Driving CAR-T therapy down the GPRC5D fast lane

Immunotherapy has revolutionized cancer treatment by harnessing the host immune system to selectively target malignant cells. In particular, chimeric antigen receptor (CAR)-T cell therapy has achieved durable remissions and shifted the paradigm in the treatment of selected hematologic malignancies, including multiple myeloma (MM) (1). MM is the second most prevalent hematologic malignancy in the United States and represents a substantial source of morbidity and mortality (2). Each year, approximately 35,000 new cases of MM are diagnosed, predominantly affecting older adults with a typical diagnosis occurring in the late 60’s (3). Despite approval of various agents, such as immunomodulatory drugs (IMiDs), proteasome inhibitors (PIs), bi-specific antibodies and CAR-T for MM, determining the optimal treatment sequencing remains an ongoing clinical challenge (4). Management of MM is rapidly evolving with the development of many novel immune-based treatment strategies (5).

Although treatment outcomes have improved, relapsed or refractory multiple myeloma (RRMM) still remains incurable (6). After relapse, the disease typically becomes more aggressive with shortened subsequent progression-free survival (PFS) and limited treatment options (7). RRMM continues to pose a significant clinical challenge due to genomic instability, clonal heterogeneity, and treatment resistance, especially for high-risk patients who have undergone all available treatments (8). Hence, there is a pressing need for novel antigen targets with improved safety and efficacy, as well as strategies to overcome resistance in RRMM.

For nearly a decade, B cell maturation antigen (BCMA)-directed CAR T-cell therapy has been the leading cellular immunotherapy for RRMM (9). Recent studies have identified G protein-coupled receptor class C group 5 member D (GPRC5D) as a potential new target and cellular immunotherapy target, achieving greater efficacy in RRMM. In their first-in-human, single-center, single-arm, phase 1 trial published in The Lancet Haematology, Jin et al. evaluate the safety, cellular kinetics, and clinical response of CT071, a GPRC5D-targeted CAR-T cell therapy in RRMM (10). The study builds on a decade of transformative progress in immunotherapy. GPRC5D is an orphan G protein-coupled receptor with no specific known ligand (11). It is a seven-transmembrane receptor protein; the short extracellular epitope of GPRC5D facilitates tighter immunological binding between T cells and target cells (12). It is overexpressed in malignant plasma cells, specifically myeloma cells and GPRC5D overexpression is associated with high risk of MM (13). This specificity makes it an ideal candidate for CAR-T cell therapy in RRMM.

In this study, CT071 demonstrated early durability, with an overall response rate (ORR) of 100%. Additionally, 50% of patients achieved a stringent complete response (sCR), and 90% achieved residual disease negativity. These results extend to patients who have previously received anti-BCMA CAR-T therapies. All five such patients having received previous anti-BCMA CAR-T therapies responded [2 partial responses (PRs), 1 very good partial response (VGPR) and 2 sCR]. CT071 now joins a rapidly expanding landscape of GPRC5D-directed cellular therapies, including MCARH109 (14), BMS-986393 (15), OriCAR-017 (16), and emerging dual-antigen BCMA/GPRC5D constructs (17). The MCARH109 trial, the first published GPRC5D CAR-T cell dose escalation study, demonstrated an ORR of 71% overall and 100% at the highest dose (450×10⁶ cells). Subsequent multicenter studies, such as BMS-986393, reported an ORR of 86% with 38% achieving complete or sCRs across a broad dose range (25×10⁶–450×10⁶ cells), reinforcing GPRC5D as a clinically relevant and druggable target in RRMM. Similarly, OriCAR-017 (POLARIS study) demonstrated durable responses (100% ORR and 60% sCR) even among high-risk and heavily pretreated patients that had greater than 20% GPRC5D expression. These studies reinforce GPRC5D as a clinically potent antigen for immune-targeting strategies.

BCMA-directed CAR-T cell therapies have yet to produce plateauing survival curves in MM, indicating that most patients ultimately experience disease relapse (14). Importantly, dual-target BCMA/GPRC5D CAR-T platforms have recently demonstrated an ORR of 100% and a complete response rate (CRR) of 44.4% in RRMM with extramedullary disease (17). Using two CAR constructs increases the strength of CAR-T cell/target cell interactions and shows the emergence of combinatorial targeting strategies to prevent BCMA-negative antigen escape (18). Furthermore, preclinical models indicate that GPRC5D CAR-T cells retain activity in BCMA-antigen-escape settings, suggesting a compelling role for GPRC5D-directed therapy in both combinatorial and sequential treatment strategies (14,19). CT071 stands out for achieving comparable antitumor activity at substantially lower cellular doses and without patient selection based on GPRC5D expression.

The study by Jin et al. was conducted at Shanghai Changzheng Hospital, a level A, grade 3 center. The patients had a median age of 63 years and three or more prior lines of treatment (95% double-class refractory (one or more PIs + IMiD), 65% triple-class refractory (one or more PIs + IMiDs + anti-CD38 antibody), 25% penta-drug refractory therapy (two or more PIs + IMiDs + anti-CD38 antibody), 50% autologous hematopoietic stem cell transplantation, 25% relapsed anti-BCMA or anti-BCMA and CD19 CAR-T cell therapy). Of 23 patients with RRMM, 20 successfully underwent apheresis and CT071 infusion. CT071 is a second-generation, autologous CAR-T cell product manufactured through the CARcelerator platform (Figure 1).

Figure 1 CT071 manufacturing workflow and treatment course. Created with BioRender.com. CAR, chimeric antigen receptor; CAR-T, Chimeric antigen receptor-T cell; GMP, good manufacturing practice; GPRC5D, G protein-coupled receptor class C group 5 member D.

The findings of this study deserve attention for their expedited CAR-T cell manufacturing time of 31 hours, efforts to reduce vein-to-vein time, enhanced perfusion of functional T cells, and reducing the need for bridging therapies that may compromise immune fitness. Compared with the MCARH109 trial, where the median interval from leukapheresis to infusion was approximately 68 days, the CT071 platform demonstrated a significantly shorter median vein-to-vein time of only 25 days. Reducing the vein-to-vein time is one of the most clinically meaningful and challenging goals in CAR-T therapy. RRMM is an aggressive disease. Prolonged manufacturing timelines can result in clinical deterioration and increased risk of progression or death before infusion. Studies indicate that 10-20% of eligible patients fail to receive their CAR-T product due to rapid progression during manufacturing (20,21). A faster production cycle also enables earlier immune engagement, preserving CAR T-cell function before exhaustion and antigen burden escalation (22,23). Moreover, the CAR-T cell manufacturing success rate of 96% is notable, given that the patient population was heavily pretreated and had received three or more prior lines of therapy. Thus, the streamlined manufacturing duration for CT071 is not merely a technical refinement but it represents a paradigm shift in how cellular therapies can be delivered at a faster pace to match the biology of aggressive myeloma and to achieve successful remission.

Safety optimization remains critical in CAR-T therapy, particularly given the risk of cytokine release syndrome (CRS), cytopenias, and neurotoxicity. As expected for CAR-T therapy, all patients experienced grade 3–4 cytopenias following lymphodepletion and infusion, comparable to the hematologic toxicity profile reported with MCARH109 (14). Despite this, the overall safety profile of CT071 was manageable: CRS occurred in 60% of patients, all grade 1–2, and only a single case of grade 3 Immune Effector Cell Associated Neurotoxicity Syndrome (ICANS) was observed. Importantly, no treatment-related deaths were reported. The authors demonstrated encouraging safety outcomes with a reduced cellular dose of CT071 to mitigate treatment-related adverse events, including hematological and non-hematological toxicity.

The study originally planned a dose-escalation schema but ultimately proceeded only with two single-dose levels (0.1×10⁶ and 0.3×10⁶/kg). The authors observed no dose-limiting toxicities (DLTs) at the two single-dose levels. The study evaluated the cellular kinetics of CT071, specifically CAR-T cell expansion and persistence as secondary pharmacokinetic endpoints in patients. CAR-T cell expansion was observed in all treated patients, and quantitative real-time polymerase chain reaction was used to monitor CAR transgene copies in peripheral blood. CT071 demonstrated a consistent expansion profile across dose levels, with peak proliferation occurring around day 14. Although the median peak expansion reached 24,103 copies/µg genomic DNA, the similarity between the 0.1×10⁶ and 0.3×10⁶ cells/kg cohorts suggests that higher dosing did not enhance in vivo pharmacokinetics. The comparable area under the curve (0–4 weeks) and parallel clinical responses across the two dose levels reinforce that CT071 achieves robust expansion even at very low cell doses. These data, coupled with similar response rates across cohorts, support selecting 0.1×10⁶ CAR-T cells/kg as the recommended phase 2 dose. Nonetheless, the therapeutic window of CT071 remains to be fully defined, and future studies will need to refine dose-response relationships to balance efficacy, persistence, and toxicity.

Key outcomes such as duration of response (DOR), PFS, and overall survival (OS) have not yet been determined for the study due to a median follow-up of 10.7 months (interquartile range, 6.13–12.02 months). Thus, the long-term efficacy of CT071 remains to be established. The estimated PFS rates at 6, 9, and 12 months were 78%, 64%, and 64%, respectively. Six patients eventually progressed, and most of those had high-risk or penta-refractory disease. Longer follow-up will be essential to determine whether these early responses translate into durable remissions and to monitor whether relapse is driven by antigen escape, T cell exhaustion, or a suppressive microenvironment. CAR-T therapy carries substantial bone marrow suppression and heightened infection risks that need to be taken into consideration. Although the study reports no infection-related deaths during treatment, adverse events including bacterial infection, pneumonia, cytomegalovirus infection, upper respiratory tract infection and urinary tract infection were still observed. Therefore, extended follow-up is required to capture delayed cytopenias, infections, secondary malignancies, and late neurotoxicity.

It is essential to acknowledge that CAR-T cell therapy remains vulnerable to antigen escape. GPRC5D represents a promising therapeutic target (Table 1) (10,12,14-17,24-29). However, its antigen density, potential modulation (antigen loss), genetic deletion, epitope masking, lineage switch and expression heterogeneity should be carefully evaluated (30). Notably, MCARH109 demonstrated possible GPRC5D antigen loss in 6 of 10 (60%) patients assessed at relapse, suggesting antigen escape as a potential mechanism of resistance (24). In a study by Ma et al., whole-genome and bisulfite sequencing of 10 patients with relapsed MM following GPRC5D CAR-T cell therapy revealed GPRC5D loss in 8 cases and mixed expression (GPRC5D^+/−) in 2 patients. These alterations were driven by either biallelic deletions or epigenetic silencing driven by promoter hypermethylation. Azacitidine treatment restored GPRC5D expression in hypermethylated cell lines, indicating that both genetic and epigenetic mechanisms contribute to antigen loss and resistance after GPRC5D-targeted therapy (31). Additional studies are needed to understand the mechanisms of relapse after GPRC5D-targeted therapies. These findings highlight that even for CT071, durable responses may be subject to antigen escape.

Jin et al. note that GPRC5D expression heterogeneity should not exclude patients from eligibility for CT071 therapy. However, its physiological expression in keratinized epithelial structures of the skin, hair/nail, and tongue (32) raises concerns for low-grade on-target, off-tumor effects. Similar to MCARH109 trial, grade 1 onychomadesis (20%) and rash (5%) were observed. These outcomes indicate the importance of integrating antigen expression profiling into dose-optimization strategies, as a “one-size-fits-all” dosing approach may overlook patient variability in target expression and tissue susceptibility. Future research should incorporate single-cell RNA sequencing (scRNA-seq) of both tumor and peripheral immune compartments to map GPRC5D expression heterogeneity and identify predictive transcriptomic signatures. Such approaches may provide mechanistic insights into the CAR-T cell differentiation states that predict durable remission versus immune exhaustion.

The CT071 product is based on a proprietary GPRC5D CAR-T cell platform. However, the study offers limited detail on manufacturing parameters and quality-control metrics, including transduction efficiency, CD4:CD8 composition, and memory phenotype optimization. Maintaining T cell fitness is crucial for the therapeutic efficacy of CAR-T cell therapy. T cells obtained from patients earlier in the myeloma disease course demonstrate superior fitness for CAR-T cell manufacturing and may enhance therapeutic efficacy compared with those from relapsed or refractory patients (33). A greater transparency in these parameters will be essential for reproducibility, cross-trial comparison and standardization as GPRC5D-targeted CAR-T therapies advance. In addition, validation in multicenter cohorts that include more ethnically diverse patient populations is urgently needed. Currently, no data are available to characterize potential racial or ethnic variations in GPRC5D expression (12). Moving forward, scalability, cost, accessibility, particularly outside of China and logistical feasibility will represent key challenges in translating these results into a globally accessible therapy.

Additionally, the study does not include information on the application of the CT071 shortened CAR-T manufacturing protocol to cancers beyond multiple myeloma. However, given the CT071’s favorable safety profile and rapid manufacturing timeline, the platform could open the door for earlier-line CAR-T cell therapy and potentially be applied to other cancer types. The streamlined platform behind CT071 sets a new standard for CAR-T logistics manufacturing by significantly shortening vein-to-vein time and making treatment more accessible to patients. Moving forward, careful patient selection and the identification of biomarkers (such as CAR-T expansion and persistence, antigen density, and tumor-microenvironmental features) will be crucial to determining which patients derive durable benefit and which remain at risk for early relapse or antigen escape.

Multiple studies have demonstrated that GPRC5D-targeted bispecific antibodies that engage T cells, such as talquetamab (28) and forimtamig (29) induce substantial responses in patients with RRMM who have exhausted at least four prior lines of therapy. However, challenges persist in refining optimal dosing, defining treatment sequencing, and mitigating immune escape (28). In contrast, CT071 delivers an autologous, “living” cellular product capable of sustained cytotoxicity and immune memory, resulting in deep, minimal residual disease (MRD)-negative responses even in heavily pretreated RRMM. While bispecifics prioritize accessibility, CT071 offers durability for long-term remission.

An important unanswered question is whether GPRC5D-targeted CAR-T cell therapy can be integrated with existing treatments, such as bispecific antibodies, antibody-drug conjugates, IMiDs, PIs, and BCMA-directed CAR-T cell therapy, in RRMM. Future studies should explore whether early GPRC5D targeting, prior to BCMA-directed therapy, could mitigate antigen escape and resistance. Ultimately, it remains unclear whether the field will move toward combination strategies, such as dual BCMA/GPRC5D targeting, or continue to position GPRC5D therapy primarily as a salvage option after BCMA CAR-T failure. These questions highlight the need to define optimal therapeutic sequencing and combinatorial strategies to minimize antigen escape and improve long-term outcomes in RRMM. Nevertheless, important questions remain and will define the next era of GPRC5D-targeted strategies.

In conclusion, GPRC5D CAR-T cell therapy could emerge as a standard salvage option for RRMM after BCMA failure and could fill a major unmet clinical need. Moreover, it may establish a paradigm in which sequential antigen-targeted CAR-T approaches (for example, BCMA followed by GPRC5D and potentially others) could become the standard of care in RRMM. The development of dual-antigen or bispecific CAR-T constructs targeting BCMA and GPRC5D may also gain momentum as a means to mitigate antigen escape and delay relapse. In the study, Jin et al. demonstrate that targeting GPRC5D with CAR-T cells can achieve high response rates in heavily pretreated RRMM with a favorable safety profile even in patients who previously failed BCMA-directed therapy. The reduction in manufacturing time represents a meaningful advancement toward improving accessibility and the timely delivery of cellular therapies. The shortened CT071 production workflow could be extended to other cancers to help reduce vein-to-vein time across CAR-T products. Future work should aim to integrate GPRC5D-directed therapy into existing treatment frameworks and to explore combinatorial strategies, including pairing with BCMA targeting or bispecific antibodies. Altogether, these findings suggest that targeting GPRC5D holds an exciting potential for preclinical and clinical use and expanding the therapeutic frontiers in RRMM.

Acknowledgments

None.

Footnote

Provenance and Peer Review: This article was commissioned by the editorial office, Annals of Blood. The article did not undergo external peer review.

Funding: This work was supported by the NIGMS/NIH (No. R35GM151109, to J.T.), NCI/NIH (No. R01CA292653, to J.T.), and the Florida Department of Health Bankhead Coley Cancer Research Grant (Bankhead Coley grant #24B15, to J.T.).

Conflicts of Interest: Both authors have completed the ICMJE uniform disclosure form (available at https://aob.amegroups.com/article/view/10.21037/aob-2025-1-53/coif). The authors have no conflicts of interest to declare.

Ethical Statement: The authors are accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved.

Open Access Statement: This is an Open Access article distributed in accordance with the Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License (CC BY-NC-ND 4.0), which permits the non-commercial replication and distribution of the article with the strict proviso that no changes or edits are made and the original work is properly cited (including links to both the formal publication through the relevant DOI and the license). See: https://creativecommons.org/licenses/by-nc-nd/4.0/.

References

1. Larson RC, Maus MV. Recent advances and discoveries in the mechanisms and functions of CAR T cells. Nat Rev Cancer 2021;21:145-61. [Crossref] [PubMed]
2. Cordas Dos Santos DM, Toenges R, Bertamini L, et al. New horizons in our understanding of precursor multiple myeloma and early interception. Nat Rev Cancer 2024;24:867-86. [Crossref] [PubMed]
3. Kyle RA, Gertz MA, Witzig TE, et al. Review of 1027 patients with newly diagnosed multiple myeloma. Mayo Clin Proc 2003;78:21-33. [Crossref] [PubMed]
4. Anderson KC, Alsina M, Atanackovic D, et al. Multiple Myeloma, Version 2.2016: Clinical Practice Guidelines in Oncology. J Natl Compr Canc Netw 2015;13:1398-435. [Crossref] [PubMed]
5. Neri P, Bahlis NJ, Lonial S. New Strategies in Multiple Myeloma: Immunotherapy as a Novel Approach to Treat Patients with Multiple Myeloma. Clin Cancer Res 2016;22:5959-65. [Crossref] [PubMed]
6. Teoh PJ, Chng WJ. CAR T-cell therapy in multiple myeloma: more room for improvement. Blood Cancer J 2021;11:84. [Crossref] [PubMed]
7. Durer C, Durer S, Lee S, et al. Treatment of relapsed multiple myeloma: Evidence-based recommendations. Blood Rev 2020;39:100616. [Crossref] [PubMed]
8. Gulla A, Anderson KC. Multiple myeloma: the (r)evolution of current therapy and a glance into future. Haematologica 2020;105:2358-67. [Crossref] [PubMed]
9. Raje N, Berdeja J, Lin Y, et al. Anti-BCMA CAR T-Cell Therapy bb2121 in Relapsed or Refractory Multiple Myeloma. N Engl J Med 2019;380:1726-37. [Crossref] [PubMed]
10. Jin L, Gu S, Ruan Q, et al. GPRC5D-targeted CAR T-cell therapy (CT071) in patients with relapsed or refractory multiple myeloma: a first-in-human, single-centre, single-arm, phase 1 trial. Lancet Haematol 2025;12:e798-807. [Crossref] [PubMed]
11. Yan P, Lin X, Wu L, et al. The binding mechanism of an anti-multiple myeloma antibody to the human GPRC5D homodimer. Nat Commun 2024;15:5255. [Crossref] [PubMed]
12. Rodriguez-Otero P, van de Donk NWCJ, Pillarisetti K, et al. GPRC5D as a novel target for the treatment of multiple myeloma: a narrative review. Blood Cancer J 2024;14:24. [Crossref] [PubMed]
13. Atamaniuk J, Gleiss A, Porpaczy E, et al. Overexpression of G protein-coupled receptor 5D in the bone marrow is associated with poor prognosis in patients with multiple myeloma. Eur J Clin Invest 2012;42:953-60. [Crossref] [PubMed]
14. Mailankody S, Devlin SM, Landa J, et al. GPRC5D-Targeted CAR T Cells for Myeloma. N Engl J Med 2022;387:1196-206. [Crossref] [PubMed]
15. Bal S, Htut M, Berdeja JG, et al. BMS-986393, a G Protein-Coupled Receptor Class C Group 5 Member D (GPRC5D)-Targeted CAR T Cell Therapy, in Patients (pts) with Relapsed/Refractory (RR) Multiple Myeloma (MM) and 1-3 Prior Regimens: Updated Phase 1 Safety and Efficacy Results. Blood 2024;144:2069.
16. Zhang M, Wei G, Zhou L, et al. GPRC5D CAR T cells (OriCAR-017) in patients with relapsed or refractory multiple myeloma (POLARIS): a first-in-human, single-centre, single-arm, phase 1 trial. Lancet Haematol 2023;10:e107-16. [Crossref] [PubMed]
17. Yao H, Ren SH, Wang LH, et al. BCMA/GPRC5D bispecific CAR T-cell therapy for relapsed/refractory multiple myeloma with extramedullary disease: a single-center, single-arm, phase 1 trial. J Hematol Oncol 2025;18:56. [Crossref] [PubMed]
18. Fernández de Larrea C, Staehr M, Lopez AV, et al. Defining an Optimal Dual-Targeted CAR T-cell Therapy Approach Simultaneously Targeting BCMA and GPRC5D to Prevent BCMA Escape-Driven Relapse in Multiple Myeloma. Blood Cancer Discov 2020;1:146-54. [Crossref] [PubMed]
19. Smith EL, Harrington K, Staehr M, et al. GPRC5D is a target for the immunotherapy of multiple myeloma with rationally designed CAR T cells. Sci Transl Med 2019;11:eaau7746. [Crossref] [PubMed]
20. Shah NN, Fry TJ. Mechanisms of resistance to CAR T cell therapy. Nat Rev Clin Oncol 2019;16:372-85. [Crossref] [PubMed]
21. Cappell KM, Kochenderfer JN. Long-term outcomes following CAR T cell therapy: what we know so far. Nat Rev Clin Oncol 2023;20:359-71. [Crossref] [PubMed]
22. Fraietta JA, Lacey SF, Orlando EJ, et al. Determinants of response and resistance to CD19 chimeric antigen receptor (CAR) T cell therapy of chronic lymphocytic leukemia. Nat Med 2018;24:563-71. [Crossref] [PubMed]
23. Ghassemi S, Nunez-Cruz S, O’Connor RS, et al. Reducing Ex Vivo Culture Improves the Antileukemic Activity of Chimeric Antigen Receptor (CAR) T Cells. Cancer Immunol Res 2018;6:1100-9. [Crossref] [PubMed]
24. Jurgens EM, Firestone RS, Chaudhari J, et al. Phase I Trial of MCARH109, a G Protein-Coupled Receptor Class C Group 5 Member D (GPRC5D)-Targeted Chimeric Antigen Receptor T-Cell Therapy for Multiple Myeloma: An Updated Analysis. J Clin Oncol 2025;43:498-504. [Crossref] [PubMed]
25. Xia J, Li H, Yan Z, et al. Anti-G Protein-Coupled Receptor, Class C Group 5 Member D Chimeric Antigen Receptor T Cells in Patients With Relapsed or Refractory Multiple Myeloma: A Single-Arm, Phase II Trial. J Clin Oncol 2023;41:2583-93. [Crossref] [PubMed]
26. Pan M, Wang D, Xu J, et al. Fully Human anti-GPRC5D CAR T-Cell Therapy RD118 Induces Durable Remissions in Relapsed/Refractory Multiple Myeloma. Blood 2025;blood.2025030559.
27. Zhou D, Sun Q, Xia J, et al. Anti-BCMA/GPRC5D bispecific CAR T cells in patients with relapsed or refractory multiple myeloma: a single-arm, single-centre, phase 1 trial. Lancet Haematol 2024;11:e751-60. [Crossref] [PubMed]
28. Chari A, Minnema MC, Berdeja JG, et al. Talquetamab, a T-Cell-Redirecting GPRC5D Bispecific Antibody for Multiple Myeloma. N Engl J Med 2022;387:2232-44. [Crossref] [PubMed]
29. Eckmann J, Fauti T, Biehl M, et al. Forimtamig, a novel GPRC5D-targeting T-cell bispecific antibody with a 2+1 format, for the treatment of multiple myeloma. Blood 2025;145:202-19. [Crossref] [PubMed]
30. Lin H, Yang X, Ye S, et al. Antigen escape in CAR-T cell therapy: Mechanisms and overcoming strategies. Biomed Pharmacother 2024;178:117252. [Crossref] [PubMed]
31. Ma S, Xia J, Zhang M, et al. Genetic and epigenetic mechanisms of GPRC5D loss after anti-GPRC5D CAR T-cell therapy in multiple myeloma. Blood 2025;146:178-90. [Crossref] [PubMed]
32. Inoue S, Nambu T, Shimomura T. The RAIG family member, GPRC5D, is associated with hard-keratinized structures. J Invest Dermatol 2004;122:565-73. [Crossref] [PubMed]
33. Garfall AL, Dancy EK, Cohen AD, et al. T-cell phenotypes associated with effective CAR T-cell therapy in postinduction vs relapsed multiple myeloma. Blood Adv 2019;3:2812-5. [Crossref] [PubMed]