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[18F]Fluorodeoxyglucose-PET/MRI-based response assessment
following BCMA-directed CAR-T-cell therapy with
ciltacabtagene autoleucel in relapsed/refractory multiple
myeloma
by Raphael Teipel, Karolin Trautmann-Grill, Luisa Kleditsch, Katharina Epp, Sebastian Böttcher,
Christoph Röllig, Heike Weidner, Andrea Gottschalk, Ingmar Glauche, Claudia Brogsitter, Ivan Platzek,
Rudi Apolle, Malte von Bonin, Martin Bornhäuser, Robert Winzer and Matthias Miederer
Received: February 3, 2026.
Accepted: May 15, 2026.
Citation: Raphael Teipel, Karolin Trautmann-Grill, Luisa Kleditsch, Katharina Epp, Sebastian Böttcher,
Christoph Röllig, Heike Weidner, Andrea Gottschalk, Ingmar Glauche, Claudia Brogsitter, Ivan Platzek,
Rudi Apolle, Malte von Bonin, Martin Bornhäuser, Robert Winzer and Matthias Miederer.
[18F]Fluorodeoxyglucose-PET/MRI-based response assessment following BCMA-directed CAR-T-cell
therapy with ciltacabtagene autoleucel in relapsed/refractory multiple myeloma.
Haematologica. 2026 May 21. doi: 10.3324/haematol.2026.300672 [Epub ahead of print]
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[18F]Fluorodeoxyglucose-PET/MRI-based response
assessment following BCMA-directed CAR-T-cell therapy
with ciltacabtagene autoleucel in relapsed/refractory
multiple myeloma
Authors: Raphael Teipel1, Karolin Trautmann-Grill1, Luisa Kleditsch1, Katharina Epp1,
Sebastian Böttcher2, Christoph Röllig1, Heike Weidner3, Andrea Gottschalk4, Ingmar
Glauche4, Claudia Brogsitter5, Ivan Platzek6, Rudi Apolle7, Malte von Bonin1, Martin
Bornhäuser1,8, Robert Winzer5 and Matthias Miederer5,7
1 Department of Internal Medicine I, Faculty of Medicine and University Hospital Carl Gustav Carus,
TU Dresden, Dresden, Germany
2 Department of Medicine III Hematology, Oncology and Palliative Care, University Hospital, Rostock,
Germany
3 Division of Endocrinology, Diabetes, and Bone Diseases, Department of Medicine III & Center for
Healthy Aging, Medical Faculty and University Hospital Carl Gustav Carus, TU Dresden, Dresden,
Germany.
4 Institute for Medical Informatics and Biometry, Faculty of Medicine Carl Gustav Carus, TU Dresden,
Dresden, Germany
5 Department of Nuclear Medicine, Faculty of Medicine and University Hospital Carl Gustav Carus, TU
Dresden, Dresden, Germany
6 Institute and Polyclinic for Diagnostic and Interventional Radiology, Faculty of Medicine and
University Hospital Carl Gustav Carus, TU Dresden, Dresden, Germany.
7 Department of Translational Imaging in Oncology, National Center for Tumor Diseases (NCT/UCC)
Dresden: a partnership between German Cancer Research Center (DKFZ), Heidelberg; Faculty of
Medicine and University Hospital Carl Gustav Carus, TUD Dresden University of Technology and
Helmholtz-Zentrum Dresden-Rossendorf (HZDR), Germany
8 National Center for Tumor Disease (NCT), Dresden, Germany
Corresponding Author:
Raphael Teipel, MD
Department of Internal Medicine I
Faculty of Medicine and University Hospital Carl Gustav Carus, TU Dresden
Dresden, Germany
E-mail: Raphael.Teipel@uniklinikum-dresden.de
Contributions
RT, KTG, RW and MM conceptualized and designed the study. RT, KTG, LK, KE, SB, HW, RW and MM
collected and interpreted data, AG and IG provided statistical input, RT, KTG, RW wrote the
manuscript. All authors reviewed and approved the final manuscript.
Data-sharing statement
The data that support the findings of this study are available from the corresponding author upon
request.
Disclosures:
RT received consulting and/or lecture fees from AbbVie, Amgen, BMS, Gilead, GSK, Johnson &
Johnson, Oncopeptides, Pfizer, Sanofi, Stemline and Takeda, received research grants from Johnson
& Johnson; KTG received Honoraria from Amgen, Novartis, Grifols, Roche, Sanofi, SOBI, Takeda and
served in advisory boards from Amgen, Grifols, Novartis, Novonordisk, SOBI, Sanofi; MM reports
consulting fees from Novartis and Roche; payment or honoraria for Telix and Novartis. All outside the
submitted work.
Acknowledgement:
This trial was reviewed and approved by the institutional review board and local ethics committee
(BO-EK-57022024) and was conducted in accordance with the Declaration of Helsinki and Good
Clinical Practice guidelines.
Funding:
Malte von Bonin is supported by CAMINO, the Advanced Clinician Scientist Program of TU
Dresden, funded by the BMFTR.
Letter to the editor
Chimeric Antigen Receptor ( CAR)-T-cell therapy has demonstrated remarkable efficacy in
patients with relapsed or refractory multiple myeloma (RRMM), inducing high response rates
even in heavily pretreated patients .1 Several diagnostic modalities are currently used for
response assessment, including classical serologic evaluation of monoclonal proteins, bone
marrow–based assessment of minimal residual disease (MRD), and functional imaging such as
PET. However, it remains unclear how treatment response after CAR -T-cell therapy should
best be evaluated, as conventional serologic assessments and bone marrow MRD testing
alone are unlikely to adequately capture the depth, spatial heterogeneity, and kinetics of
response indu ced by cellular immunotherapy, especially in patients with extramedullary
disease (EMD). In this context, the role of PET-based diagnostics continues to be investigated.
Still, data on PET -based response assessment after CAR -T-cell therapy remain limited i n
multiple myeloma, particularly with regard to its optimal application, timing, and added value
compared to other available response assessment methods. PET/MRI is an evolving
technology with promising results mainly in newly diagnosed MM2, but data on its use before
and after CAR-T-cell therapy are lacking.
To specifically address the current knowledge gap regarding PET/MRI-based response
assessment in cilta cabtagene autoleucel (cilta-cel) recipients, we retrospectively evaluated
RRMM patients exclusively treated with cilta -cel, eliminating the confounding prognostic
heterogeneity introduced by different CAR-T-cell constructs. A particular focus was placed on
the prognostic impact and outcome of patients with EMD.
A total of 26 patients undergoing CAR-T-cell therapy with cilta-cel from December 2023 until
April 2025 at an academic hospital in Germany were included . Per institutional standard,
whole-body [¹⁸F]Fluorodeoxyglucose-PET/MRI was performed prior to CAR -T-cell therapy, at
2 months, and at ≥12 months post cilta -cel in all patients with respective follow -up and
without prior clinical or serological relapse. Additionally, a standardized flow -cytometry–
based MRD assessment 3 (sensitivity: 10⁻⁵) was performed 2 an d 8–12 months post cilta-cel.
Serological response assessments according to IMWG criteria4 were conducted at 2, 6, 8, and
12 months after cilta-cel.
PET/MRI scans were assessed by two nuclear medicine specialists and radiologists using the
IMPeTUs criteria5, focusing on Deauville score (DS), bone marrow patterns, focal lesions, and
extent of EMD. A methodological limitation is that MRI does not allow reliable assessment of
CT-based osteolytic lesions (including their progression) or fractures . Diffuse myeloma
involvement was defined as homogenous uptake above liver threshold (PET) or diffuse
increased signal on high b -value images (DW-MRI). For evaluation of therapeutic response,
complete metabolic response (CMR) was defined as a DS <4 in all focal lesions and bone
marrow, whereas a persistent DS ≥4 was considered non–complete metabolic response (Non-
CMR), as previously described .6 Based on PET/MRI findings, patients were categorized as
either having bone-restricted (intraosseous and/or paraskeletal) lesions only (noEMD; n=17),
or exhibiting extramedullary involvement not adjacent to bone (EMD; n=9). The study was
approved by the institutional review board and local ethics committee (BO-EK-57022024).
The median patient age was 63 years at the time of cilta -cel infusion. Patients were heavily
pretreated (median of 4 prior lines of therapy) . All patients were triple-class exposed and
19/26 (73%) of patients were triple-class refractory. A significant proportion of patients (73%)
had cytogenetic high-risk disease (Table 1).
In total, 22/26 patients were evaluable by serolog y, while 4 patients had oligo -/asecretory
disease and could not be evaluated accordingly. All patients with measurable disease (n=22)
achieved an objective se rological response at month +2 ( ≥CR=12; VGPR=7; PR=3) , with
deepening of response over time (Figure 1A). Bone marrow assessment at month +2 showed
a high rate of early MRD negativity (MRDneg) (24/26 patients ; 92 %), with 11/26 patients
achieving MRDneg and CR. Of 24 patients with MRDneg at month +2, 17 were evaluable for
sustained MRD negativity (>6 months), which maintained in 13 patients. Three patients
developed early progressive disease, and one converted to MRD positivity (MRDpos) at the
second assessment. Seven patients were excluded due to immature follow-up (n=6) or refusal
(n=1). Of the two patients, with MRDpos at month +2 one converted to MRDneg, wh ile the
other patient experienced a clinical relapse 7 months post cilta-cel (Figure 1B/D).
Diffuse infiltration at baseline was detected in 5 patients by PET compared to 10 patients by
DW-MRI. All diffuse manifestations detected by PET displayed also diffuse uptake in MRI.
Discrepancies between the two modalities were either due to diffuse uptake in PET not
extending above liver threshold or inhomogeneous, micronodular signal in MRI classified a s
diffuse uptake. At month +2 diffuse uptake consistently resolved for all patients in PET and in
all but one patient in DW-MRI.
Further, 19/26 patients (73%) showed CMR on PET/MRI at month +2, whereas in 7/26 patients
at least one lesion (average of 1,7 +/- 0,76) with persistent increased metabolic uptake (Non-
CMR) was detectable. All except one lesion were classified as DS 4 (one lesion DS 5) on PET.
On DW-MRI, all of the lesions were also classified as responders (MY-RADS 1 or 2), except the
one lesion with persistent DS 5 in PET . Of the 7 patients with Non -CMR at month +2, 5
converted to CMR over time, whereas 2 patients experienced clinical relapse, both of whom
had EMD prior to CAR -T-cell therapy (Figure 1C/D). All patients with conversion to CMR at a
later time point remained in ongoing complete remission at last follow up. This raises further
questions regarding the optimal time point and interpretation of early PET -based response
assessment after CAR-T-cell therapy in multiple myeloma. The high rate of later conversion to
CMR in our cohort might indicate that month +2 is not the optimal time point for PET
evaluation alone, as it might be too early to sufficiently distinguish between residual metabolic
uptake and clinically relevant active myeloma . Here, the addition of DW -MRI might help for
further distinction . In p revious reports different potential reasons for persistent residual
metabolic uptake such as spatially heterogeneous delayed clearance, or inflammatory and
immune-mediated flare-up phenomena after BCMA-directed therapy have been discussed.7,8
This could be particularly relevant to avoid unnecessary intensification of therapy, for example
through consolidative radiotherapy of residual lesions.
Another key area of interest is the evaluation of potential biomarkers and their prognostic
impact on outcomes after CAR-T-cell therapy. Recent studies evaluated the role of PET-based
metabolic tumor volume (MTV) and soluble B -cell maturation antigen (sBCM A) in mixed
cohorts treated with cilta -cel, ide -cel, or an academic CAR -T-cell construct .9–11 High MTV,
defined by different thresholds, was reported as a negative prognostic factor in two studies.
Furthermore, elevated sBCMA levels were associated with high baseline tumor burden and
inferior outcomes.
We assessed PET-based MTV using PERCIST 1.0 liver reference normalization with automated
lesion detection. Levels of sBCMA were measured by ELISA (R&D®).
Serum levels of sBCMA before cilta -cel infusion corr elated well with pre –CAR-T-cell MTV
(R=0.72; p<0.001; Supplementary figure 1A). Furthermore, we observed a strong correlation
between the change in MTV from baseline to month +2 after CAR -T-cell therapy and the
change in sBCMA over the same period (R=0.84; p<0.001; Supplementary Figure 1B). Baseline
MTV also correlated with the rate of serological CR (p=0.0 08), but not with CMR (p >0.9) at
month +2 and it did not correlate with outcome (Supplementary figure 2C/D). This supports
the potential role of sBCMA and MTV as biomarkers of tumor burden in this setting. Th ese
findings could be particularly relevant in patients with high tumor burden, especially patients
with EMD.
EMD is a well-established adverse prognostic factor in multiple myeloma, particularly in the
context of conventional therapies. Although early trials of BCMA-directed CAR-T-cell therapies
demonstrate superior efficacy over standard treatments, published data on their use in
patients with EMD remain sparse. Available evidence suggests that, whilst response rates are
higher than with conventional therapy, outcomes for patients with extramedullary
involvement are still markedly inferior to those without such dise ase.12,13 Cilta-cel is
presumably the most effective approved CAR-T-cell in myeloma and can also lead to durable
responses in patients with high -risk features such as adverse cytogenetics and triple -class
refractory status .1415 Nevertheless, its ef ficacy in patients with EMD remains insufficiently
defined.
To further assess the influence of extramedullary disease, the cohort was divided into noEMD
vs. EMD patients. Baseline MTV (p=0.047) and levels of sBCMA (p=0.038) were significantly
higher in patients with EMD . Further patients with EMD had a higher number of lesions per
patient (p=0.021).
When c omparing response patterns, patients without EMD achieved higher rates of early
serological ≥CR (63% vs. 33%) as well as highe r rates of C MR (82% vs. 56%) at month +2.
However, these differences were not statistically significant based on the given sample size.
In contrast, comparison of bone-marrow MRD-levels revealed similarly high rates of MRDneg
at month +2 in both groups (93% vs. 92%).
After a median follow up of 12 months (range=5.8-23.2) patients with EMD prior to CAR-T-cell
therapy showed a worse PFS (12-month-PFS=65% in EMD-group versus 94% in noEMD-group,
p=0.044), while OS did not reach significance (12-month-OS=88% in EMD-group versus 93% in
noEMD-group, p=0.37). Comparing specific response patterns of EMD lesions, MRI showed
reduction of EMD lesion size at month +2, with persistent measurable disease in most
patients, whereas PET demonstrated CMR in all but one patient despite residual morphology.
Relapses after CAR -T in the EMD group occurred at previously involved EMD in all patients
(Supplementary table 1).
Our data, derived from a small but well-defined and uniformly treated RRMM patient cohort,
provide detailed insight into multimodal and longitudinal response assessments after CAR -T-
cell therapy including preliminary data on PET/MRI -based imaging. Nevertheless, given the
limitations of a small, single-center cohort, the results of this exploratory analysis should be
considered in context and require confirmation in l arger, prospective cohorts to further
determine the use of PET/MRI and its optimal timing after CAR-T-cell therapy. Our findings
suggest that EMD may remain an adverse prognostic factor even in cilta-cel treated patients
and indicate, that PET imaging prior to CAR -T-cell therapy and the incorporation of other
biomarkers like sBCMA could add essential information for prognostic stratification. This may
facilitate the implementation of more effecti ve bridging and debulking strategies to further
improve outcomes in this difficult-to-treat patient population.
References
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Table 1: Patient and PET/MRI characteristics at baseline
Baseline patient characteristics N = 26
Age at CAR-T infusion (median, range) 63 (41-74)
Sex, n (%)
Male
Female
14/26 (54%)
12/26 (46%)
Prior lines of therapy (median, range) 4 (2-9)
R-ISS-Score at CAR-T, n (%)
I
II
III
10/26 (38%)
9/26 (35%)
7/26 (27%)
Triple class exposed, n (%) 26/26 (100%)
Triple class refractory, n (%) 19/26 (73%)
Prior autologous SCT, n (%) 24/26 (92%)
Cytogenetic high-risk *, n (%) 19/26 (73%)
Time from primary diagnosis to CAR-T infusion in months (median, range) 57 (15 - 205)
Baseline PET/MRI characteristics (prior to CAR-T)
Diffuse bone marrow uptake per modality, n (%)
PET
DW-MRI
5/26 (19%)
10/26 (38 %)
Number of metabolic active lesions per patient, median (range) 5 (0-17)
Localization of lesions, patients in n (%)
Bone-restricted (intraosseous and/or paraskeletal)
Extramedullary (not adjacent to bone)
17/26 (65%)
9/26 (35%)
Metabolic Tumor Volume (MTV) in cm3, median (range) 8 (0 - 1.430)
sBCMA in ng/ml, median (range) 18 (2 - 186)
*Defined as presence of one or more: del17p13; t(4;14); t(14;16); gain/amp1q21
Abbr.: CAR-T - chimeric antigen receptor T-cell; EMD – extramedullary disease; [¹⁸F]FDG –
fluorodeoxyglucose; MRI - magnetic resonance imaging; MTV – metabolic tumor volume; PET -
positron emission tomography; R-ISS – Revised International Scoring System; sBCMA – soluble b-cell
maturation antigen; SCT – stem cell transplantation
Legend to figures:
Figure 1. Different patterns of response over time . (A) Longitudinal serologic response after
CAR-T-cell. (B) Bone marrow MRD-status (sensitivity-level: 10-5) at months +2 and at months
+8-12 post cilta-cel. (C) PET response measured by [¹⁸F]FDG-PET/MRI at months +2 and at ≥
12 months post cilta-cel. Patients with progressive disease (PD) after cilta-cel are illustrated in
each figure irrespective to the modality defining progression. Response categories are defined
by IMWG-criteria: PD= progressive disease; SD= stable disease; PR= partial response; VGPR=
very good partial response; ≥ CR= Complete response (includes stringent CR and CR); NE= Non
evaluable. (D) Patient individual follow-up. Colored bars prior to cilta-cel infusion (time point
“0”) represent the overall response (imaging and serology) to bridging therapy (all patients
received bridging therapy). After car-t cell infusion, colored bars indicate serological response
categories according to IMWG-criteria. PET/MRI assessments are indicated by stars (red star=
Non-CMR; green star= CMR). Bone marrow MRD assessments are indicated by dots (red dot=
MRDpos; green dot= MRDneg). An arrow indicates ongoing response at the time of data cut -
off. Progression (“PD”) is shown irrespective to the modality defining progression (imaging,
serological or clinical).
Figure 2. PFS and OS in EMD vs. noEMD patients. (A) Progression-free survival in patients with
EMD (red curve) vs. patients without EMD (blue curve). (B) Overall survival in patients with
EMD (red curve) vs. patients without EMD (blue curve). Survival analyses were performed
using the Kaplan -Meier estimator for survival curve estimation, and group differences were
assessed using the log-rank test.
Supplementary data:
Supplementary figure 1
Legend to supplementary figure 1: Correlation of sBCMA and MTV before and after
cilta-cel (A) Correlation of sBCMA and MTV at baseline (before cilta-cel). (B) Correlation
of the change in sBCMA-levels and MTV-levels from baseline to month +2 after cilta -cel.
At month +2, MTV levels were undetectable (0) in 25 out of 26 patients.
Spearman's rank correlation coefficient was used to assess associations. To enable
visualization of log -transformed data, a value of 1 was added to both sBCMA and MTV
Supplementary data
prior to log₁₀ transformation. This adjustment does not affect the Spearman correlation
results.
Supplementary figure 2
Legend to supplementary figure 2: PFS and OS dependent on MRD -status and
baseline MTV (A) Progression-free survival in patients with MRDneg (bone marrow) and
CMR (PET) at month 2 (blue curve) vs. patients with either MRDpos (bone marrow) and/or
Non-CMR (PET) at month 2 (red curve). (B) Overall survival in patients with MRDneg (bone
marrow) and CMR (PET) at month 2 (blue curve) vs. patients with either MRDpos (bone
marrow) and/or Non -CMR (PET) at month 2 (red curve). (C) Progression-free survival in
patients with baseline MTV ≥ 38.3 cm3 (red curve) vs. baseline MTV < 38.3 cm3 (blue
curve). ( D) Overall survival in patients with baseline MTV ≥ 38.3 cm3 (red curve) vs.
baseline MTV < 38.3 cm3 (blue curve). Survival analyses were performed using the Kaplan-
Meier estimator for survival curve estimation. The cut -off for MTV (38.3 cm 3; median
specificity: 70%; median sensitivity: 90.3 %) was calculated by ROC-analysis.
Supplementary table 1
Sites and response patterns of EMD lesions
Patient EMD sites at baseline Metabolic response
of EMD lesions at
month 2
Morphologic
response of
EMD lesions
at month 2
EMD sites at
relapse after
CAR-T
#2 pleura CMR PR
#4 pancreas CMR PR pancreas
#11 mediastinum Non-CMR SD
#12 liver, muscle, spleen CMR CR
#17 peritoneum, corpus
cavernosus penis
CMR PR
#22 pleura CMR CR pleura
#23 lymphnodes,
peritoneum, pleura,
liver, kidney, adrenal
glands
CMR PR pleura
#25 muscle CMR PR
#26 retrocrural space CMR CR retrocrural
space
Abbr.: EMD – extramedullary disease; CMR – complete metabolic response; Non-CMR – Non complete metabolic response; CR –
complete response; PR – partial response; SD – stable disease