Outcomes of CAR T-Cell Therapy in Relapsed/Refractory Multiple Myeloma by Race: A Multicenter Real-World Study

doi:10.21203/rs.3.rs-7208369/v1

Racial and ethnic minorities have been underrepresented in pivotal trials of idecabtagene vicleucel (ide-cel) and ciltacabtagene autoleucel (cilta-cel), limiting the generalizability of findings. This multicenter retrospective study evaluated real-world outcomes in minority patients (MP) versus White patients (WP) treated with cilta-cel or ide-cel across five U.S. centers between May 2022 and April 2024. Among 223 patients, 21% self-identified as racial minorities (39 Black, 2 Asian, 2 Hispanic, 3 other). MPs were younger at infusion (mean age 61.3 vs. 64.8 years; p = 0.012) and more likely to have impaired renal function (CrCl < 45 mL/min: 22% vs. 8.5%; p = 0.011). Other baseline disease characteristics were similar between groups. At 6 months, overall response rate (ORR) was 84% in MPs and 71% in WPs. Median progression-free survival was 16.1 months in MPs and 14.1 months in WPs, while median overall survival was 26.4 vs. 27.9 months, respectively; these differences were not statistically significant. Toxicity profiles were comparable overall; however, MPs experienced significantly higher rates of grade 4 neutropenia (41% vs. 21%; p = 0.01 ). In this real-world cohort, cilta-cel and ide-cel demonstrated similar efficacy and safety in MPs compared to WPs. These results support the use of BCMA-targeted CAR-T therapies across diverse populations and highlight the continued need to improve minority representation in clinical trials to ensure equitable access and outcomes in multiple myeloma care.

Biological sciences/Cancer/Cancer therapy/Cancer immunotherapy

Health sciences/Medical research/Translational research

Ciltacabtagene autoleucel (cilta-cel) and idecabtagene vicleucel (ide-cel) are B- cell maturation antigen (BCMA)-directed chimeric antigen receptor T-cell (CAR T) therapies that have become established treatments for heavily pretreated patients with relapsed/refractory multiple myeloma (RRMM) based on early, deep, and durable responses.^1,2 Supported by randomized phase III trials, CARTITUDE-4 (for cilta-cel) and KarMMA-3 (for ide-cel), both therapies have shown superior efficacy compared to standard-of-care treatments.^3,4 As a result, cilta-cel and ide-cel are increasingly being used earlier in the treatment course, often after the first or second relapse.

Despite the clinical success of CAR T therapies, several logistical challenges persist, including the need for administration at specialized centers, intensive toxicity monitoring, and high out-of-pocket costs. These barriers, along with broader socioeconomic disparities, contribute to unequal access to CAR T therapy both within clinical trials and in general clinical practice. Historically, racial minority populations have been underrepresented in CAR T clinical trials. For example, in the CARTITUDE-4 trial, only 2.9% of participants were Black or African American, while the KarMMA-3 trial included just 7% Black patients and 3% Asian patients.^3,4 This underrepresentation could lead to disparities in outcomes and limit the widespread use of these therapies as they become more accessible.

While few studies have examined the impact of race on the efficacy and toxicity of CAR T therapy, most have focused on non-Hodgkin lymphoma (NHL) and B-cell acute lymphoblastic leukemia (B-ALL), ^5–7 with limited research in MM. One earlier study examined racial and ethnic differences in adverse events and outcomes among patients with RRMM treated with ide-cel in the standard-of-care setting.⁸ It found that safety and response varied across various racial and ethnic subgroups, though no differences were observed in overall survival (OS) and progression-free survival (PFS).

Given the scarcity of data from both real-world settings and clinical trials, this multicenter retrospective study compares the outcomes of ide-cel and cilta-cel in racial minority groups versus White patients, aiming to identify potential disparities and inform more inclusive and equitable treatment strategies for diverse patient populations.

Study Population

This study pooled data from consecutive patients with RRMM who received either commercial cilta-cel or ide-cel between May 2022 and April 2024 at five participating centers: Levine Cancer Institute, Ohio State University, University of Kansas Cancer Center, University of Iowa, and Medical University of South Carolina. The study was approved by the relevant institutional review boards or ethics committees at each institution, and a waiver of informed consent was obtained for the retrospective record review.

Demographic and clinical data were collected from electronic medical records. Baseline characteristics included age at CAR T therapy initiation, sex, race, Eastern Cooperative Oncology Group (ECOG) performance status, isotype, Revised International Staging System (R-ISS) stage, presence of high-risk features, extramedullary disease, prior lines of therapy, and refractory status to major drug classes. Race and ethnicity were self-reported. Treatment protocols for cytokine release syndrome (CRS) and immune-effector cell-associated neurotoxicity syndrome (ICANS), infectious disease prophylaxis, and the administration of growth factors support adhered to institutional guidelines.

Statistical Methods

For analysis, race/ethnicity was categorized into two broad groups: White and racial minority (which includes African American or Black, Asian, Hispanic or Latino, and other). Outcome measures, including CRS, ICANS, cytopenia, response rates, PFS, and OS, were compared between the two racial groups. Treatment response was assessed by treating investigators according to the International Myeloma Working Group criteria⁹ at one, three-, and six-months post-CAR T infusion. Descriptive analyses were conducted using R Core Team (2024) software. Continuous variables were summarized as mean (min, max) and median (IQR), while dichotomous factors were reported by total numbers and frequencies. Fisher’s exact test was used for categorical comparisons, and the Wilcoxon rank-sum test was applied to assess differences in continuous variables between groups.

To evaluate the relationship between predictor variables and time-to-event outcomes, univariate Cox proportional hazards analysis was performed, calculating hazard ratios (HRs) and 95% confidence intervals (CIs) while accounting for censored data. OS was calculated as the time from CAR T infusion to death or last contact, and PFS was calculated as the time from CAR T infusion to disease progression, death, or last contact. Kaplan-Meier survival curves and log-rank tests were used to examine OS and PFS by race and ethnicity. Univariate Cox proportional hazards models were then used to estimate HRs and 95% CIs for the association of race and ethnicity with OS and PFS, adjusting for baseline characteristics.

Of the 223 patients who received either cilta-cel or ide-cel, 79% of patients were White, and 21% were racial minority. Among the 46 racial minority patients, 39 were Black or African American, 2 were Asian, 2 were Hispanic or Latino, and 3 identified as belonging to other racial or ethnic backgrounds. The distribution of baseline characteristics based on race/ethnicity is provided in Table 1.

Racial minority patients were younger at the time of CAR T infusion, with a median age of 61.5 (range, 41-83) years compared to 66 (range, 34-84) years in White patients (p = 0.012). Additionally, 43% of racial minority patients were male, compared to 59% of White patients (p = 0.054). An ECOG performance status of 2 or higher was observed in 18.8% of racial minority patients, compared to 7.5% of White patients (p = 0.0795). Renal dysfunction, defined as creatinine clearance below 45 mL/min, was more common in racial minority patients (22%) compared to White patients (8.5%; p = 0.011). Otherwise, the two groups were similar in terms of demographics, prior treatments, and disease characteristics, including the presence of high-risk cytogenetics. Notably, 41% of racial minority population and 24% of White patients would have been ineligible for KarMMa and or CARTITUDE clinical trials due to factors such as EF <45%, creatinine clearance <45%, plasma cell leukemia, concomitant AL amyloidosis, and previous anti-BCMA therapy (Table 2).

Among racial minority patients, 35% received cilta-cel and 65% received ide-cel, compared to 32% and 68%, respectively, among White patients. No statistically significant differences in overall response rate (ORR) or depth of response were noted at one, three and six months (Figure 1). For instance, at six months, the overall response rate (ORR) was 84% among racial minority patients and 71% among White patients (p = 0.4), with a stringent complete response (sCR) observed in 17% versus 25%, complete response (CR) in 25% versus 17%, very good partial response (VGPR) in 25% versus 24%, partial response (PR) in 17% versus 4.7%, and progressive disease (PD) in 17% versus 26%, respectively. Data on minimal residual disease (MRD) was not available for a substantial proportion of patients in both groups (Supplementary Table 1).

No significant differences in toxicities and adverse events following CAR T therapy were observed between racial minority and White patients. The hematologic toxicities are shown in Figure 2 and Supplementary Table 2, and nonhematologic toxicities in Table 3. The incidence of any grade CRS was 87% in racial minority patients and 80% in White patients (p= 0.30). Any grade ICANS within the first 30 days post-infusion occurred in 30% of racial minority patients compared to 18% of White patients (p = .065). Infections of any grade post CAR T infusion were reported in 30% of racial minority patients and 21% White patients (p = 0.20). The incidence of cytopenia was generally comparable between the groups, except for neutropenia at 60 days post-infusion. At that point, the median absolute neutrophil count (ANC) was 1.46 k/µL in racial minority patients, compared to 2.50 k/µL in White patients (p = 0.003; data not shown). A total of 8 patients (17%) in the minority group and 18 patients (10%) in the White group required a stem cell boost due to persistent cytopenia. The overall incidence of grade 4 neutropenia was significantly higher in the minority group (41%) compared to White patients (21%, p = 0.012). Similarly, the incidence of grade 3/4 thrombocytopenia was higher among minority patients (61%) than White patients (48%), although this difference did not reach statistical significance (p = 0.15) (Supplementary Table 2).

The median follow-up for the study population was 27.8 months (IQR 11 to N/A). Median follow-up was similar between the two groups: 26.4 months for racial minority and 27.8 months for White patients. The median PFS was 16.1 months [95% CI: 8.9, N/A] for racial minority patients, compared to 14.1 months [95% CI: 11.1,17.1] for White patients. Median OS was 26.4 months [95% CI: 16.5, N/A] in racial minority patients and 27.9 months [95% CI: 26.3, N/A] in White patients. No statistically significant difference was observed in PFS (p = 0.8079; HR 1.07, 95% CI: 0.64, 1.78) or OS (p = 0.4174; HR 0.78, 95% CI: 0.44, 1.39) between the two groups (Figures 3 and 4). Even after adjusting for clinically relevant covariates, no differences in PFS were observed between the two groups (Supplementary Table 3).

Given the historical underrepresentation of minority populations in both early-phase clinical trials and pivotal registration studies, real-world data are essential for providing a more comprehensive understanding of treatment outcomes across diverse patient groups. This study evaluates the impact of race on patients with RRMM treated with Ide-cel and Cilta-cel, the two CAR T therapies currently approved for commercial use. Conducted across multiple academic centers, including those serving racially diverse catchment areas, racial minority patients were well-represented, comprising 21% of the overall study population. Among these, African American patients made up the largest subgroup, accounting for 39 of the 46 racial minority patients. Similarly, two other real-world studies of CAR T-cell therapy in RRMM reported Black patient representation at 17% and 15%, respectively.^8,10 While the proportion of African American and or Black patients in these studies exceeds that reported in clinical trials for ide-cel and cilta-cel, the absolute number remains modest, especially when considering the 2- to 3-fold higher incidence of multiple myeloma in African American population compared to the White population. Additionally, the comparatively younger age of minority patients receiving CAR T-cell therapy may reflect selection bias in referral patterns or access to care, rather than accurately representing the true median age at diagnosis among minority populations. These findings underscore the ongoing need for more inclusive and representative research efforts.

Emerging data suggest that response to CAR T-cell therapy may be influenced by immune-related factors such as T-cell fitness and immune diversity.¹¹ The U.S. MM Immunotherapy Consortium study reported that non-Hispanic Black patients (n =36) had higher median levels of C-reactive protein and ferritin, were more likely to develop any grade of CRS, and had a higher best ORR compared to Hispanic (n = 22) and non-Hispanic White patients (n = 149).⁸ In contrast, our study did not observe significant differences in incidence of CRS or ICANS between racial minority and white patients, though data on inflammatory marker data were not collected. Similarly, no significant differences were seen in ORR, including VGPR or CR at predefined time points.

We also did not observe any significant differences in PFS or OS by race or ethnicity following CAR T therapy. These findings align with the consortium study, which reported no racial or ethnic disparities in PFS or OS despite observed differences in CRS and ORR.⁸ Similarly, other studies of CAR T-cell therapy in NHL and ALL have shown comparable overall survival across racial groups.^5-7 Notably, this pattern extends to autologous stem cell transplantation, where emerging evidence suggests that, after adjusting for sociodemographic confounders, Black patients may experience survival outcomes equal to or better than those of White patients.^12,13 These findings suggest that when access to care is equitable, racial disparities in treatment outcomes can be significantly reduced. Consequently, race or ethnicity should not influence clinical decision-making or patient counseling regarding the risks or expected outcomes of CAR T therapy.

In our study, 41% of the minority patients and 24% of the White patients (p-value = 0.017) would not have met the eligibility criteria for the KarMMa or CARTITUDE clinical trials that led to the FDA approval of ide-cel and cilta-cel. This figure is likely an underestimate, as baseline ANC and platelet counts at the time of lymphodepleting chemotherapy were not collected. The U.S. MM Immunotherapy Consortium study similarly found that 75% of patients would not have been eligible for the KarMMa trial, underscoring the restrictive nature of current trial criteria.⁸ One key exclusion factor among clinical trials was renal dysfunction, defined as a creatinine clearance <45 mL/min, which was more common among racial minority patients (22%) in our cohort compared to White patients (8.5%; p = 0.011). These findings highlight how current trial eligibility criteria, while intended for safety, may inadvertently exclude a significant proportion of minority patients with comorbidities and limit the applicability of trial results to real-world settings. Revisiting and potentially broadening these criteria through more flexible trial designs is necessary to ensure equitable access to emerging therapies and to improve the representation of historically underrepresented groups in clinical research.

A key limitation of this study is that it includes only patients with RRMM who were referred to academic centers and received CAR T therapy, without accounting for those who may have faced physical, socioeconomic, or systemic barriers to access. CAR T therapy remains largely confined to specialized centers, and access is influenced by geography, healthcare infrastructure, referral patterns, insurance coverage, and stringent eligibility criteria.^14,15 As such, our cohort may not fully represent the broader RRMM population, especially those facing access challenges.

Moreover, the absence of data on insurance type, treatment denials, and distance from treatment centers limits our ability to assess how these factors influence disparities in access and outcomes. Previous studies have shown that socioeconomic stratum and insurance coverage are critical determinants of access to CAR T therapy and contribute to racial and ethnic disparities in outcomes.^6,14 As with other observational studies, our analysis is also subject to missing data, as data collection was site-dependent and aligned with routine clinical practice. Finally, most patients in our study had heavily pretreated RRMM at the time of referral, and therefore, survival outcomes may not be generalizable to patients treated earlier in their disease course, which is particularly relevant as CAR T-cell therapy is increasingly used in earlier lines of treatment.

In conclusion, racial minority patients achieved similar OS, PFS and ORR compared to White patients following treatment with cilta-cel or ide-cel for RRMM. Toxicity profiles were also comparable between the groups. These findings suggest that among patients who can access CAR T therapy, real-world efficacy and safety outcomes are consistent across racial groups. Ongoing evaluation of CAR T therapy in diverse populations is essential to ensure equitable improvements in outcomes for all individuals with RRMM. Future prospective trials should prioritize improved representation of racial and ethnic minority groups to better inform treatment strategies and reduce disparities in access and outcomes.

Acknowledgments

The authors gratefully acknowledge the support of the U.S. Myeloma Innovations and Research Collaborative (USMIRC) for its contributions to this work, including assistance with study design, critical review of the manuscript, and administrative coordination.

Author Contributions

MB and SA wrote the first draft of the manuscript. Data collection: AH, AV, HS, DC, CS, KG, MUM, ZM, AK. Statistical analysis: SA. All authors participated in reviewing and approving this paper.

Conflict of Interest (COI)

MB: Consulting or Advisory Role: Caribou Biosciences; Research Funding: Janssen (Inst), Amgen (Inst), Bristol Myers Squibb/ Celgene (Inst), Takeda (Inst), Abbvie (Inst), Caribou Biosciences (Inst), and The Binding Site (Inst).

MUM: Research Funding: Iovance Biotherapeutics (Inst).

ZM: Leadership: Hematology Oncology Pharmacists Association; Honoraria: Bristol Myers Squibb Foundation, Kite/Gilead, Genentech, Pfizer, and Sanofi.

JPM: Honoraria: Kite, a Gilead company, AlloVir, Nektar, Sana Biotechnology, Bristol Myers Squibb/Sanofi, Novartis, crispr therapeutics, CARGO Therapeutics, Autolus, Legend Biotech; Consulting or Advisory Role: Kite, a Gilead company, Juno Therapeutics, Allovir, Magenta Therapeutics, EcoR1 Capital, crispr therapeutics, Fosun Kite Biotechnology Co, Ltd, Sanofi US Services, Inc, Novartis, Nektar, Sana Biotechnology, Inc; Speakers’ Bureau: Kite/Gilead; Research Funding: Novartis (Inst), Fresenius Biotech (Inst), Astellas Pharma (Inst), Bellicum Pharmaceuticals (Inst), Novartis (Inst), Gamida Cell (Inst), Pluristem Therapeutics (Inst), Kite, a Gilead company (Inst), AlloVir (Inst).

PV: Consultancy or Advisory Role: AbbVie, AstraZeneca, BMS, Karyopharm, Lava Therapeutics, Sanofi, Regeneron, Janssen, GSK; Research Funding: AbbVie, GSK, Janssen, Regeneron.

A-OA: Research Funding: Celgene (Inst), Seagen (Inst), AbbVie (Inst), Bristol Myers Squibb/Medarex (Inst), Sanofi (Inst), GlaxoSmithKline (Inst). Patents, Royalties, Other Intellectual Property: PSA vaccine patent.

NA: Consulting or Advisory Role: Kite/Gilead, BMS, Legend Biotech, Invivyd; Research Funding: Kite/Gilead (Inst).

SA: Leadership ACCRU; Consulting or Advisory Role: Pfizer, Sanofi: Research Funding: GlaxoSmithKline, Amgen, Karyopharm Therapeutics, Janssen Oncology (Inst), Celgene/Bristol Myers Squibb (Inst); Honoraria: Janssen, GSK, Sanofi.

AH, AV, AN, ES, HS, DC, CS, KG and AMK: These authors declare no competing financial interests.

Data Availability Statement

The datasets generated during and/or analyzed during the current study are not publicly available due to HIPPA but are available from the corresponding author on reasonable request.

Berdeja JG, Madduri D, Usmani SZ, et al: Ciltacabtagene autoleucel, a B-cell maturation antigen-directed chimeric antigen receptor T-cell therapy in patients with relapsed or refractory multiple myeloma (CARTITUDE-1): a phase 1b/2 open-label study. Lancet 398:314-324, 2021
Munshi NC, Hege K, San-Miguel J: Idecabtagene Vicleucel in Relapsed Myeloma. Reply. N Engl J Med 384:2357-2358, 2021
San-Miguel J, Dhakal B, Yong K, et al: Cilta-cel or Standard Care in Lenalidomide-Refractory Multiple Myeloma. N Engl J Med 389:335-347, 2023
Rodriguez-Otero P, Ailawadhi S, Arnulf B, et al: Ide-cel or Standard Regimens in Relapsed and Refractory Multiple Myeloma. N Engl J Med 388:1002-1014, 2023
Faruqi AJ, Ligon JA, Borgman P, et al: The impact of race, ethnicity, and obesity on CAR T-cell therapy outcomes. Blood Adv 6:6040-6050, 2022
Karmali R, Machhi R, Epperla N, et al: Impact of race and social determinants of health on outcomes in patients with aggressive B-cell NHL treated with CAR-T therapy. Blood Adv 8:2592-2599, 2024
Locke FL, Siddiqi T, Jacobson CA, et al: Real-world and clinical trial outcomes in large B-cell lymphoma with axicabtagene ciloleucel across race and ethnicity. Blood 143:2722-2734, 2024
Peres LC, Oswald LB, Dillard CM, et al: Racial and ethnic differences in clinical outcomes among patients with multiple myeloma treated with CAR T-cell therapy. Blood Adv 8:251-259, 2024
Kumar S, Paiva B, Anderson KC, et al: International Myeloma Working Group consensus criteria for response and minimal residual disease assessment in multiple myeloma. Lancet Oncol 17:e328-e346, 2016
Wesson W, Dima D, Suleman N, et al: Timing of Toxicities and Non-Relapse Mortality Following CAR T Therapy in Myeloma. Transplant Cell Ther 30:876-884, 2024
Dhodapkar KM, Cohen AD, Kaushal A, et al: Changes in Bone Marrow Tumor and Immune Cells Correlate with Durability of Remissions Following BCMA CAR T Therapy in Myeloma. Blood Cancer Discov 3:490-501, 2022
Dong J, Garacci Z, Buradagunta CS, et al: Black patients with multiple myeloma have better survival than white patients when treated equally: a matched cohort study. Blood Cancer J 12:34, 2022
Mikhael J, Cichewicz A, Mearns ES, et al: Overall Survival in Patients With Multiple Myeloma in the U.S.: A Systematic Literature Review of Racial Disparities. Clin Lymphoma Myeloma Leuk 24:e1-e12, 2024
Ahmed N, Shahzad M, Shippey E, et al: Socioeconomic and Racial Disparity in Chimeric Antigen Receptor T Cell Therapy Access. Transplant Cell Ther 28:358-364, 2022
Snyder S, Chung KC, Jun MP, et al: Access to Chimeric Antigen Receptor T Cell Therapy for Diffuse Large B Cell Lymphoma. Adv Ther 38:4659-4674, 2021

Table 1. Baseline clinical and disease characteristics

Characteristic	Minority, N = 46^a	White, N = 177^a	p-value^b
Age (median, years)	61.5 (41.0-83.0)	66.0 (34.0-84.0)	0.012
Male	20 (43%)	105 (59%)	0.054
ECOG			0.033
0	2 (4.4%)	22 (14%)
1	35 (78%)	125 (79%)
2	7 (16%)	12 (7.5%)
3	1 (2.2%)	0 (0%)
Heavy Isotype			0.8
IgA	7 (15%)	35 (20%)
IgG	29 (63%)	104 (59%)
Light chain disease	10 (22%)	37 (21%)
Light Chain			0.6
Kappa	26 (57%)	109 (62%)
Lambda	20 (43%)	67 (38%)
R-ISS stage			0.082
1	5 (16%)	34 (24%)
2	12 (39%)	70 (50%)
3	14 (45%)	35 (25%)
Unknown	15	38
High-risk cytogenetics
Deletion 17p	7 (15%)	38 (21%)	0.3
t(4;14)	4 (8.7%)	18 (10%)	>0.9
t(14;16)	2 (4.3%)	8 (4.5%)	>0.9
Plasma cell leukemia	1 (2.2%)	3 (1.7%)	>0.9
EMD	16 (35%)	67 (38%)	0.7
CrCl <45	10 (22%)	15 (8.5%)	0.011
Prior transplant	37 (80%)	148 (84%)	0.6
Prior lines of therapy	5.0 (0.0-12.0)	6.0 (1.0-13.0)	0.5
Refractory Status
Bortezomib refractory	28 (61%)	95 (54%)	0.6
Carfilzomib refractory	33 (72%)	125 (71%)	0.4
Lenalidomide refractory	36 (78%)	137 (77%)	0.5
Pomalidomide refractory	38 (83%)	131 (74%)	0.5
Anti-CD38 refractory	42 (91%)	163 (92.1%)	0.6
Previous anti-BCMA exposed	7 (15%)	22 (12%)	0.6
Product			0.7
Cilta-Cel	16 (35%)	57 (32%)
Ide-Cel	30 (65%)	120 (68%)

Table 2. Clinical trial eligibility by race as based on ejection fraction, creatinine clearance, presence of plasma cell leukemia, prior BCMA exposure, and AL amyloidosis

Characteristic	Race		p-value
Characteristic	Minority N = 46	White N = 177	p-value
Total number of Ineligible patients	19 (41%)	42 (24%)	0.017
EF < 45%	2 (4.3%)	2 (1.1%)	0.2
CrCl <45 ml/min	10 (22%)	15 (8.5%)	0.011
PCL	1 (2.2%)	3 (1.7%)	>0.9
Concomitant AL Amyloidosis	1 (2.2%)	5 (2.8%)	>0.9
Previous anti-BCMA	7 (15%)	22 (12%)	0.6

^{Note: Values are presented as n (%). p-values are from Pearson’s Chi-squared test.}

Table 3. Summary of non-hematologic toxicities by race

Characteristic	Minority (N = 46), n(%)	White N = 177, n(%)	p-value*
CRS any grade	40 (87%)	142 (80%)	0.3
Max CRS			0.7
0	6 (13%)	35 (20%)
1	28 (61%)	101 (57%)
2	12 (26%)	39 (22%)
3	0 (0%)	2 (1.1%)
ICANS any grade	14 (30%)	32 (18%)	0.065
Max ICANS			0.1
0	32 (70%)	141 (80%)
1	6 (13%)	20 (11%)
2	4 (8.7%)	13 (7.3%)
3	2 (4.3%)	1 (0.6%)
4	1 (2.2%)	2 (1.1%)
5	1 (2.2%)	0 (0%)
Infection of any grade	14 (30%)	37 (21%)	0.2
Hospitalization (days)	11 (8, 17)	10 (7, 15)	0.13
Parkinsonian	0 (0%)	1 (0.6%)	>0.9

Note: Hospitalization duration is reported as median (interquartile range).

*P-values were calculated using Pearson's Chi-squared test; Fisher's exact test; and Wilcoxon rank sum test.

Yes there is potential conflict of interest.

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Outcomes of CAR T-Cell Therapy in Relapsed/Refractory Multiple Myeloma by Race: A Multicenter Real-World Study

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