Introduction
Chimeric antigen receptor T-cell (CAR-T) therapy has advanced the treatment landscape for patients with relapsed/refractory multiple myeloma (RRMM), providing high response rates and durable responses [ 1 – 3 ]. Two CAR-T therapies are currently approved in RRMM: ciltacabtagene autoleucel (cilta-cel) and idecabtagene vicleucel (ide-cel) [ 4 , 5 ]. Cilta-cel is approved by the European Medicines Agency (EMA) and the US Food and Drug Administration (FDA) in patients who have received at least one prior line of therapy (LOT), including an immunomodulatory agent and a proteasome inhibitor (PI), and are lenalidomide-refractory, based on the CARTITUDE-4 trial [ 4 , 6 , 7 ]. Ide-cel is approved by the EMA and FDA for patients who have received two or more prior LOTs, including an immunomodulatory agent, a PI and an anti-CD38 monoclonal antibody (mAb), based on the KarMMa-3 trial [ 5 , 8 , 9 ]. In CARTITUDE-4, at a median follow-up of 33.6 months, median progression-free survival (PFS) was not reached (NR) in the cilta-cel group (hazard ratio [HR] versus standard of care [SOC], 0.29; 95% CI, 0.22–0.39); median overall survival (OS) was also NR with cilta-cel (HR versus SOC, 0.55; 95% CI, 0.39–0.79) [ 10 ]. In KarMMa-3, at a median follow-up of 30.9 months, median PFS was 13.8 months with ide-cel versus 4.4 months with SOC (HR, 0.49; 95% CI, 0.38–0.63); median OS was 41.4 months with ide-cel versus 37.9 months with SOC (HR, 1.01; 95% CI, 0.73–1.40) [ 11 ].
B-cell maturation antigen (BCMA)-targeting CAR-T therapies are manufactured from autologous T cells, genetically engineered to recognise BCMA on plasma cells [ 12 ]. Manufacturing is complex and typically takes 4–6 weeks [ 12 – 14 ], during which time disease control must be maintained to prevent progression and preserve patient fitness [ 13 ]. Bridging therapy (BT) is recommended to be administered between T-cell leukapheresis and lymphodepleting chemotherapy [ 13 , 15 ]; however its use varies widely in practice [ 16 ]. BT options in earlier LOTs include chemotherapy, immunomodulatory drugs, PI, mAbs, and targeted agents [ 7 , 9 ]. However, effective BTs in later LOTs remain limited [ 1 , 2 ], prompting the exploration of novel therapies such as bispecific T-cell engagers in RRMM [ 17 , 18 ].
In CARTITUDE-4, all patients in the cilta-cel group received BT with daratumumab, pomalidomide, and dexamethasone (DPd) or pomalidomide, bortezomib, and dexamethasone (PVd), with better BT responses correlating with longer PFS [ 19 , 20 ]. KarMMa-3 allowed various BT combinations including PIs, immunomodulatory drugs and mAbs [ 9 ]. Patients who received BT and had a decrease/no change in disease burden had longer PFS than patients who had an increase in disease burden [ 20 ]. In early-phase trials (CARTITUDE-1 and KarMMa), low BT response rates were observed [ 1 , 2 ], possibly due to heavy pretreatment (median 6 prior LOT), and use of novel therapies such as bispecific T-cell engagers was not permitted.
Real-world data show that effective BT before cilta-cel or ide-cel can minimise adverse events and improve outcomes in RRMM [ 18 , 21 ]. While one study reports worse outcomes with ide-cel in patients who received alkylator-based BT versus those who did not, use of BT was more likely in patients with aggressive disease [ 22 ]. Additionally, intensity of cytotoxic chemotherapy BT has been associated with impaired hematopoietic recovery [ 23 ]. These data highlight the need for expert guidance to optimise BT selection, efficacy, safety, and post–CAR-T outcomes.
Objective
This publication summarises the clinical experience and consensus recommendations of a panel of experts from multiple European centres proficient in managing RRMM with CAR-T therapy. We recognised a high need for guidance around optimal BT to CAR-T therapy in the European multiple myeloma (MM) community. Hence, we aim to provide guidance for BT before anti-BCMA CAR-T therapy, with particular focus on heavily pretreated patients and emerging BT options, such as bispecific T-cell engagers, to address current challenges and support harmonised clinical decision-making.
Methods
A panel of 10 experts was assembled, with strong clinical backgrounds in haematology and experience in novel MM therapies, including CAR-T therapy. Within this, a steering committee guided the process to ensure consensus workshop objectives were met. Our approach involved qualitative individual interviews and a consensus workshop, both focused on BT in RRMM, including bispecific T-cell engagers as BT options before anti-BCMA CAR-T therapy.
Qualitative interviews
In January 2025, three steering committee members developed interview questions addressing BT concepts and options for later treatment lines. Topics selected were areas where practical guidance would be highly beneficial to healthcare professionals (HCPs) using BT in anti-BCMA CAR-T therapy. One-hour individual interviews were conducted to capture uninfluenced opinions. Results were summarised in April 2025 to prepare for the workshop.
Consensus workshop
In the workshop, we reviewed interview insights and resolved areas lacking consensus, covering topics like BT definition and objectives, patient eligibility, balancing duration and response, regimen selection, difficult-to-treat groups, and clinical and safety management. We discussed evolving practices, including shifting from minimising BT duration to optimising the balance between duration and response to BT.
The virtual meeting used structured dialogue and voting to encourage active participation and discussion, which was consolidated into key expert recommendations. While our guidance offers flexible direction based on our experience and emerging evidence, it does not replace clinical judgment or legal advice.
Expert guidance and opinions: BT in anti-BCMA CAR-T therapy
Scope of the recommendations
For the purposes of this publication, BT was defined as therapy administered after leukapheresis and before lymphodepleting chemotherapy preceding anti-BCMA CAR-T infusion, in alignment with previous publications [ 13 , 24 , 25 ]. It was deemed important to distinguish between BT and pre-bridging/holding treatments, defined as treatments administered before apheresis [ 13 , 18 ]. Treatment goals and considerations may be different for BT and pre-bridging/holding treatments. This publication focuses on BT before anti-BCMA CAR-T therapy in triple-class exposed patients with RRMM.
Recipients of BT
The recent International Myeloma Working Group (IMWG) guidelines recommend consideration of BT in patients with high disease burden and/or at risk of developing morbidity from MM during T-cell manufacturing [ 13 ]. Based on our experience, BT should be used for a vast majority of patients undergoing anti-BCMA CAR-T therapy, regardless of prior LOTs; effective BT enables most patients to receive CAR-T infusion. Patients experiencing smouldering relapse (typically in earlier LOTs) or slowly progressing disease will still benefit from BT. In exceptional circumstances, for example where contraindications or substantial comorbidities are present, BT may not be administered; however, such decisions would be made on an individual basis rather than reflecting a clearly defined population unsuitable for BT.
Although anticipated future reductions in vein-to-vein time may lessen the need for BT in some patients, it should still be considered an opportunity to reduce tumour load before infusion, particularly as effective BT has been associated with improved efficacy and safety outcomes of CAR-T therapy [ 26 , 27 ].
Objectives of BT
We agreed that the short-term objectives of BT are to: Bring patients to anti-BCMA CAR-T therapy, maintain or improve performance status and organ function until CAR-T infusion and reduce tumour burden, while avoiding treatment-related toxicity and worsening cytopenia that could delay or prevent CAR-T infusion. Long-term objectives include maximising efficacy post–CAR-T therapy and reducing the risk of post–CAR-T toxicities, as high tumour burden is a major risk factor for development of typical CAR-T associated toxicities (cytokine-release syndrome [CRS], immune effector cell-associated neurotoxicity syndrome [ICANS] and non-ICANS neurotoxicities) [ 28 ]. These objectives are supported by literature [ 13 , 24 , 29 – 32 ]. Available evidence suggests effective BT is associated with improved efficacy and safety of subsequent CAR-T therapy [ 18 – 22 , 27 ]. Within these objectives, the optimal balance between treatment duration and achieving an adequate response must be considered.
Balancing duration and response
Although data on optimal duration of BT in CAR-T therapy are limited [ 25 ], HCPs should balance duration with achieving an adequate response. BT should last as ‘short as possible’ and ‘as long as necessary’ to reach the deepest response without delaying or preventing CAR-T infusion. We generally agreed that reaching ≥complete response during BT is not always possible; ≥partial response is an appropriate target. In patients with low tumour burden, however, this may not be required – a lower level of response and absence of progressive disease might be sufficient.
In some cases, extending BT to optimise response may be considered if a deeper response is achievable, though no consensus exists on extending BT by 1–2 or >2 cycles. Substantially prolonged BT is discouraged due to risks of disease progression and infections, which may delay or prevent CAR-T infusion. Patients should proceed to CAR-T infusion if CAR-T manufacturing was successful, even if achieving a deep response (e.g., ≥very good partial response) during BT. Extension of BT to optimise response should follow careful monitoring of disease and toxicity parameters. Guidance priorities are: 1: Stop proliferative disease and gain some response. 2: Add 1 cycle if good response occurs rapidly.
We agreed that patients who do not achieve ≥partial response after initial BT should switch to a different (second-line) BT regimen; the objectives of this may differ. In this context, attaining minor response or control of stable disease may be a reasonable goal, aiming to preserve eligibility for CAR-T and avoid further progression of disease. Importantly, patients with rapid disease progression or high/uncontrolled tumour burden on BT may not be recommended for CAR-T.
Choice of BT
The literature shows heterogeneity in BT options [ 23 , 24 ], reflecting differences in prior LOTs, patient factors (e.g., age and cytogenetics) and status (e.g., extramedullary disease [EMD], renal impairment, central nervous system [CNS] involvement, bone marrow reserve, and cytopenias/infections risk), tumour dynamics, and drug availability. Patient characteristics and prior therapies should guide BT selection. Patients with progressive disease on BT should be promptly evaluated for alternative BT regimens, depending on availability/access and prior treatments, to avoid delay or prevention of CAR-T infusion. Typically, more BT options are available in earlier lines; effective BT is more challenging in heavily pretreated patients. BTs that have been most frequently used in RRMM after ≥3 prior LOTs include chemotherapy, immunomodulatory drugs, PI, monoclonal antibodies, targeted inhibitors (BCL-2 and XPO1), and talquetamab (Table 1 ). Table 1 Bridging therapy options in CAR-T therapy in patients with RRMM who have received ≥3 lines of therapy a . Chemotherapy combinations mAb combinations PI combinations Targeted inhibitors (BCL-2 and XPO1) and combinations Unique/Novel therapies: Bispecific antibodies Cisplatin + doxorubicin + cyclophosphamide + etoposide (PACE)-like therapy [ 58 ] Anti-CD38 mAb + pomalidomide + dexamethasone Carfilzomib + dexamethasone Venetoclax [ 1 , 13 ] Talquetamab [ 18 , 37 ] Dexamethasone + cisplatin + doxorubicin + cyclophosphamide + etoposide (DPACE) [ 58 ] Anti-CD38 mAb + carfilzomib + dexamethasone Carfilzomib + Anti-CD38 mAb + dexamethasone Selinexor [ 13 ] Dexamethasone + cyclophosphamide + etoposide + cisplatin (DCEP) [ 53 ] Anti-CD38 mAb + PI + immunomodulatory drug + dexamethasone Carfilzomib + cyclophosphamide + dexamethasone [ 53 ] Selinexor + bortezomib or pomalidomide Cyclophosphamide in combination [ 1 , 2 ] Elotuzumab + pomalidomide + dexamethasone Carfilzomib + cyclophosphamide + Anti-CD38 mAb BRAF inhibitors +/- MEK inhibitor Cyclophosphamide + etoposide + dexamethasone Carfilzomib + pomalidomide + Anti-CD38 mAb Bendamustine [ 1 ] Carfilzomib + pomalidomide + isatuximab Melphalan [ 1 ] Bortezomib + dexamethasone [ 53 ] BCL-2 B-cell lymphoma 2, CAR-T chimeric antigen receptor T-cell, mAb monoclonal antibodies, PI proteasome inhibitor, RRMM relapsed/refractory multiple myeloma, XPO1 exportin 1. a The bridging therapy categories are listed alphabetically.
Table 1
Bridging therapy options in CAR-T therapy in patients with RRMM who have received ≥3 lines of therapy a .
BCL-2 B-cell lymphoma 2, CAR-T chimeric antigen receptor T-cell, mAb monoclonal antibodies, PI proteasome inhibitor, RRMM relapsed/refractory multiple myeloma, XPO1 exportin 1. a The bridging therapy categories are listed alphabetically.
| Chemotherapy combinations | mAb combinations | PI combinations | Targeted inhibitors (BCL-2 and XPO1) and combinations | Unique/Novel therapies: Bispecific antibodies |
| Cisplatin + doxorubicin + cyclophosphamide + etoposide (PACE)-like therapy [ 58 ] | Anti-CD38 mAb + pomalidomide + dexamethasone | Carfilzomib + dexamethasone | Venetoclax [ 1 , 13 ] | Talquetamab [ 18 , 37 ] |
| Dexamethasone + cisplatin + doxorubicin + cyclophosphamide + etoposide (DPACE) [ 58 ] | Anti-CD38 mAb + carfilzomib + dexamethasone | Carfilzomib + Anti-CD38 mAb + dexamethasone | Selinexor [ 13 ] | |
| Dexamethasone + cyclophosphamide + etoposide + cisplatin (DCEP) [ 53 ] | Anti-CD38 mAb + PI + immunomodulatory drug + dexamethasone | Carfilzomib + cyclophosphamide + dexamethasone [ 53 ] | Selinexor + bortezomib or pomalidomide | |
| Cyclophosphamide in combination [ 1 , 2 ] | Elotuzumab + pomalidomide + dexamethasone | Carfilzomib + cyclophosphamide + Anti-CD38 mAb | BRAF inhibitors +/- MEK inhibitor | |
| Cyclophosphamide + etoposide + dexamethasone | Carfilzomib + pomalidomide + Anti-CD38 mAb | |||
| Bendamustine [ 1 ] | Carfilzomib + pomalidomide + isatuximab | |||
| Melphalan [ 1 ] | Bortezomib + dexamethasone [ 53 ] |
In patients who do not achieve ≥partial response to initial BT, treatment decisions should be guided by treatment history and patient characteristics.
Additional considerations for regimen selection include: Avoid agents to which the patient was previously refractory. Prioritise conventional RRMM therapies; consider prior exposure and refractory status in triple-class exposed patients. Consider mAb-based regimens in patients with limited exposure/prolonged period since exposure. Consider high-dose melphalan and DPACE (dexamethasone + cisplatin + doxorubicin + cyclophosphamide + etoposide) only for fit, non-elderly patients who have exhausted most options and have sufficient bone marrow reserve and/or an autologous back-up available. Consider chemotherapy-based regimens for patients with high tumour burden and/or EMD. Consider talquetamab in heavily pretreated patients who have exhausted other effective therapies. Avoid anti-BCMA BT before anti-BCMA CAR-T therapy due to unknown effects of short-term use and resistance concerns. Consider local reimbursement policies and accessibility; no regimen is FDA or EMA-approved specifically for BT and available treatments differ widely by country.
Choice of BT – Talquetamab
Talquetamab, a GPRC5DxCD3 bispecific antibody, is EMA-approved for patients with RRMM who have received at least three prior therapies, including an immunomodulatory agent, a PI, and an anti-CD38 mAb, and have demonstrated disease progression on the last therapy [ 33 ], and FDA-approved after at least four prior lines of therapy, including a PI, an immunomodulatory agent, and an anti-CD38 mAb [ 34 ]. In MonumenTAL-1, talquetamab demonstrated a high ORR of 67–74%, median duration of response of 17.5 months at a dosing schedule of 0.8 mg/kg every other week [ 35 ], and rapid responses with a median time to first response of 1.2 and 1.3 for 0.4 mg/kg every week and 0.8 mg/kg every other week, respectively [ 36 ]. The safety profile showed lower risk of high-grade infections versus approved anti-BCMA bispecific antibodies [ 35 ].
Based on the favourable efficacy outcomes and rapid response rates in MonumenTAL-1 [ 35 , 36 ], we recommend considering talquetamab as BT, particularly for patients who have exhausted other effective treatments. Retrospective studies from multiple centres in Germany and the US also support the efficacy and manageable safety of talquetamab as BT before anti-BCMA CAR-T therapy [ 17 , 18 , 37 ]. These studies reported ORRs of talquetamab BT at 62–100% [ 17 , 18 , 37 ], with talquetamab outperforming chemotherapy or other antibody-based regimens [ 17 ], enabling most patients to successfully proceed to CAR-T infusion [ 17 , 18 , 37 ].
Patients eligible for CAR-T therapy may be considered eligible for bridging with talquetamab, considering their characteristics, pre-existing conditions, and clinically relevant impairments such as taste changes, skin conditions, or weight loss. As supported by recent findings [ 18 ], talquetamab is favourable for difficult-to-treat groups including renal impairment, advanced age, high disease burden, functional high-risk status, or EMD, especially since patients with EMD often do not respond well to other therapies.
Consistent with other BT regimens, the typical duration of talquetamab as BT is 6–8 weeks. We noted safety considerations with talquetamab including those related to GPRC5D targeting, such as early-onset taste changes and skin reactions, which rarely lead to discontinuation but require supportive care [ 36 – 39 ]. Nail toxicity typically occurs later (median onset of 64–69 days) [ 38 ] and is less relevant during bridging. CRS and ICANS are expected, with ICANS seen in <10% of cases and mostly low grade; delayed neurotoxicity is rare (<2%) [ 17 , 18 , 37 , 38 ].
Bispecific antibodies like talquetamab may serve as salvage options after anti-BCMA CAR-T relapse [ 40 ], but data on reuse in patients who previously received it as BT is lacking. We would consider reusing talquetamab after CAR-T progression if a non-BCMA targeting agent is needed as alternatives are limited, especially if there was a prior response to talquetamab. Efficacy may be reduced shortly after CAR-T therapy, highlighting the need for prospective studies to guide clinical practice.
BT in difficult-to-treat patient groups
Patients with EMD
In the pivotal cilta-cel and ide-cel trials, EMD incidence in patients with RRMM was 13–39% [ 2 , 7 , 9 , 41 ]. In general, studies have shown negative correlations between EMD and treatment outcomes in patients with RRMM [ 16 , 42 – 44 ]. Although superior outcomes were observed across all patient subgroups (including EMD) with CAR-T therapy vs SOC [ 9 , 10 ], studies such as LocoMMotion showed worse PFS outcomes in patients with versus without EMD (median 2.7 vs 5.1 months) [ 42 ]. In addition to systemic treatment, we recommend considering radiation as BT in RRMM with EMD (depending on tumour location and size), painful osteolytic lesions, or risk of fracture. One study found this approach safe and feasible in patients with EMD [ 45 ]. Talquetamab may also be considered for BT in these patients [ 18 ]. EMD should be controlled when CAR-T therapy is administered.
Patients eligible for molecular-driven therapies
The t(11;14) chromosomal translocation, present in 16–24% MM cases, represents the most common primary translocation in plasma cell disorders [ 46 ]. There are no approved mutation-targeted agents for MM; however, venetoclax, a BCL-2 inhibitor, is suggested in recent IMWG recommendations for patients with RRMM with the t(11;14) translocation, though its off-label use should be guided by local regulatory frameworks and clinical judgment [ 13 ]. This is particularly relevant to patients with limited treatment options.
BRAF V600E is the most common BRAF mutation, seen in ~4% of newly diagnosed MM and ~8% of RRMM [ 47 – 50 ]. BRAF inhibitors, potentially in combination with a MEK inhibitor, may be a BT option for patients harbouring BRAF mutations, who have limited treatment options.
Patients with CNS involvement
CNS involvement, a rare form of EMD, affects <1% of patients with MM [ 51 , 52 ]. Although there are concerns that anti-BCMA CAR-T therapy could increase the incidence or severity of neurotoxicity including ICANS, a recent study suggests that CAR-T therapy in MM with CNS involvement is safe and feasible [ 53 ]. Here, patients were given BT similar to our recommendations [ 53 ]. We recommend considering various options including intrathecal therapy (e.g., dexamethasone, methotrexate and/or cytarabine), combination of selinexor and pomalidomide (repeated until clearance of plasma cells in the CNS), chemotherapy combination (methotrexate, dexamethasone, and cytarabine-arabinoside), with or without radiation therapy, or PACE-based regimens (cisplatin + doxorubicin + cyclophosphamide + etoposide) [ 54 , 55 ].
Clinical management
In our experience, duration of BT ranges from 6–8 weeks (i.e., 1–2 cycles), which is generally sufficient to induce meaningful disease control. If feasible, we recommend an approximate 2-week wash-out period between BT and lymphodepleting chemotherapy, regardless of BT regimen.
In clinical practice, obtaining a deep response (≥very good partial response) during the typical BT (1–2 cycles) period is not always possible; similarly, full response assessment work-up according to IMWG guidelines [ 15 ] may not be feasible. Thus, from a practical perspective, achieving ≥partial response may be a reasonable treatment goal with BT; such responses may be assessed by measuring serum and urine M-protein, in combination with imaging (to assess EMD before CAR-T infusion). This is supported by a recent analysis of the CARTITUDE-4 study showing that ≥25% paraprotein reduction from baseline after BT was associated with longer PFS post–cilta-cel versus <25% [ 19 ] and findings from a real-world cohort from Germany, where BT success correlated with safety and PFS after CAR-T therapy, regardless of whether patients received ide-cel or cilta-cel [ 21 ].
Safety consideration
Ongoing infections or organ toxicities may delay or prohibit CAR-T infusion in patients with RRMM [ 7 , 9 ]. Minimising toxicity risk during BT is paramount to avoiding any delay or prevention of CAR-T infusion. This includes avoiding excessive haematotoxicity, which may delay lymphodepletion or increase infection risk, awareness of effective management of specific adverse events associated with bridging agents, and monitoring and preventing infections. The CAR-HEMATOTOX score, a tool used to predict haematological toxicity in patients receiving CAR-T therapy [ 56 ], may help with risk assessment and BT regimen selection. However, a high CAR-HEMATOTOX score should not prevent CAR-T therapy. Based on our clinical observations, haematotoxic BT should be avoided in patients with high CAR-HEMATOTOX scores.
Conclusions
BT is a vital component of anti-BCMA CAR-T therapy in RRMM, requiring careful balance of efficacy, safety, and timing. HCPs should aim for the deepest possible response without risking any delay or prevention of CAR-T infusion. This consensus provides guidance on selecting BTs tailored to patients and their disease characteristics, and highlights potential challenges, particularly in heavily pre-treated patients. Analyses of talquetamab as BT in real-world clinical practice have generated promising findings, aligned with our clinical experience. Additionally, recently published EMN guidance considers talquetamab a valid BT option for patients who have exhausted other treatments [ 57 ]. Our consensus is based on clinical experience and is intended to serve as a reference for HCPs using anti-BCMA CAR-T therapy in RRMM. Continued research and shared clinical experience will enhance standardisation and optimise care delivery in this rapidly evolving field.
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These authors contributed equally: Leo Rasche, Maria Theresa Krauth.
Acknowledgements
We thank all participating experts and institutions for their valuable contributions to the interviews and consensus workshop discussions. The expert interviews and consensus workshop were facilitated by Metaplan ® . Questions for individual qualitative interviews were developed and validated by the three members of the Scientific Committee: Prof. Maria Krauth, Prof. Leo Rasche, and Prof. Marc Raab. Medical writing and editorial support for the development of this manuscript, under the direction of the authors, was provided by Ntando Mnisi, Ashfield MedComms, an Inizio company, and funded by Janssen Global Services, LLC.
Author contributions
LR, MK, and MR served on the steering committee, contributed to the interview questionnaire design and ensured the workshop objectives were met. All authors fully participated in the consensus-gathering process via interviews and a virtual workshop, and provided critical review, editorial input and final approval of the manuscript.
Funding
The advisory board meeting and this manuscript were supported by Johnson & Johnson Research & Development, LLC., EMEA Medical Affairs. Open Access funding enabled and organized by Projekt DEAL.
Data availability
The data sharing policy of Johnson & Johnson Innovative Medicine is available at https://www.janssen.com/clinical-trials/transparency . Requests for access to the study data can be submitted through Yale Open Data Access (YODA) Project site at http://yoda.yale.edu .
Competing interests
LR: has received research support from BMS, has served in advisory boards for Amgen, BMS, Roche, Johnson & Johnson, Sanofi, GSK, and Pfizer, and received honoraria from Amgen, BMS, Roche, Johnson & Johnson, Sanofi, GSK, Pfizer, and Takeda. MTK: consultant for and has served in advisory boards for: Amgen, Celgene, Novartis, BMS, J&J, Sanofi, GSK, Takeda, Pfizer, Oncopeptides, and Stemline. HA: has received honoraria from Amgen, BMS, GSK, Johnson & Johnson, Pfizer, and Takeda, and has received research support from Johnson & Johnson. CR: has served in advisory boards for BMS/Celgene, BeiGene, Roche, Johnson & Johnson, Sanofi, GSK, and Pfizer, and received honoraria from BMS/Celgene, Roche, Johnson & Johnson, Sanofi, Pfizer, and Stemline. IS: has served in advisory boards for: Amgen, BMS, GSK, Johnson & Johnson, Pfizer, and Sanofi, and received honoraria from Abbvie, Amgen, BMS, Gilead, GSK, Johnson & Johnson, Pfizer, Sanofi, Stemline, and Takeda. RT: has served in advisory boards for AbbVie, Amgen, BMS, Gilead, GSK, Johnson & Johnson, Oncopeptides, Sanofi, Stemline and Takeda, received research support from Johnson & Johnson, received travel grants from Amgen and Johnson & Johnson and received honoraria from AbbVie, Amgen, AstraZeneca, Bristol Myers Squibb, Gilead, GSK, Johnson & Johnson, Pfizer and Stemline. VV: has received research support from Amgen, has served on advisory boards for Amgen, BMS/Celgene, Johnson & Johnson, Gilead/Kite, AstraZeneca, Abbvie and received honoraria from Johnson & Johnson, Gilead/Kite, Abbvie, AstraZeneca, Elli Lilly, and Roche. KW: has received research support from Abbvie, Amgen, BMS, Johnson & Johnson, GSK, and Sanofi, received honoraria from Abbvie, Adaptive Biotech, Amgen, Astra Zeneca, BeiGene, BMS, Johnson & Johnson, GSK, Karyopharm, Novartis, Oncopeptides, Pfizer, Regeneron, Roche Pharma, Sanofi, Stemline, Takeda, has received consulting fees from Abbvie, Adaptive Biotech, Amgen, Astra Zeneca, BeiGene, BMS, CellCentric, Johnson & Johnson, GSK, Karyopharm, Oncopeptides, Pfizer, Regeneron, Roche Pharma, Sanofi, Stemline, Takeda WW: has received research support from Amgen, Astra-Zeneca, BMS/Celgene, Johnson & Johnson, Novartis, Pfizer, Roche, Sanofi, and Takeda, has participated in steering and safety committees, advisory boards and given lectures for Amgen, Abbvie, Astra Zeneca, BeiGene, BMS/Celgene, Blueprint, CSL-Behring, Dayton, DSMM, EUSA Pharma, Gilead, GSK, IQVIA, Incyte, Johnson & Johnson, Kite, Merck, Myelom- and Lymphomselbsthilfe Österreich, MedMedia, Morphosys, Novartis, Onconovum, Pharma&, Pfizer, Roche, Sandoz, Sanofi, Stemline-Menarini, Takeda MSR: has received research funding from BMS, Johnson & Johnson, Sanofi, and Heidelberg Pharma, has received honoraria from BMS, Johnson & Johnson, AbbVie, Sanofi, Oncopeptides, has performed a consulting or advisory role for BMS, Amgen, GSK, Johnson & Johnson, Sanofi, Pfizer, AbbVie and has received travel funding from BMS, Amgen, Johnson & Johnson, Oncopeptides
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