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Long-term Cancer Risk with Targeted Therapy in SpA

Jun 12, 2026 7:33 am

Dr. Antoni Chan reports on abstract OP0238 presented at EULAR 2026 in London

Transcription
I'm Anthony Chan reporting for RheumNow here in London at EULAR 2026. Increasingly we are using more targeted therapies, biologics and also targeted synthetic DMARDs in the field of SpA, and one of the questions we ask is does this actually increase the risk of malignancy in the long term. One possible explanation is that by using these agents we might reduce the immunosurveillance and possibly there could be a long-term malignancy risk with continuous immunosuppression or the use of targeted therapies.

To test this there was a presentation which is the oral presentation OP0238. This looked at long-term cancer risk with targeted therapies in spondyloarthritis. It was a French nationwide cohort. So they had a lot of patients. Nearly 56 and a half thousand patients took part and were evaluated in this study. So this was trying to address the question of is there a concern about long-term use of these agents with malignancy?

The study was done as a nationwide study, lots of patients, and these included both PsA, axial SpA and also other SpA subtypes. These were patients who were studied between 2014 and 2022 and they were included when they were treated with the biologic therapies but also JAK inhibitors. The median follow-up was 5 years. These patients were studied and those with known prior cancer, HIV or transplantation were excluded because that obviously could affect the follow-up in terms of their incidence of malignancy.

The primary outcome was incident cancer and they looked at the outcome of this in the study. So during the follow-up, there were around 1,200 cancers that occurred across the cohort. The overall incidence rate was 479 per 100,000 patient years. When looked at in terms of the weighted hazard ratio, those exposed for 6 months or less, the hazard ratio was 0.86. The confidence interval was 0.75 to 0.99. Breaking it down by cancer type, the protective association was significant. In other words, using the biologics conferred a protection and reduced the hazard ratio in these patients. In hematological malignancy specifically, the weighted hazard ratio was 0.65 and for solid cancers the direction was the same and did not reach statistical significance with a weighted hazard ratio of 0.92. These results were consistent across sensitivity analyses across the SpA subtypes including PsA.

What do we learn from this? The finding is that sustained therapies in SpA is associated with reduced rather than increased cancer risk, and this should reassure us that with earlier use of these targeted therapies with early diagnosis, which means a longer duration of exposure over the lifetime of the patient, does not increase the risk of malignancy. The explanation for this is that uncontrolled inflammation itself from the underlying disease is the reason there is an increased risk of cancer. So by actually treating and controlling inflammation, that will reduce the drive towards cancer. This is particularly so in the hematological context with hematological malignancy such as lymphoma and leukemia, and these are tightly linked to the inflammatory burden or the inflammatory severity, and by reducing inflammation we therefore could reduce the cancer risk.

Obviously the caveat from this study is there could be some residual confounding. This is observational data and therefore patients who could receive a more sustained therapy may be different from those who may have shorter courses of treatment. Also the 5-year follow-up may not be long enough for us to know across a longer period of time what we could see. Nevertheless, this is quite a robust real-world cancer study. The safety signals should reassure us that we should continue to drive towards treating our patients' inflammation, controlling their disease, and this could in the long term reduce their cancer risk. So this data is reassuring from this presentation. I'm Anthony Chan reporting here in London at EULAR 2026.

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