Psoriasis does not directly cause cancer, but it is linked to a modestly higher cancer risk. A large prospective study of 200,000 psoriasis patients found a small but statistically significant increase in overall cancer risk, with an adjusted hazard ratio of 1.06 compared to the general population. That number climbs meaningfully for specific cancer types, particularly lymphoma, non-melanoma skin cancer, and certain solid tumors. The severity of your psoriasis matters: people with mild disease face little to no additional risk, while severe psoriasis carries a notably higher one.
How Psoriasis Increases Cancer Risk
The connection between psoriasis and cancer centers on chronic inflammation. Psoriasis keeps your immune system in a constant state of activation, and the same inflammatory signals that drive psoriatic plaques can, over years, create conditions that favor cancer development.
Immune cells involved in psoriasis release molecules called reactive oxygen species that can damage DNA directly. When this happens repeatedly over months and years, the genetic errors accumulate. Repair mechanisms get overwhelmed, and key protective genes (including p53, one of the body’s most important tumor-suppressing genes) can become inactivated. This is essentially how chronic inflammation anywhere in the body raises cancer risk, and psoriasis creates exactly this environment in the skin and, through circulating immune signals, potentially elsewhere.
The specific immune messengers elevated in psoriasis, including TNF-alpha, IL-17, and IL-23, don’t just drive skin inflammation. They activate pathways that promote cell survival, new blood vessel formation, and immune evasion, all processes that tumors need to grow. TNF-alpha, for instance, activates a molecular switch called NF-kB that regulates both inflammation and cell survival. IL-17 stimulates the production of growth factors that help tumors build their own blood supply. These aren’t theoretical links; they’re well-documented molecular pathways shared between psoriasis and cancer biology.
Which Cancers Are More Common
Not all cancers are equally affected. The strongest associations are with non-melanoma skin cancer, lymphoma, and a handful of solid organ cancers.
Non-melanoma skin cancer (the category that includes squamous cell and basal cell carcinomas) shows the most consistent elevation. A Taiwanese population study following psoriasis patients over 10 years found non-melanoma skin cancer was the most common malignancy, occurring at 7.5 times the expected rate. The risk scaled with severity: patients with severe psoriasis had roughly double the rate of those with mild disease.
Lymphoma, particularly non-Hodgkin lymphoma, is the other well-established association. A 2013 meta-analysis found the risk of non-Hodgkin lymphoma was 40% higher in psoriasis patients than in the general population. The Taiwanese cohort reported even higher figures for people with severe disease, with a lymphoma rate nearly five times above expected levels.
More recent genetic research using data from the UK Biobank has strengthened the case for links to solid tumors as well. A Mendelian randomization study, which uses genetic variants to establish causal direction, found that psoriasis is causally associated with breast cancer and lung cancer. A separate meta-analysis identified elevated risks across 11 site-specific cancers, including colorectal, kidney, liver, esophageal, pancreatic, and oral cavity cancers.
Severity Is the Key Variable
The difference between mild and severe psoriasis is dramatic when it comes to cancer outcomes. A meta-analysis published in JAMA Dermatology found no significant increase in overall cancer mortality for people with psoriasis as a whole (pooled relative risk of 1.05). But when researchers looked only at severe psoriasis, cancer mortality risk jumped to a relative risk of 1.22. Certain cancers stood out: esophageal cancer risk was 2.5 times higher, liver cancer 1.4 times higher, and pancreatic cancer 1.3 times higher in people with severe disease.
Swedish and Taiwanese population studies have confirmed this pattern. In both countries, severe psoriasis patients showed cancer mortality rates clearly above the general population, while mild psoriasis patients did not. Severe psoriasis is generally defined as disease covering more than 10% of body surface area or requiring systemic medications, phototherapy, or hospitalization.
How Much Is Psoriasis and How Much Is Lifestyle
This is a critical nuance. People with psoriasis smoke more, drink more alcohol, and have higher rates of obesity than the general population. All three are independent cancer risk factors. When researchers account for these lifestyle differences, the apparent cancer risk from psoriasis shrinks considerably.
The JAMA Dermatology systematic review noted a “marked attenuation of risk” in studies that adjusted for smoking, alcohol, and obesity. Some of the specific cancers linked to psoriasis, like esophageal and liver cancer, are also strongly associated with alcohol and smoking independently. This makes it difficult to separate the contribution of psoriasis itself from the behaviors that tend to accompany it.
That said, the genetic evidence from Mendelian randomization studies suggests the link isn’t entirely explained by lifestyle. Because these studies use inherited genetic variants that predispose to psoriasis, they’re less susceptible to confounding by behavior. The fact that they still show causal associations with breast and lung cancer suggests psoriasis-related inflammation contributes independently, even if lifestyle factors amplify the signal.
Do Psoriasis Treatments Affect Cancer Risk
Some treatments for psoriasis have their own relationship with cancer risk, and this is worth understanding separately from the disease itself.
PUVA phototherapy, which combines a light-sensitizing medication with ultraviolet A light, carries a dose-dependent skin cancer risk. Patients who undergo more than 250 PUVA sessions see a meaningful increase in both melanoma and non-melanoma skin cancers. When PUVA and UVB phototherapy are used together, the effect may be synergistic. Narrowband UVB alone carries a lower risk, but caution is still advised beyond 300 sessions. Because of these concerns, PUVA use has declined significantly over the years.
Biologic medications that block TNF-alpha are widely used for moderate-to-severe psoriasis, and their cancer profile has been closely studied. A systematic review and meta-analysis of long-term TNF-alpha inhibitor use found no increased risk of cancer overall, melanoma, lymphoma, prostate cancer, or breast cancer compared to the general population. The one exception was squamous cell carcinoma of the skin: patients on TNF-alpha inhibitors had roughly 2.8 times the expected rate. Patients with psoriatic arthritis on these drugs also showed elevated non-melanoma skin cancer rates. This is worth discussing with your dermatologist, particularly if you have a history of skin cancer or have had extensive phototherapy.
What This Means in Practical Terms
The absolute increase in cancer risk for most people with psoriasis is small. An overall hazard ratio of 1.06 means that for every 100 cancers expected in a comparable group without psoriasis, you’d expect about 106 in the psoriasis group. That’s not a dramatic difference for any individual person.
Where the risk becomes more clinically meaningful is in severe, long-standing disease. If you have widespread psoriasis that requires systemic treatment, the combination of chronic inflammation, potential treatment effects, and the lifestyle factors that often accompany severe disease creates a higher cumulative risk. Regular skin checks are particularly important if you’ve had extensive phototherapy. Paying attention to the modifiable risk factors, especially smoking and alcohol use, is one of the most effective things you can do, since reducing those exposures appears to meaningfully lower the cancer risk that gets attributed to psoriasis in population studies.