Authors
Jiaqi Fan, Nadine Kutsch, Jan-Michel Heger, Philipp Gödel, Eva Heger, Henning Gruell, Philipp Linde, Simone Ferdinandus, Johannes Rosenbrock, Hendrik Dapper, Emmanouil Fokas, Peter Borchmann, Christian Baues
Published in
Acta oncologica (Stockholm, Sweden). Volume 65. Pages 749-757. Sep 17, 2026. Epub Sep 17, 2026.
Abstract
While Chimeric antigen receptor (CAR) T-cell therapy has transformed treatment of relapsed/refractory diffuse large B-cell lymphoma (DLBCL), over half of patients relapse within 1 year with poor prognosis. Salvage radiotherapy (sRT) achieves high local response rates, but which subgroups benefit most and whether CAR T-cell persistence influences sRT response remains unclear. Patient/material and methods: We retrospectively analyzed DLBCL patients receiving sRT after CAR T-cell therapy at our center. CAR transgene levels were quantified by quantitative polymerase chain reaction (qPCR), and associations between CAR T-cell kinetics at relapse, sRT response, and survival were evaluated.
CAR transgene data were available for 13 patients, (18 lesions treated with sRT). Toxicity was mild (grade ≤ 2). The local response rate was 83% (15/18 lesions). Three CAR transgene kinetic patterns were identified at relapse: increased-CAR (second increase in transgene levels, n = 4), persisted-CAR (persistence > 6 months, n = 4), and decreased-CAR (decline or absence, n = 5). Local response rates were 100% in both the increased- and persisted-CAR groups versus 57% (4/7 lesions) in the decreased-CAR group, 12-month local control rates were 83, 100, and 14%, respectively. Twelve-month overall survival was 100% in both increased-CAR and persisted-CAR groups versus 20% in the decreased-CAR group.
sRT may provide durable local control in relapsed DLBCL after CAR T-cell therapy. Persistent CAR T-cell activity at relapse may help identify patients most likely to benefit from comprehensive sRT. Given the small, heterogeneous cohort, these findings are hypothesis-generating and require validation in larger series.
PMID:
42752612
Bibliographic data and abstract were imported from PubMed on 18 Sep 2026.
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