"Eczema may reduce risk of skin cancer: Condition means sufferers are more likely to shed skin containing cancerous cells," reports the Mail Online.
This headline follows a study which found that mice with a defect in their skin barrier were less likely to develop benign skin tumours. But the mice that did develop tumours were more likely to develop malignant tumours.
The laboratory study used mice that were engineered to have similar symptoms to humans with atopic dermatitis, the most common form of eczema. Researchers exposed the engineered mice and an additional group of wild mice to chemicals that can cause tumours.
After 16 weeks, half of the engineered mice had developed benign skin tumours compared with almost all of the wild mice. The wild mice also had six times more benign tumours.
From this, the researchers conclude that the likelihood of developing allergic diseases reduces the risk of tumour formation in experimental conditions in mice.
However, the study does not directly prove that people with eczema have a reduced risk of skin cancer because they shed more skin. There may be other important factors at play that were not considered in this lab experiment.
And importantly, this study does not mean that people with eczema can ignore the known risks of sun and UV exposure for developing skin cancer.
The study was carried out by researchers from King's College London, Cancer Research UK Cambridge Research Institute in the UK, Hokkaido University in Japan, and Otto von Guericke University in Germany.
It was funded by the UK Medical Research Council, the Wellcome Trust, the European Union and Cancer Research UK.
The Mail Online reported on the study accurately, although the headlines somewhat exaggerated the link between this study of mice and its implications for humans with eczema.
This was a laboratory study using mice. It aimed to see if there was a link between atopic dermatitis (the most common type of eczema) and the risk of skin cancer.
Previous epidemiological studies of humans have shown that atopic dermatitis is associated with lower levels of skin cancers. But it is not known if this is because of the disease process or the drugs that are used to control it, such as topical corticosteroids.
This research assessed the link by using genetically engineered mice that they called "triple knockout mice". The mice are called this because they do not have three essential proteins that are required for the outer layer of skin. They say that this skin defect can be used to study how atopic dermatitis would behave and respond to external influences.
The researchers used two tumour-causing chemicals on the triple knockout mice and wild-type mice to see which grew skin tumours.
The mice were first covered in a chemical called DMBA, which causes mutations in a gene called HRas. They were then repeatedly covered in TPA, a chemical that helps tumours grow from HRas cells that have mutations.
They then measured how many skin tumours each mouse had after 16 weeks. The researchers also carried out experiments using either DMBA or TPA.
Sixteen weeks after being covered in DMBA and then TPA:
Mice did not develop tumours if they were exposed to just one of the chemicals.
Triple knockout mice and wild-type mice responded in the same way to DMBA alone.
Triple knockout mice had an increased response to TPA compared with the wild-type mice. Their skin was thickened, red, dry and scaly. The skin also had increased numbers of cells involved in inflammation and infection.
The researchers suggest that the immune cells that were present when the triple knockout mice were exposed to TPA are the same as those involved in flare-ups of atopic dermatitis in humans.
They conclude that, "Atopy is protective against skin cancer in our experimental model and that the mechanism involves keratinocytes communicating with cells of the immune system via signalling elements that normally protect against environmental assaults."
This study has shown that mice with a defective skin barrier mount a greater immune response to the chemical TPA than wild mice. This immune response appears to reduce their likelihood of developing benign tumours. However, if they do develop a benign tumour, it is more likely to turn into a malignant tumour.
The researchers suggest that it is this heightened immune response that may be why people with eczema appear to be less likely to develop skin cancer.
However, it is not clear how close a match the triple knockout mice would be to humans with atopic eczema. In addition, most squamous skin cancers are associated with increased exposure to UV light, not chemicals.
This study is therefore an important precursor for understanding the possible mechanisms that reduce the risk of cancer, but the results are not yet directly applicable to humans.
As yet, it is unclear how we could use the potential protective effect of the immune response associated with eczema without exposing people to the downsides of this chronic condition.