel funds;janssen cilag:Honoraria, Other: advisory board, travel funds;roche:Other: travle funds;abbvie:Honoraria, Other: advisory board, travel funds.Ysebaert:AbbVie:Consultancy;Janssen:Consultancy;Roche:Consultancy.Fornecker:Roche:Consultancy;Takeda:Consultancy.Broséus:Gilead:Honoraria;AstraZeneca:Consultancy, Honoraria;Janssen:Honoraria, Research Funding;Novartis:Honoraria, Research Funding.Feugier:astrazeneca:Consultancy, Honoraria, Research Funding;abbvie:Consultancy, Honoraria, Research Funding;roche:Consultancy, Honoraria, Research Funding;gilead:Consultancy, Honoraria, Research Funding;janssen:Consultancy, Honoraria, Research Funding. OffLabel Disclosure: Blinatumomab is a bi-specific T-cell engaging antibody construct that transiently links CD3-positive T cells to CD19-positive B-cells. It has been approved as a second line treatment for Philadelphia chromosome-negative relapsed or refractory acute lymphoblastic leukemia.