Vitiligo and the risk for skin cancer

Vitiligo is an autoimmune disease in which the immune system targets melanocytes. Interestingly, this autoimmune response appears to offer a protective effect, as patients with vitiligo exhibit a reduced risk of developing melanoma or experiencing melanoma progression. This may be attributed to enhanced immune surveillance and the presence of shared antigens between melanocytes and melanoma cells. In addition, patients with vitiligo also have a lower risk of non-melanoma skin cancer, though the underlying mechanisms remain less well understood.

Non-segmental vitiligo is characterised by a progressive loss of skin pigmentation. Genetic predisposition and environmental factors that trigger a local immune response in the skin may induce the development of the disease. Dr Rosalie Luiten (Cancer Center Amsterdam, the Netherlands) expressed that natural killer cells and cytotoxic CD8-positive T lymphocytes play a central role in attacking melanocytes [1]. “Also, the genetic basis of vitiligo overlaps with that of other autoimmune diseases such as type 1 diabetes and rheumatoid arthritis,” Dr Luiten noted, adding that this explains the frequent co-occurrence of vitiligo with other autoimmune conditions.

Dr Luiten also highlighted that certain chemical substances, such as monobenzone, may disrupt melanin synthesis. Monobenzone, previously used for skin bleaching, was found to cause depigmentation not only at the site of application but also at distant skin sites. “The resulting pattern is indistinguishable from the one seen in vitiligo vulgaris, suggesting that monobenzone can potentially induce vitiligo,” explained Dr Luiten.

Interestingly, melanoma-associated vitiligo has emerged as a favourable prognostic factor in patients with melanoma undergoing immunotherapy. In fact, the risk of disease progression in these patients may be reduced by half compared with those without vitiligo. Even more striking, the risk of mortality could be 4 times lower in patients with melanoma-associated vitiligo [2]. “The explanation behind this result is quite straightforward,” said Dr Luiten. “Melanocytes and melanoma cells share common antigens, so an immune response against melanocytes is also effective against melanoma cells.” Next, Dr Luiten mentioned that the induction of vitiligo through a combination of monobenzone, used to induce skin depigmentation, plus imiquimod, an immune response stimulator, could be used as a therapy against melanoma [3].

Another interesting question is whether patients with vitiligo have a decreased risk for skin cancer overall. Studies have shown that patients with vitiligo indeed have a significantly lower risk not only for melanoma but also for non-melanoma skin cancer, even after controlling for sun exposure and light therapy [4,5]. This finding is counterintuitive since the autoimmune response of vitiligo is directed against melanocytes and not keratinocytes. Dr Luiten hypothesised that the enhanced immune surveillance seen in vitiligo patients could contribute to this protective effect, possibly extending the reduced cancer risk to other tumour types.

There is growing interest in the bystander-lysis hypothesis, which proposes that melanocyte-specific CD8-positive T cells from patients with vitiligo could be presented to other tissues. If these T cells recognise melanocytes in adjacent structures, interferon-γ and other cytokines could be released, potentially damaging surrounding cells like keratinocytes. This mechanism is especially relevant for basal cell carcinoma, which often contains melanocytes. Dr Luiten stressed that non-immune-mediated mechanisms could also explain the decreased risk for non-melanoma skin cancer in patients with vitiligo. “The skin of patients with vitiligo contains increased levels of TP53, which may promote keratinocyte apoptosis and DNA repair, thereby reducing the risk for carcinogenesis,” she said.

In summary, patients with vitiligo have a reduced risk of melanoma and non-melanoma skin cancer. This protective effect likely reflects a combination of immune-driven processes and non-immune factors. In recent years, researchers have unravelled some of these underlying mechanisms and have actively been investigating other potential mechanisms.

1. Luiten R. Vitiligo and skin cancer: auto-immunity as a guide for effective tumour-immunity. Dermatologendagen 2025, 10–11 April, Apeldoorn, the Netherlands.
2. Teulings H-E, et al. et al. J Clin Oncol. 2015.33(7):773-781.
3. Teulings H-E, et al. Oncoimmunology. 2018;7(4):e1419113.
4. Teulings H-E, et al. Br J Derm. 2013;168(1):162-171.
5. Rooker A, et al. J Invest Derm. 2024;144(2):234-242.

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Posted on 5 June 20255 June 2025