scholarly journals Does Trauma Heighten the Risk of Hematologic Malignancies? a Retrospective Study of U.S. Combat Veterans

Blood ◽  
2019 ◽  
Vol 134 (Supplement_1) ◽  
pp. 4130-4130
Author(s):  
Christin Destefano ◽  
Krista Shaw ◽  
Ian Stewart ◽  
Eduard Poltavskiy ◽  
Kevin Chung ◽  
...  
Keyword(s):  
T Cell ◽  
B Cell ◽  
Plasma Cell ◽  
Combat Veterans ◽  
Medical Center ◽  
Hematologic Malignancies ◽  
B Cell Lymphomas ◽  
Traumatic Injuries ◽  
Plasma Cell Dyscrasias

Introduction: Multiple case reports have described lymphomas and plasma cell neoplasms developing after trauma 1-4. It has been hypothesized that trauma-induced inflammation may contribute to the neoplasia, and that the site of trauma may serve as the nidus (locus minoris resistentiae) 1, 5. However, to our knowledge there are no studies demonstrating causality. Traumatic injuries sustained during combat have been linked with higher rates of hypertension, coronary artery disease, diabetes mellitus and chronic kidney disease 6. Whether severe injury also increases the risk of hematologic malignancies is unknown. We hypothesized that combat injured veterans have higher rates of lymphoma and plasma cell dyscrasias than un-injured combat veterans. Methods: This was a retrospective cohort study of US military personnel injured during combat operations in Iraq or Afghanistan from 2002-2015 extracted from the Department of Defense (DoD) Trauma Registry. Patients were excluded if they died in theater, had multiple battle injuries, had pre-existing cancer diagnoses or missing data. A comparator arm of deployed and un-injured Iraq and Afghanistan combat veterans was obtained from the Military Health System Data Repository (MDR) matched for year of birth, branch of service, and sex. Cancer diagnoses were defined using International Classification of Diseases, Ninth Revision (ICD-9) and Tenth Revision (ICD-10) Clinical Modification codes obtained from both the DoD and the Veterans Health Administration through the MDR and the Veterans Informatics and Computing Infrastructure, respectively. Malignancy classifications by ICD codes are demonstrated in Table 1 and broken down into aggressive B-cell lymphomas, indolent B-cell lymphomas, Hodgkin lymphoma, T-cell lymphomas and plasma cell dyscrasias. Statistical analyses were performed with the chi-square test and fisher's exact test. This study was approved by the IRB at David Grant USAF Medical Center. Results: There were 9,654 subjects each in the injured and un-injured cohorts. Baseline demographics are demonstrated in Table 2. The mean age was 26 and most patients were junior enlisted, members of the Army, males, and of non-Hispanic white ethnicity/race. The average post-trauma follow-up time was 5.3 years. Overall rates of aggressive B-cell lymphomas, indolent B-cell lymphomas, Hodgkin lymphoma, T-cell lymphomas and plasma cell dyscrasias were low, as demonstrated in Table 3, and there were no statistically significant differences in incidence rates between the two cohorts. Discussion: Traumatic injuries can activate innate immune responses involving inflammatory cytokines, complement, coagulation and dendritic cells, resulting in a pro-inflammatory state 7. Preclinical studies reveal that such inflammation may hamper T-cell immune-surveillance needed to eradicate malignancy 8. However, in our cohort of severely injured combat veterans, rates of lymphomas and plasma cell dyscrasias were not increased over un-injured combat veterans. Strengths of this study include a well-characterized cohort with a matched comparator arm enabling vigorous examination of the impacts of traumatic injuries on cancer. Limitations include retrospective design and relatively short follow up. It is possible that differences will emerge with longer follow up. Conclusions: Despite critical combat trauma injuries being associated with a heightened risk of multiple chronic comorbidities, they do not appear to heighten the risk of lymphoid or plasma cell neoplasms within the first 5-years. The opinions and assertions expressed herein are those of the authors and do not necessarily reflect the official policy or position of the U.S. Air Force, David Grant USAF Medical Center, the Uniformed Services University or the Department of Defense. References: 1. Kriwalsky MS, Oral Surg, 2010. 2. Huang J, Medicine, 2019. 3. Stemberga V, Hematol Oncol, 2003. 4. Erdogan B, Eur Spine J, 2005. 5. Lo Schiavo A, Clin Dermatol, 2014. 6. Stewart IJ, Circulation, 2015. 7. Huber-Lang M, Nature Immunology, 2018. 8. Krall J, Science, 2018. Disclosures No relevant conflicts of interest to declare.

scholarly journals Advances and Perspectives in the Treatment of B-Cell Malignancies

Cancers ◽  
2021 ◽  
Vol 13 (9) ◽  
pp. 2266
Author(s):  
Marta Cuenca ◽  
Victor Peperzak
Keyword(s):  
Cell Differentiation ◽  
B Cell ◽  
Plasma Cell ◽  
Heterogeneous Group ◽  
B Cell Differentiation ◽  
B Cell Lymphomas ◽  
B Cell Malignancies ◽  
Plasma Cell Dyscrasias

B-cell malignancies arise from different stages of B-cell differentiation and constitute a heterogeneous group of cancers including B-cell lymphomas, B-cell leukemias, and plasma cell dyscrasias [...]

Other Tumours in Primary Cutaneous Lymphomas.

Blood ◽  
2007 ◽  
Vol 110 (11) ◽  
pp. 4417-4417
Author(s):  
Serena Rupoli ◽  
G. Goteri ◽  
P. Picardi ◽  
S. Pulini ◽  
A. Tassetti ◽  
...  
Keyword(s):  
T Cell ◽  
B Cell ◽  
Cell Lymphoma ◽  
B Cell Lymphoma ◽  
Skin Carcinoma ◽  
B Cell Lymphomas ◽  
T Cell Lymphomas ◽  
Cutaneous Lymphomas ◽  
Other Neoplasms

Abstract Patients with primary cutaneous lymphomas (PCLs) are treated with multiple therapeutic regimens, which may increase the risk of subsequent solid and haematological neoplasms. The aim of our study was to assess the incidence of other malignancies in our series of PCLs. From March 1994 to January 2007, 272 patients with PCLs (179 M, 93 F, median age 65 yr, range 14–88) were referred to our center for staging, treatment and follow-up. The clinical charts were reviewed to detect the incidence of malignancies occurred before or after the diagnosis of PCL or concomitantly. The series was composed by 228 patients (150 M, 78 F, median age 66 yrs) with T-cell lymphomas (202 Mycosis Fungoides/MF, 10 Sézary Syndrome/SS, 9 CD30+ PCL, 7 non MF/non CD30+ T cell PCL); 43 patients (28 M, 15 F, median age 60 yrs) with B-cell lymphomas (25 Follicular/FL, 14 marginal/MZL, 3 Leg-type, 1 Lymphoblastic) and one patient with CD4+/CD56+ hematodermic neoplasm. Chemotherapy was administered to 48 patients. During follow-up 12 patients died for the disease and 24 for other causes. A second tumor was observed in 41 patients (15%): 6 of them experienced more than one neoplasms: overall we observed 48 malignancies, 38 solid and 10 haematological. The other neoplasms appeared similarly before (20) and after (21) the diagnosis of PCL; in 7 cases they were diagnosed simultaneously. Solid tumours (17 preceding, 4 concurrent, 17 subsequent) were diagnosed in: skin (11), colon (5), lung (4), breast (3), CNS (3), bladder (2), liver (2), kidney (2), uterus (2), testis (1), prostate (1), stomach (1), thyroid (1). The haematological malignancies (3 preceding, 3 concurrent, 4 subsequent) were: B-cell lymphomas (4), acute myeloid leukemias (3), plasmocytoma (1), T-cell lymphoma (1), Hodgkin’s lymphoma (1). Among the six patients with more than one adjunctive neoplasms one patient had lung and kidney carcinoma preceding PCL; two patients a preceding carcinoma (skin and bladder, respectively) and subsequently a lung carcinoma; other two patients showed both a preceding and a concurrent neoplasm (skin and colon carcinoma, B-cell lymphoma and skin carcinoma, respectively). Finally a patient had a preceding skin carcinoma, a concurrent nodal Hodgkin’s lymphoma and a subsequent nodal B-cell lymphoma. So we have reported 48 other neoplasms in 41 patients within 272 PCLs (15%). The occurrence of the other malignancy was not related to the B/T phenotype of PCLs, as it was observed in 35/228 (15.4%) T-cell lymphomas (32 MF, 2 SS, 1 non MF/non CD30+ T cell lymphoma) and in 6/43 (14%) B-cell lymphomas (3 FL, 3 MZL; χ2 test: P=0.88). The interval of occurrence was longer for tumors preceding (median 60 mo.s, range 8–180) than for tumors following PCL (median 45, range 6–122). The administration of chemotherapy for PCL was not associated with an increased incidence of second neoplasm(χ2 test, P=0.77). Multicentric studies might help in elucidating the role of genetic and immunitary factors in the pathogenesis of multiple neoplasms in patients with PCLs.

scholarly journals Factors Associated with Seroconversion after COVID-19 Vaccination in Patients with Hematologic Malignancies

Blood ◽  
2021 ◽  
Vol 138 (Supplement 1) ◽  
pp. 3511-3511
Author(s):  
Thomas A. Ollila ◽  
Rebecca Masel ◽  
John L Reagan ◽  
Kimberly Paiva ◽  
Shaolei Lu ◽  
...  
Keyword(s):  
Monoclonal Antibody ◽  
B Cell ◽  
Plasma Cell ◽  
Lymphocyte Count ◽  
Research Funding ◽  
Hematologic Malignancies ◽  
Categorical Variables ◽  
B Cell Lymphomas ◽  
Cell Antibody ◽  
Active Disease

Abstract Background: Recent studies reported low rates of seroconversion response to COVID-19 vaccination in patients (pts) with hematologic malignancies (HMs). Vaccine choice among the 3 FDA-authorized products (BNT162b2/Pfizer-BioNTech, mRNA-1273/Moderna, or Ad26.COV2.S/J&J), prior therapy, and disease-specific factors may affect seroconversion. Addressing these factors may improve seroconversion rates and identify pts at risk of severe COVID-19 infection despite vaccination. Methods: We conducted a retrospective study of adults with HMs vaccinated in our center between 2/2021 and 7/2021, excluding pts with prior COVID-19 infection. Seroconversion was assessed by the qualitative SARS-CoV-2 Total Antibody Test (IgG/IgM against Receptor Binding Domain [RBD], Wondfo USA, Willowbrook, IL). A subset of samples was tested by the semi-quantitative Abbott AdviseDx SARS-CoV-2 IgG II assay (IgG against RBD). For univariate associations (UVA) we used Fisher's exact test for categorical variables, and fractional polynomial fits for continuous variables to examine non-linearity. Multivariable analysis (MVA) used a robust Poisson model reporting risk ratio (RR) with 95% confidence intervals (CI). Results: Among 239 eligible pts, median age was 70 (range, 28-94), and 112 (47%) were female. HMs included aggressive B-cell lymphomas (n=74, 31%), indolent B-cell lymphomas (n=52, 22%), chronic lymphocytic leukemia (CLL, n=30, 13%), other lymphomas (n-19, 8%), plasma cell neoplasms (n=43, 18%), and myeloid cancers (n=21, 9%); 140 pts (59%) received BNT162b2/Pfizer, 74 (31%) mRNA-1273/Moderna, and 23 (10%) Ad26.COV2.S/J&J vaccines (2 pts had undetermined vaccine type). HM was active in 100 pts (42%), whereas 108 (45%) pts were in remission after treatment, and 31 (13%) on watchful waiting (WW, never treated); 141 (59%) had a prior exposure to an anti-B-cell monoclonal antibody, and 22 (9%) prior stem cell transplantation. Overall, 99 pts (41%; binomial 95% CI, 35-48%) showed post-vaccination seroconversion upon testing at median 10 weeks from first vaccine. Seroconversion was significantly less frequent among pts with lymphomas compared with plasma cell or myeloid neoplasms (overall P=.020; Fig A). It was also less frequent after prior anti-B-cell antibody exposure (29% vs 59%, P<.0001; Fig. B), and in those with active disease (28%, vs 49% for remission [P=.0027], vs 58% for WW [P=.0045]; Fig. C). Furthermore, seroconversion was significantly more frequent after mRNA-1273/Moderna vaccine (57%) compared with BNT162b2/Pfizer (36%, P=.006) or Ad26.COV2.S/J&J (22%, P=.004; Fig. D). It was not associated with age (Fig. E), WBC (Fig. G), or time from vaccination (Fig. I), but was significantly higher with increased lymphocyte count (P<.0001; Fig F) and time elapsed from last chemotherapy (P=.0039; Fig. H). In a MVA (Fig. J), vaccination with mRNA-1273 remained significantly associated with higher rate of seroconversion compared with BNT162b2 (RR=0.59; 95%CI, 0.44-0.79) or Ad26.COV2.S (RR=0.35; 95%CI, 0.16-0.77). Higher seroconversion rate was also associated with remission (RR=1.98; 95%CI, 1.42-2.76) or WW status (RR=1.72; 95%CI 1.02-2.89) compared with active disease, and higher lymphocyte count. Exposure to anti-B-cell antibodies remained associated with lack of seroconversion (RR=0.66; 95%CI, 0.44-0.99). Seroconversion was borderline less frequent in CLL than lymphomas, and higher with plasma cell or myeloid disorders. Results were similar in the subset of pts (n=191) with prior treatment, adjusting for time from last chemotherapy(data not shown). The anti-COVID-19 IgG titers on semiquantitative test (n=47, all after mRNA-based vaccines) were also lower in pts with active disease compared with those in remission (P=.065) or under WW (P=.028), and in those with prior anti-B-cell antibody (P=.0095). Conclusions: Pts with HMs demonstrate overall low rates of seroconversion after vaccination against COVID-19, particularly when they have active disease or are on/after B-cell depleting monoclonal antibody therapy. The mRNA vaccines (particularly mRNA-1273) appear to have elicited superior responses compared with the adenovirus-based product. Pts with active HMs or those within 2 years of last therapy should be particularly aware of the risk of infection despite vaccines and should be considered for strategies to enhance anti-COVID-19 immunity regardless of age. Figure 1 Figure 1. Disclosures Olszewski: TG Therapeutics: Research Funding; PrecisionBio: Research Funding; Celldex Therapeutics: Research Funding; Acrotech Pharma: Research Funding; Genentech, Inc.: Research Funding; Genmab: Research Funding.

scholarly journals A Phase 1 Study of Nivolumab in Combination with Ipilimumab for Relapsed or Refractory Hematologic Malignancies (CheckMate 039)

Blood ◽  
2016 ◽  
Vol 128 (22) ◽  
pp. 183-183 ◽  
Author(s):  
Stephen Ansell ◽  
Martin E Gutierrez ◽  
Margaret A. Shipp ◽  
Douglas Gladstone ◽  
Alison Moskowitz ◽  
...  
Keyword(s):  
T Cell ◽  
B Cell ◽  
Research Funding ◽  
Cell Lymphoma ◽  
Objective Response ◽  
B Cell Lymphoma ◽  
Hematologic Malignancies ◽  
Clinical Activity ◽  
Food And Beverage

Abstract Introduction: Nivolumab (nivo) is a fully human IgG4 monoclonal antibody (mAb) targeting programmed death receptor-1 (PD-1). Nivo has demonstrated clinical activity and an acceptable safety profile in a phase 1b study (NCT01592370; CheckMate 039) in patients (pts) with relapsed/refractory hematologic malignancies. In pts diagnosed with Hodgkin lymphoma (HL), after a median 86 weeks of follow-up, 7/20 responders maintained a response for >1.5 years (Ansell S et al. Blood 2015;126:583), and after a median follow-up of 67 weeks, clinical activity (investigator-assessed objective response rate) was demonstrated in follicular lymphoma (FL; 40%), diffuse large B-cell lymphoma (DLBCL; 36%), mycosis fungoides (15%), and peripheral T-cell lymphoma (PTCL; 40%) (Lesokhin AM et al. J Clin Oncol 2016;34:2698). CheckMate 039 also included a cohort of pts who had received nivo in combination with ipilimumab (ipi), a fully human mAb targeting cytotoxic T-lymphocyte antigen 4 (CTLA-4). Combination of CTLA-4 and PD-1 blockade has shown superior efficacy compared with nivo or ipi alone in preclinical studies and solid tumor malignancies (Wolchok JD et al. N Engl J Med 2013;369:122; Larkin JM et al. N Engl J Med 2015;373:22; Antonia SJ et al. Lancet Oncol 2016;17:883). The aim of this cohort study was to evaluate the safety and efficacy of combined immune checkpoint blockade (nivo+ipi) in pts with the following hematologic malignancies: HL, B-cell non-Hodgkin lymphoma (B-NHL; FL and DLBCL), T-cell NHL (T-NHL; cutaneous T-cell lymphoma [CTCL] and PTCL]), and multiple myeloma (MM). Methods: Nivo+ipi were given at 3 mg/kg IV and 1 mg/kg IV, respectively, every 3 weeks for 4 doses, followed by nivo monotherapy (3 mg/kg) every 2 weeks for up to 2 years. Pts with any of the above histologies, relapsed or refractory disease after ≥2 prior lines of therapy, and adequate organ function were included in the study. Prior systemic therapy may have included chemotherapy and autologous hematopoietic stem cell transplantation (auto-HSCT). Prior anti-PD-1 therapy and allogeneic (allo)-HSCT were not permitted. The primary endpoint was safety. Secondary endpoints included investigator-assessed objective response rate (ORR), best overall response, duration of response (DOR), and progression-free survival (PFS). Results: In total, 65 pts were treated with nivo+ipi (31 HL, 15 B-NHL, 11 T-NHL, 7 MM, and 1 with primary mediastinal B-cell lymphoma [PMBL] who was included in the overall safety cohort only). Median (range) number of prior systemic therapies was 4 (2, 10; HL), 3, (1, 16; B-NHL), 4 (1, 11; T-NHL), and 5 (2, 20; MM). Among patients with HL, only 13% (4/31) had prior auto-HSCT. 2 pts with HL and 1 with T-NHL proceeded to allo-HSCT after stopping study therapy. Across all cohorts, median follow-up was 11.4 months. 5 pts (8%) discontinued due to a drug-related adverse event (AE). The most common drug-related AEs of any grade were fatigue (17 pts [26%]), pyrexia (15 [23%]), and diarrhea (12 [18%]). 19 pts (29%) had a drug-related AE of grade ≥3. 31 pts (48%) had a serious AE. 24 pts (37%) died: HL 2 pts, B-NHL 11, T-NHL 6, MM 4, PMBL 1. Among those pts, 22 (34%) were from disease progression (HL 2 pts, B-NHL 10, T-NHL 5, MM 4, PMBL 1); no deaths were due to an AE. Clinical outcome data are presented (Table). Conclusions: These are the first reported data of combination checkpoint blockade therapy in hematologic malignancies. Overall, the combination of nivo+ipi in these heavily pretreated patients demonstrated a safety and efficacy profile similar to that previously reported for nivo monotherapy in HL, NHL, and MM. Additional follow-up may further clarify the role of ipi in this cohort of patients. In this predominantly transplant-naïve group of patients with HL, the efficacy of nivo+ipi was similar to that seen in patients with relapsed/refractory HL treated with nivo alone. Funding: Bristol-Myers Squibb (BMS). Medical writing: S Addison, Caudex, funded by BMS Disclosures Ansell: BMS, Seattle Genetics, Merck, Celldex and Affimed: Research Funding. Gutierrez:Bayer Health Care Pharmaceuticals, Inc.: Other: Traveling and Lodging- Food and Beverage; E.R. Squibb & Sons, LLC (Bristol Myers Squibb): Consultancy, Other: Travel and Lodging; Incyte Corporation: Consultancy; Pfizer Inc: Consultancy; Merck Sharp & Dohme Corporation: Consultancy, Other: Travel and Lodging; Pharmacyclics LLC, An AbbVie Company: Other: Food and Beverage. Shipp:Cell Signaling: Honoraria; Bristol-Myers Squibb: Consultancy, Research Funding; Bayer: Research Funding; Merck, Gilead, Takeda: Other: Scientific Advisory Board. Moskowitz:Seattle Genetics: Research Funding; Seattle Genetics, Merck: Consultancy. Borello:Bristol-Myers Squibb: Research Funding, Speakers Bureau. Popa-Mckiver:Bristol-Myers Squibb: Employment, Equity Ownership. Farsaci:Bristol-Myers Squibb: Employment. Zhu:Bristol-Myers Squibb: Employment. Armand:Sequenta Inc: Research Funding; Pfizer: Research Funding; Bristol-Myers Squibb: Consultancy, Research Funding; Infinity Pharmaceuticals: Consultancy; Roche: Research Funding; Merck: Consultancy, Research Funding.

scholarly journals Among diffuse large B-cell lymphomas, T-cell-rich/histiocyte-rich BCL and CD30 + anaplastic B-cell subtypes exhibit distinct clinical features

2001 ◽  
Vol 12 (6) ◽  
pp. 853-858 ◽  
Author(s):  
B. Maes ◽  
A. Anastasopoulou ◽  
J.C. Kluin-Nelemans ◽  
I. Teodorovic ◽  
R. Achten ◽  
...  
Keyword(s):  
T Cell ◽  
B Cell ◽  
Clinical Features ◽  
B Cell Lymphomas ◽  
Large B Cell

scholarly journals Enhancer mutations of Akv murine leukemia virus inhibit the induction of mature B-cell lymphomas and shift disease specificity towards the more differentiated plasma cell stage

Virology ◽  
2007 ◽  
Vol 362 (1) ◽  
pp. 179-191 ◽  
Author(s):  
Karina Dalsgaard Sørensen ◽  
Sandra Kunder ◽  
Leticia Quintanilla-Martinez ◽  
Jonna Sørensen ◽  
Jörg Schmidt ◽  
...  
Keyword(s):  
B Cell ◽  
Plasma Cell ◽  
Murine Leukemia Virus ◽  
Leukemia Virus ◽  
B Cell Lymphomas ◽  
Cell Stage ◽  
Disease Specificity ◽  
Murine Leukemia

Cells Reactive with Anti-T-Cell Monoclonal Antibodies in Malignant Cutaneous B-Cell Lymphomas and Pseudolymphomas

1984 ◽  
Vol 10 (4) ◽  
pp. 313-314 ◽  
Author(s):  
PETER KAUDEWITZ ◽  
GÜNTER BURG ◽  
K. KLEPZIG ◽  
R. MUNKER ◽  
P. RIEBER ◽  
...  
Keyword(s):  
Monoclonal Antibodies ◽  
T Cell ◽  
B Cell ◽  
B Cell Lymphomas

scholarly journals Long-Term Follow-Up of Anti-CD19 Chimeric Antigen Receptor T-Cell Therapy

2020 ◽  
Vol 38 (32) ◽  
pp. 3805-3815
Author(s):  
Kathryn M. Cappell ◽  
Richard M. Sherry ◽  
James C. Yang ◽  
Stephanie L. Goff ◽  
Danielle A. Vanasse ◽  
...  
Keyword(s):  
T Cell ◽  
Cell Therapy ◽  
B Cell ◽  
Cell Lymphoma ◽  
B Cell Lymphoma ◽  
T Cell Therapy ◽  
Car T Cell ◽  
Car T

PURPOSE Anti-CD19 chimeric antigen receptors (CARs) are artificial fusion proteins that cause CD19-specific T-cell activation. Durability of remissions and incidence of long-term adverse events are critical factors determining the utility of anti-CD19 CAR T-cell therapy, but long-term follow-up of patients treated with anti-CD19 CAR T cells is limited. This work provides the longest follow-up of patients in remission after anti-CD19 CAR T-cell therapy. METHODS Between 2009 and 2015, we administered 46 CAR T-cell treatments to 43 patients (ClinicalTrials.gov identifier: NCT00924326 ). Patients had relapsed B-cell malignancies of the following types: diffuse large B-cell lymphoma or primary mediastinal B-cell lymphoma (DLBCL/PMBCL; n = 28), low-grade B-cell lymphoma (n = 8), or chronic lymphocytic leukemia (CLL; n = 7). This report focuses on long-term outcomes of these patients. The CAR used was FMC63-28Z; axicabtagene ciloleucel uses the same CAR. Cyclophosphamide plus fludarabine conditioning chemotherapy was administered before CAR T cells. RESULTS The percentages of CAR T-cell treatments resulting in a > 3-year duration of response (DOR) were 51% (95% CI, 35% to 67%) for all evaluable treatments, 48% (95% CI, 28% to 69%) for DLBCL/PMBCL, 63% (95% CI, 25% to 92%) for low-grade lymphoma, and 50% (95% CI, 16% to 84%) for CLL. The median event-free survival of all 45 evaluable treatments was 55 months. Long-term adverse effects were rare, except for B-cell depletion and hypogammaglobulinemia. Median peak blood CAR-positive cell levels were higher among patients with a DOR of > 3 years (98/µL; range, 9-1,217/µL) than among patients with a DOR of < 3 years (18/µL; range, 0-308/μL, P = .0051). CONCLUSION Complete remissions of a variety of B-cell malignancies lasting ≥ 3 years occurred after 51% of evaluable anti-CD19 CAR T-cell treatments. Remissions of up to 9 years are ongoing. Late adverse events were rare.

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