Current prognostic models fail to capture the biological complexity of primary central nervous system lymphoma (PCNSL). We integrated whole-genome sequencing and multiplex immunofluorescence in 68 treatment-naïve patients to define four genomic subtypes (C1, C2, C3, and C4) with divergent survival (C4 worst: median overall survival [OS], 26 months). In parallel, a novel tumor microenvironment (TME) classification based on CD8+T/M2 macrophage ratio stratified patients into High (> 1.5), Intermediate (0.8-1.5), and Low (< 0.8) groups. Unexpectedly, the Intermediate TME group showed the poorest outcomes (5-year OS: 10%). Integration revealed a lethal subgroup (C4 + Intermediate TME; 9.8% of cohort) with a median OS of 3.0 months (hazard ratio = 7.24, p = 0.006). Prognostic nomograms incorporating these subtypes showed promising discriminative performance in internal validation (C-index > 0.78), but external validation is needed. Together, these findings identify a high-risk biological subset and provide a hypothesis-generating framework for future biomarker-driven risk stratification and therapeutic discovery in PCNSL.

IntroductionThe clinical management of relapsed or refractory diffuse large B‑cell lymphoma (R/R DLBCL) has been transformed by chimeric antigen receptor T‑cell therapy (CAR‑T), yet a significant challenge remains in predicting which patients will derive long‑term benefit.MethodsThis multicenter retrospective real‑world study aimed to validate a previously developed efficacy prediction model for CD19 CAR‑T in Chinese patients with R/R DLBCL. A total of 92 patients with DLBCL who received CD19 CAR‑T across four Chinese centers from August 1, 2021, to November 30, 2024 were included. The 5‑index prediction model (incorporating double‑expressor lymphoma status, TP53 alterations, ECOG performance status ≥2, bulky disease ≥5 cm, and prior therapy lines ≥4) was applied to predict treatment outcomes. The primary endpoints were overall response rate (ORR), complete response (CR) rate, progression‑free survival (PFS), and overall survival (OS).ResultsThe median follow‑up was 14.6 months. The C‑index for the 5‑index model was 0.767, indicating good predictive performance. The model effectively stratified patients into different risk groups, with significant differences observed in PFS (P < 0.0001) and OS (P = 0.0007) across groups. The model outperformed traditional prognostic indices such as IPI and R‑IPI.DiscussionThe 5‑index risk model demonstrated robust predictive ability in a real‑world setting, providing a reliable basis for personalized treatment decisions in Chinese DLBCL patients undergoing CAR‑T. Future work will focus on further optimizing the model and conducting multi‑regional validation.

TPS7106 Background: Diffuse large B-cell lymphoma (DLBCL) is the most common type of lymphoma. Aberrant activation of the Bruton's tyrosine kinase (BTK)-related signaling pathway is present in the non-GCB subtype of DLBCL (Davis et al. Nature 2010). Multiple BTK inhibitors (BTKi) have demonstrated efficacy in relapsed or refractory (R/R) non-GCB DLBCL (Strati et al. Haematologica. 2021; Wilson et al. Nat Med. 2015; Yang et al. Blood Adv. 2022), however, there remains room for further improvement. Rocbrutinib is a novel, highly selective, the fourth generation covalent (irreversible) and non-covalent (reversible) BTKi. Phase 1 study showed that in 45 patients with R/R non-GCB DLBCL who had received ≥2 prior lines of systemic therapy, rocbrutinib monotherapy achieved an overall response rate (ORR) of 57.8% and a complete response (CR) rate of 31.3%( Song et al. CSCO. 2025). This article describes the design and progress of a phase 2 pivotal study aimed at comparing the efficacy and safety of rocbrutinib versus investigator's choice of therapy in patients with R/R non-GCB DLBCL. Methods: ROCK-2 (NCT07189065; CTR20253693) is an open-label, randomized, multicenter phase 2 study conducted in China. Eligible patients must have non-GCB DLBCL, not otherwise specified (NOS) per the 2017 WHO classification, received ≥2 prior lines of systemic therapy. Additionally, patients must have measurable disease, an ECOG performance status of 0-2, and adequate hematologic and organ function. Key exclusion criteria include central nervous system involvement, DLBCL transformed from indolent lymphoma, prior refractoriness to BTK-targeting agents, uncontrolled systemic diseases, active infection. Approximately 150 eligible subjects will be randomized 1:1 to receive either rocbrutinib or BR/R 2 , stratified by the number of prior lines of therapy (2 vs ≥3) and International Prognostic Index (IPI) score (0-2 vs 3-5). Subjects in the experimental group will receive rocbrutinib [200 mg once daily (QD)] until disease progression or unacceptable toxicity. Subjects in the control group will receive either BR or R 2 according to the investigator's choice. The BR regimen consists 6 cycles of rituximab (375 mg/m² on day 1) plus bendamustine (90 mg/m²/d on days 1-2). The R 2 regimen consists of rituximab (375 mg/m² on day 1 of cycles 1-6) plus lenalidomide (20 mg QD on days 1-21 of each 28d-cycle until disease progression or unacceptable toxicity). The primary endpoint is ORR assessed by Independent Review Committee (IRC) according to the 2014 Lugano criteria. Secondary endpoints include ORR assessed by investigator (INV), and CR rate, progression-free survival (PFS), duration of response (DOR), time to response (TTR), overall survival (OS) assessed by IRC or INV. The first subject was enrolled on Nov 27 th ,2025. Recruitment is ongoing. Clinical trial information: NCT07189065 .

Abstract The multicenter, noninterventional, observational MMY4032 study is a large-scale, real-world study exploring daratumumab (DARA) in Chinese patients (n = 212) with multiple myeloma (MM) who have received ≤ 3 prior lines of therapy. In the first interim analysis (median follow-up, 10.5 months), DARA was often initiated in second-line therapy, often given in combination with a proteasome inhibitor and/or immunomodulatory drug, and induced high response rates (overall response rate [ORR], 71.8%) and acceptable safety. Here, we report treatment patterns, efficacy, and safety from the second interim analysis with a longer median follow-up of 16.2 months. At the time of this analysis, median duration of DARA exposure was 8.2 months. Among 189 response-evaluable patients, the ORR was 74.1% and the very good partial response or better rate was 55.6%. Minimal residual disease–negativity rate was 60.0% among tested patients. Median progression-free and overall survival were 32.8 months and not reached, respectively; 12-month rates were 77.9% and 87.8%. Response and survival rates were higher with DARA initiation in earlier lines of therapy. Median time to next treatment was not reached with most DARA-based regimens. Adverse drug reactions and serious adverse events were reported in 20.3% and 15.6% of patients, respectively. Overall, with longer follow-up of the MMY4032 study, responses deepened, and survival rates remained high with DARA-based regimens, with more favorable outcomes observed with earlier DARA initiation. No new safety concerns were observed. These real-world data continue to support early use of DARA-based regimens as a standard of care for Chinese patients with MM.

Representativeness of Study Participants

Figure S1. A, control CAR (HBsAg CAR T), BCMA CAR and BCMA CAR-CD27 constructs were transduced into T cells, and CAR expression was detected by protein L assay. B, mock T, BCMA CAR and BCMA CAR-CD27 T cells were stained with anti-human CD27 antibodies. C, mock T and BCMA CAR-CD27 T cells were stained with fluorescence dye-labeled recombinant protein L and BCMA (rp), respectively. D, flow cytometry was used for detection of BCMA and CD70 on the cell surface of multiple cell lines. E, cell coculture was set-up as described in materials and methods. At Day 1 and 2 after coculture, supernatants were harvested for IFNγ measurement by ELISA. F, the transduced or non-transduced T cells were co-cultured with medium in the presence of anti-human CD107a for 1h, monensin was then added; and after 3h, cells were stained for CD3/CD4/CD8 antibodies and recombinant BCMA protein, and detected by flow cytometry. G and H, on day 15 after transduction, CAR-T cells were harvested and stained with CD4/CD8/ki67 antibodies and recombinant BCMA protein, and analyzed using flow cytometry (E); the percentage of Ki76+ cells in CD4+ and CD8+ CAR T cells were shown (F). * P<0.05.

OBJECTIVE:Several recent studies have focused on human endogenous retroviruses (HERVs). HERVs entered the human genome millions of years ago and are associated with various diseases including cancer and immune regulation. Among these, the HERV-K family exhibits the highest transcriptional activity. However, little is known about the expression of HERVs in acute myeloid leukemia (AML) and their potential as biomarkers or therapeutic targets. This study primarily investigated the role of HERV-K102 in AML development and explored the underlying mechanisms. METHODS:The expression profiles of HERV K102 in AML and normal samples were analyzed using The Cancer Genome Atlas (TCGA) database and AML cell lines. Knockout models were generated using CRISPR-Cas9-mediated deletion of the HERV-K102 envelope (K-Env). Cell viability and pyroptosis rates were measured using the MTT assay and flow cytometry, respectively. Transcriptome analysis was performed to identify differentially expressed genes and related pathways. Pyroptosis markers were detected using qRT-PCR and western blotting. The role of HERV-K102 in AML was validated using an inducible knockout xenograft tumor model. RESULTS:HERV-K102 was aberrantly activated and highly expressed in AML cells. K-Env depletion inhibited AML cell proliferation and promoted apoptosis. Furthermore, K-Env knockout induced pyroptosis, as indicated by increased lactate dehydrogenase (LDH) release and enhanced cleavage of caspase-1 and gasdermin D (GSDMD). Transcriptomic and functional analyses demonstrated that this process is mediated by S100A9 upregulation and activation of the NOD-like receptor protein 3 (NLRP3) inflammasome pathway. CONCLUSION:Our findings suggest that HERV-K102 Env may play an important role in AML pathogenesis and represents a novel diagnostic and therapeutic target.

The clinical utility of histone deacetylase inhibitors (HDACi) like vorinostat (SAHA) in lymphoma is constrained by poor pharmacokinetics and off-target toxicity. To address this, we developed a reactive oxygen species (ROS)-responsive homodimeric SAHA prodrug (SAHA-tk-SAHA) linked via a thioketal bridge, which self-assembled into PEGylated nanoparticles (tk-diSAHA NP). These monodisperse nanoparticles (119.3 ± 4.0 nm) demonstrated excellent stability and ROS-triggered drug release (68.18 ± 2.25% with 10 mM H2O2 vs 6.24% in PBS over 48 h). In vitro, tk-diSAHA NP induced G0/G1 cell cycle arrest and apoptosis in lymphoma cells. In A20 lymphoma-bearing mice, intravenous tk-diSAHA NP achieved superior tumor growth inhibition (615.18 ± 147.88 mm3) compared to oral SAHA (1134.78 ± 311.31 mm3, p < 0.05), with enhanced histone H3 acetylation in tumors and no appreciable systemic toxicity. This ROS-activatable nanoprodrug platform presents a promising strategy to enhance the efficacy and safety of HDACi-based epigenetic therapy for lymphoma.

BACKGROUND:Despite advances in lymphoma therapy, significant challenges persist including R-CHOP resistance and CAR-T toxicity. Hydroxamate-based histone deacetylase inhibitors (HDACi) like vorinostat (SAHA) offer epigenetic therapeutic potential but are limited by poor bioavailability and rapid clearance. METHODS:To overcome these barriers, we rationally designed an esterase- activatable dimeric prodrug by conjugating two SAHA molecules via a glutaric acid linker (SAHA-cc-SAHA). This prodrug co-assembled with DSPE-PEG2000 into nanoparticles (cc-diSAHA NPs). The system was characterized (DLS/TEM), and its drug release profile was assessed with/without porcine liver esterase (PLE). Antitumor activity was evaluated in EL4/A20 lymphoma cells (apoptosis/cycle assays, etc) and EL4 allograft. Transcriptomic mechanisms were deciphered by RNA-seq. RESULTS:The cc-diSAHA NPs were uniform spheres (∼74 nm, PDI = 0.187) with excellent colloidal stability and minimal drug leakage (<4 % in 7 days), while enabling rapid drug release upon esterase stimulation (92.4 % within 7 h with PLE). In vitro, they demonstrated broad-spectrum anti-lymphoma activity, inducing G0/G1 arrest and apoptosis, albeit with delayed kinetics versus free formulations, consistent with a sustained-release profile. Transcriptomics revealed multifaceted mechanisms, including potent activation of interferon-mediated immunogenic stress and hematopoietic differentiation, alongside enriched adhesion and redox metabolism pathways. In vivo, intravenous cc-diSAHA NPs suppressed EL4 tumor growth significantly more than oral SAHA (819.36 vs 1594.40 mm³; p < 0.01), without inducing systemic toxicity or organ damage. CONCLUSION:This nanoplatform overcomes HDACi delivery barriers by reconciling the stability-activation paradox, providing a therapeutically viable option for lymphoma patients ineligible for standard intensive therapies.

Effective therapy for relapsed or refractory central nervous system lymphoma (r/r CNSL) remains an unmet medical need. Meanwhile, developing antitumor drugs for CNS malignancies faces the dual challenge of achieving effective blood‒brain barrier (BBB) penetration and potent tumor cell killing. To address these challenges, a comprehensive predictive system was established to support decision-making during the discovery of HZ-A-018, a potent and BBB-permeable Bruton tyrosine kinase (BTK) inhibitor. This study further presents key preclinical results for HZ-A-018, as well as efficacy/safety data from a multicenter Phase 1 trial in r/r CNSL patients. HZ-A-018 demonstrated manageable safety, with only 19.2% of patients experienced grade 3 or higher adverse events according to the Common Terminology Criteria for Adverse Events version 5.0. Treatment with HZ-A-018 at the recommended phase II dose (RP2D) of 600 mg achieved an overall response rate (ORR) of 72.7% (95% CI, 39.0–94.0) and a 12-month survival rate of 90.5%. The Center for Drug Evaluation in China has authorized the initiation of this single-arm Phase II study as a pivotal registrational clinical trial for accelerated approval of HZ-A-018 for monotherapy in patients with r/r PCNSL. This trial has been registered under the identifiers ChiCTR2400091821 at www.chictr.org.cn and CTR20210181 at www.chinadrugtrials.org.cn.

A, the peak CAR copies were compared between non-responders and responders (Mann-Whitney; P=0.006). B, CAR copies detected by qPCR following infusion of CBG-002 in patient 1. d: day; m: month.

Abstract Purpose: This report presents long-term outcomes of third-generation anti-CD30 chimeric antigen receptor (CAR) T-cell therapy in patients with relapsed/refractory (r/r) CD30+ lymphoma. Patients and Methods: In this single-arm, multicenter, phase I/II trial, patients received a lymphodepletion regimen comprising fludarabine and cyclophosphamide, followed by infusion of anti-CD30 CAR T cells. Primary endpoints included safety and overall response rate (ORR), whereas secondary endpoints were progression-free survival (PFS) and overall survival (OS). Results: Forty-four patients were enrolled, including 33 cases of Hodgkin lymphoma. Of 44 patients, 23 achieved complete response (CR) to CAR T, and 19 achieved PR, resulting in a CR rate of 52.3% and an ORR of 95.5%. The most frequent toxicities were hematologic adverse events of grade 3 or higher (68.2% of neutropenia). Cytokine release syndrome occurred in 18 (40.9%) patients, with 2 (4.5%) cases being ≥ grade 3. In the follow-up period, 24 patients underwent autologous hematopoietic stem cell transplantation (auto-HSCT) after CAR T within a median of 3 months. The best ORR was 95.5%, with 27 (61.4%) patients achieving CR. The best CR rate was higher in patients receiving CAR T followed by auto-HSCT compared with those receiving CAR T alone (75% vs. 45%). Three-year OS and PFS rates for all patients were 79% [95% confidence interval (CI), 66.1%–91.9%] and 74.2% (95% CI, 60.3% –88.1%), respectively. Patients receiving consolidated auto-HSCT following CAR T exhibited significantly longer OS and PFS compared with those treated with CAR T alone. Conclusions: Third-generation anti-CD30 CAR T demonstrates high efficacy and a favorable safety profile in patients with r/r CD30+ lymphoma. Addition of auto-HSCT following CAR T-cell therapy improves depth of remission and potentially enhances OS and PFS.

Abstract Background Chimeric Antigen Receptor T‐cell (CAR‐T) therapy has evolved from its initial application in hematological cancers to treating solid tumors and autoimmune diseases. Despite iterative advancements in CAR design improving efficacy and safety, challenges including limited persistence, immune‐related toxicities, tumor resistance mechanisms, and barriers posed by the tumor microenvironment (TME) remain critical obstacles. Methods This review synthesizes current evidence on CAR‐T resistance mechanisms and therapeutic strategies. Key approaches analyzed include CAR design optimization (e.g., dual‐targeting), pre‐infusion tumor burden reduction, combination therapies to mitigate immune suppression, and cytokine support (e.g., IL‐2/IL‐15) to enhance persistence. The role of the TME (hypoxia, metabolic competition, immunosuppressive factors) and tumor‐intrinsic resistance drivers (antigen loss, anti‐apoptotic signaling) are systematically evaluated. Results Major resistance mechanisms include antigen escape (masking/loss), high tumor burden, and TME‐mediated suppression (hypoxia, immune checkpoints). Clinical challenges involve manufacturing delays, insufficient CAR‐T cytotoxicity, and poor persistence. Strategies such as dual‐target CARs, preconditioning regimens, and cytokine‐augmented persistence demonstrate preclinical/clinical promise in overcoming these limitations. Conclusions CAR‐T therapy holds transformative potential but requires addressing resistance and toxicity barriers. Future directions include allogeneic CAR‐T platforms, in vivo CAR‐T delivery, and novel combinatorial approaches. While these innovations offer exciting prospects, scalability, safety, and long‐term efficacy necessitate further translational and clinical research.

7059 Background: Marginal zone lymphoma (MZL) is a heterogeneous B-cell malignancy that is often managed with chemoimmunotherapy in the first-line setting, but chemotherapy entails considerable toxicity. Orelabrutinib, a novel oral BTK inhibitor which offers improved target selectivity and fewer off-target effects. This study evaluates the chemo-free combination of orelabrutinib plus rituximab in untreated MZL. Methods: This is a prospective, single-arm, multicenter phase II clinical trial (NCT07022223). Patients with untreated MZL who met ECOG criteria of 0–2 and were in need of treatment, or who had failed local, were eligible. All participants will receive induction therapy with the orelabrutinib and rituximab regimen. The treatment cycle is 28 days, with a total of 4~6 cycles. The induction treatment period is as follows: Cycle 1: Rituximab, 375 mg/m², on day 1. Cycles 2-6: Orelabrutinib, 150 mg, once daily orally, from day 1-28, plus rituximab 375 mg/m² on day 1. Patients who achieve a partial response (PR) or better will enter a 2-year maintenance period with orelabrutinib. The primary endpoint is the overall response rate (ORR). Secondary endpoints include complete response (CR) rate, PR rate, progression-free survival (PFS), and overall survival (OS). Safety is assessed by monitoring adverse events (AEs). Results: From March 2025 to December 2025, a total of 40 patients with MZL (32 MALT, 6 NMZL, 2 SMZL) were enrolled. The median age at diagnosis was 68 years (range 44–84), and 82.5 % of patients were older than 60 years. 21 (52.5%) were female. Most patients had an ECOG score of 0-1 (28/40), Ann Arbor Stage Ⅲ-IV disease (35/40). Twelve patients had an MZL-International Prognostic Index score of ≥2. Thirteen patients had failed prior local therapy, the majority of whom had undergone surgical resection. After three cycles, 25 patients were evaluable, with an ORR of 80 % (20/25) and a CRR of 24 %. Following six cycles, 13 patients were evaluable, achieving an ORR of 100 % (13/13) and a CRR of 62 % (8/13). The median time to response was 72 days. With a median follow-up of 5.7 months (range, 5.1-6.8), the median PFS and OS were not reached, the 1-year PFS rates were 97.2% and the 1-year OS rates were 100%. Next-generation sequencing (NGS) was performed on 16 patients, a total of 158 mutated genes were identified, with missense mutations predominating (62.7%). The most frequently mutated genes were NOTCH2, FAT4, LRP1B, PCLO, and SYNE1, all at 31.2 %. Treatment was generally well tolerated, only 13 patients experienced adverse events, the most common adverse events were anemia (15 %), infection (12.5 %) and neutropenia (10 %). Notably, BTK inhibitor–associated atrial fibrillation (0 %) and bradycardia (0 %) were absent. Conclusions: The combination of orelaburtinib and rituximab shows significant activity in MZL, with a manageable toxicity profile. Clinical trial information: NCT07022223 .

Background B cell-targeting chimeric antigen receptor (CAR) T cell therapy has shown efficacy in autoimmune diseases but is limited by toxicity, complex manufacturing, and high cost. Umbilical cord blood (UCB)-derived CAR-natural killer (CAR-NK) cells offer an alternative “off-the-shelf” platform with a potentially superior safety profile. We developed a UCB-derived CD19-targeting CAR-NK product incorporating the 4-1BB costimulatory domain (CD19-BBz) and evaluated its safety and efficacy in refractory systemic lupus erythematosus (SLE). This study was registered at ClinicalTrials.gov (ClinicalTrials.gov: NCT06421701). Methods In this phase 1, open-label, dose-escalation study, five patients with refractory SLE received lymphodepletion chemotherapy followed by infusion of allogeneic CD19-BBz CAR-NK cells. Dosing followed a step-up regimen, with the highest total dose being 1.35 × 109 cells—2.2- to 3.3-fold lower than the highest doses previously reported for CAR-NK therapy in SLE. Findings Treatment was exceptionally well tolerated. No grade ≥2 cytokine release syndrome and no neurotoxicity or graft-versus-host disease occurred. All patients achieved profound B cell depletion, with nadir circulating B cell levels ranging from 0.16 to 1.44 cells/μL. All patients achieved an SLE Responder Index-4 response by month 1. The lupus low disease activity state was attained in all patients by month 9, and 80% (4/5) met the definition of remission in SLE by the last follow-up (median, 12 months). Reconstituted B cells displayed a sustained naive-dominant repertoire. Conclusions Low-dose UCB-derived CD19-BBz CAR-NK cell therapy demonstrated an excellent safety profile and induced robust, durable clinical responses in refractory SLE. Funding This study was supported by the Noncommunicable Chronic Diseases-National Science and Technology Major Project (2023ZD0501300).

HZ-A-018 represents a highly selective, covalent, novel inhibitor targeting Bruton's tyrosine kinase (BTK). This multicenter, open-label phase I study enrolled 32 patients with relapsed/refractory B cell malignancies (including diffuse large B cell lymphoma, chronic lymphocytic leukemia/small lymphocytic lymphoma, Waldenström macroglobulinemia, follicular lymphoma, mantle cell lymphoma, and marginal zone lymphoma) in dose-escalation and -expansion phases. Thirty-one patients received treatment: 15 in the dose-escalation phase (75-550 mg once daily) and 16 in the expansion phase (300 mg once daily). No dose-limiting toxicities or maximum tolerated dose were identified. The most common treatment-emergent adverse events included cytopenias, rash, and hypertension. Among 29 efficacy-evaluable patients, with a median follow-up of 4.9 months, the overall response rate was 44.8%. Pharmacokinetics revealed dose-proportional exposure, and median BTK occupancy in peripheral blood mononuclear cells surpassed 95% across all dose levels at steady state. HZ-A-018 demonstrated acceptable safety and antitumor activity, supporting further clinical development.

Cytomegalovirus (CMV) is an increasingly recognized complication of chimeric antigen receptor T-cell (CAR-T) and bispecific antibody (BsAb) therapies for hematologic malignancies, driven by therapy-related immunosuppression and cumulative exposure to lymphodepleting or steroid regimens. Given China's high adult CMV IgG seroprevalence (>90%), baseline risk, interpretation of low-level DNAemia, and operational thresholds differ from low-seroprevalence settings, requiring context-specific guidance. This China-adapted, evidence-graded consensus was developed by a multidisciplinary panel from major centers using a modified Delphi process and Oxford Centre for Evidence-Based Medicine levels to translate international guidance into a high-seroprevalence setting. Recommendations prioritize early risk stratification and pragmatic surveillance. We advise routine CMV monitoring by real-time quantitative PCR during the first 30 days after therapy, with risk-adapted extension thereafter. Interpretation and treatment triggers are anchored to WHO-traceable IU/mL and specified by specimen matrix to support comparability across assays. Consideration of prophylaxis is proposed for well-defined high-risk subgroups, acknowledging the need for prospective validation. Syndrome-based diagnostic and treatment algorithms are provided for tissue-invasive disease, including CMV pneumonia and encephalitis, with guidance on antiviral induction, step-down, and monitoring for virologic response and drug toxicity. This consensus explicitly adapts international recommendations to China's epidemiology, assay practice, and drug accessibility. By standardizing prevention, surveillance, and management in CAR T-cell and BsAb recipients, this consensus aims to lower non-relapse mortality and improve long-term outcomes. Priority research needs include harmonized viral-load thresholds, validation of risk-adapted prophylaxis strategies, and studies that clarify the significance of low-level DNAemia in this population.

Median levels of serum CRP (A), IL-6 (B), IL-10 (C), TNFα (D) and IFNγ (E) during the CRS phase were measured in serial clinical samples stratified by dose cohorts.