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Letters to the Editor
curve over time among MCL2 treated patients could possibly be related to a deeper remission and longer time to relapse, as previously demonstrated by the intensified strategy.3,11 In any case, the lack of a plateau in any of the curves is probably related to chemo-resistant disease, as previously demonstrated in biologic high-risk MCL.12,13 The favorable OS in limited-stage MCL patients receiv- ing curative radiotherapy confirms the efficacy of this strategy. 14 However, the low number of patients stud- ied, the uncertainty of defining a group based on criteria in a retrospective cohort and the potential influence of confounders, i.e., biologic good prognostic factors, should not be neglected.
A major strength of the work presented is the popula- tion-based setting and the large size of the cohort, retrieved from a time period after rituximab was intro- duced in clinical routine. Moreover, the standardized models in both overall and relative survival models improve the reliability of the results. Limitations were the lack of data on molecular markers, comorbidity, sec- ond primary malignancies and other factors with poten- tial impact on treatment choice and mortality15 as well as the low number of patients treated with maintenance rituximab. Furthermore, the delayed entry may poten- tially have excluded cases with the most treatment-resis- tant disease.
To conclude, this study demonstrates that BR may be comparable to intensified treatment strategies in a pro- portion of patients with MCL. Awaiting the results from ongoing prospective trials on novel combinatory regi- mens, future studies should focus on a deeper evaluation of predictive markers in relation to established treatment concepts.
Alexandra Albertsson-Lindblad,1 Thorgerdur Palsdottir,2,3 Karin E. Smedby,2,4 Caroline E. Weibull,2 Ingrid Glimelius,2,5 and Mats Jerkeman1
1 Division of Oncology, Skane University Hospital, Lund University, Lund; 2 Department of Medicine Solna, Clinical Epidemiology Division, Karolinska Institutet and Karolinska University Hospital, Stockholm; 3 Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm; 4Department of Medicine Solna, Division of Hematology, Karolinska University Hospital, Stockholm and 5Department of Immunology, Genetics and Pathology, Clinical and Experimental Oncology, Uppsala University and Uppsala Akademiska Hospital, Sweden
Correspondence:
ALEXANDRA ALBERTSSON LINDBLAD- Alexandra.albertsson_lindblad@med.lu.se
doi:10.3324/haematol.2021.279037 Received: April 22, 2021.
Accepted: November 5, 2021. Pre-published: November 18, 2021.
Disclosures: AAL received grant support from Janssen Pharmaceutical NV as part of a collaboration between Karolinska Institutet and Janssen Pharmaceutical NV; CW and TP are part of a research collaboration between Karolinska Institutet and Janssen Pharmaceutical NV for which Karolinska Institutet has received grant support; IG participated in educational seminars run by Janssen Pharmaceutical NV; KES received a research grant from Janssen, honoraria from Takeda and Celgene; MJ received research support from Janssen Pharmaceutica NV, Celgene, Abbvie, Gilead, Roche and Astra Zeneca and honoraria from Roche, Gilead, BMS, Astra Zeneca, Janssen Genmab and Incyte.
Contributions: AAL, TP, IG, CEW, KES, MJ designed the study; TP, CEW, IG, AAL prepared data; AAL, TP and CEW performed data analysis, tables and figures; AAL, TP, IG, CEW, KES, MJ
participated in the analysis and interpretation of results; AAL pre- pared the draft manuscript; AAL, TP, IG, CEW, KES, MJ critically reviewed the manuscript prior to submission.
Funding: This study was financed partly through the Swedish Cancer Society and partly through a public-private real-world evi- dence collaboration between Karolinska Institutet and Janssen Pharmaceutical NV.
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