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Multiple sclerosis outcomes after cancer diagnosis in people with recorded chemotherapy exposure: A real-world MSBase study
Journal article   Open access   Peer reviewed

Multiple sclerosis outcomes after cancer diagnosis in people with recorded chemotherapy exposure: A real-world MSBase study

Cassie Nesbitt, Paul Sanfilippo, Chao Zhu, Serkan Ozakbas, Alexandre Prat, Marc Girard, Pierre Duquette, Tomas Kalincik, Izanne Roos, Katherine Buzzard, …
Multiple sclerosis, Online First
2026
DOI: https://doi.org/10.1177/13524585261460658
PMID: 42543909
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cancer diagnosis1.42 MBDownloadView
Open Access CC BY V4.0

Abstract

Clinical Neurology Life Sciences & Biomedicine Neurosciences Neurosciences & Neurology Science & Technology
Background and objective: As more people with multiple sclerosis (MS) survive cancer, questions about MS management after cancer are increasingly relevant. This study aimed to describe post-cancer treatment patterns and MS outcomes in people with recorded chemotherapy exposure. Methods: Using MSBase, we identified people with MS with cancer and chemotherapy exposure. Time to first relapse and 6-month confirmed disability progression (CDP) were analysed using Cox models with disease-modifying therapy (DMT) as a time-varying covariate. Outcomes were contextualised using 1:2 propensity-matched MS controls without cancer or chemotherapy. Results: In total, 363 individuals were followed for 2.8 years (median) after cancer. Older age at cancer was associated with lower relapse hazard (hazard ratio (HR) = 0.96 per year, p = 0.008), while DMT category was not. The DMT category was not associated with CDP. In matched analysis (256 vs. 505), relapse hazard was lower during the first year after cancer (HR = 0.30, p = 0.015) with no difference thereafter; CDP risk was similar (HR = 1.13, p = 0.60). Conclusion: Post-cancer DMT category was not associated with relapse or CDP. Lower first-year relapse hazard, together with lower relapse hazard at older age, may provide cautious reassurance regarding early post-cancer inflammatory activity in similar clinical contexts, although the drivers of the first-year signal remain uncertain.

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