Psoriasis carries an established clinical correlation with an increased risk of overall malignancy. This is thought to be partially driven by the presence of chronic systemic inflammation and its effects on overlapping immune pathways. Although treatment with biologic therapies in patients with a history of cancer should be judicious, recent studies have shown that biologics for plaque psoriasis may not increase cancer recurrence or progression rates.

One of the biggest shifts in our understanding of psoriasis over the last 2 decades has been recognizing that it is not just a disease of the skin, but rather a systemic chronic inflammatory condition that involves the skin. It is therefore not surprising that psoriasis intersects with many other disease states, including malignancy.

We now have fairly robust epidemiologic evidence suggesting that psoriasis does correlate with an increased risk of malignancy, although it is important to recognize that this risk is modest and is not uniform across all malignancies. Further, a Mendelian randomization study and genomic analysis really strengthened the argument that the association between psoriasis and risk of malignancy may represent a true biological relationship, rather than simply being due to shared lifestyle risk factors. There are overlapping inflammatory pathways and genetic susceptibility loci that appear to contribute to both psoriasis and carcinogenesis. The inflammation associated with psoriasis can lead to more oxidative stress, a dysregulated immune surveillance, and dysregulated cellular proliferation, all of which can theoretically impact carcinogenesis.

To be clear, this does not mean that psoriasis causes cancer; instead, it means that psoriasis represents one manifestation of a broader inflammatory state, which, in a susceptible individual, may contribute to the development of certain malignancies. This changes how we talk to patients about treating plaque psoriasis in that it is about more than just skin clearance, and we frame it from the larger context of controlling systemic inflammation. Over time, uncontrolled disease creates this inflammatory debt that increases the risk for other conditions such as high blood pressure, diabetes, dyslipidemia, fatty liver disease, and, occasionally, malignancy. It is not that psoriasis directly causes them; it again goes back to chronic inflammation being the common denominator that certainly contributes. This reinforces something that we have been saying for years: plaque psoriasis management is about much more than treating the visible plaques—we are treating the whole patient.

Regarding the use of biologics in patients with cancer, the evidence currently does not allow us to say with 100% certainty that biologics as a class do not cause cancer recurrence, but we certainly have accumulating evidence that is remarkably reassuring. A 5-year waiting period has become the dogma in dermatology, where, in someone who has a history of cancer, you do not think about using a biologic for at least 5 years.

However, the landscape now is very different. Large real-world cohort studies consistently demonstrate no meaningful increase in new primary malignancies among patients receiving biologics compared with biologic-naive patients. Newer studies evaluating patients with plaque psoriasis who have active or recently treated malignancies have also shown no progression or no impact on recurrence-free survival with biologic therapies compared with patients taking conventional systemic agents, which I think is really important. However, cancer is incredibly heterogeneous, and this underscores the need for an individualized response. We need to learn about the biology of the individual patient’s cancer, their risk of recurrence, their treatment, and the severity of their plaque psoriasis to create a personalized approach.