Many of us might reach for the hair dye the moment those first grey hairs appear. But a groundbreaking new study suggests we may be covering up one of the body’s most ingenious defences against cancer.

Research published in Nature Cell ­Biology showed grey hair is not just a sign of ageing – it also indicates the body is busy fighting off cancer-causing cell mutations in hair follicles in the scalp.

These could potentially lead to malignant melanoma, the most dangerous form of skin cancer. 

Scientists believe that understanding how this natural defence system works could lead to new ways to prevent or treat the disease, which kills around 2,500 Britons a year.

Researchers at the University of Tokyo studied mice and found that cells in the hair follicles called melanocyte stem cells (which grow into melanocytes, the cells that give hair and skin their colour) went into self-destruct mode as soon as they detected any sign of DNA damage that might lead to ­cancer, such as cells multiplying out of control.

The stem cells shut down permanently – a process called cell ­senescence – halting potential ­cancer growth, but also depriving the hair of its colour.

This is key because studies suggest once these stem cells undergo cancer-causing changes, they can migrate to the skin’s upper layers, leading to a malignant melanoma, which can spread around the body.

Many of us might reach for the hair dye the moment those first grey hairs appear. But a groundbreaking new study suggests we may be covering up one of the body’s most ingenious defences against cancer

Emi Nishimura, a professor of ageing and regeneration, who led the study, said grey hair and melanomas are caused by the same stress response in the cells that give colour to hair. But hair follicle cells are able to detect their own DNA damage and shut themselves down before they lead to cancer.

The team now hope to try to replicate the findings in humans. Cell senescence also occurs in the skin, gut, lungs and other organs. For example, during wound healing the body shuts down repair cells once a cut has healed, to prevent excessive scarring.

And moles on the skin are just clusters of melanocytes which stopped growing ‘because one ­melanocyte acquired a cancer-­promoting mutation’, says ­Professor Dot Bennett, a cell biologist at City St George’s, University of London.

These same moles can then become cancerous if one of the ­melanocytes breaks loose and starts to rapidly divide.

‘Scientists are starting to understand how some damaged cells escape senescence and restart dividing,’ says Professor Bennett.

‘That could eventually help us find ways to push dangerous cells back towards senescence – and away from cancer.’

The latest research also tackled an important question – if hair stem cells shut down at the first sign of DNA damage, why don’t they behave the same way when that damage is caused by over-exposure to the sun’s rays, the biggest cause of malignant melanoma?

Emi Nishimura, a professor of ageing and regeneration, says grey hair and melanomas are caused by the same stress response in the cells that give colour to hair

The Tokyo team found that when hair follicle cells were exposed to UV light, it failed to trigger this same protective response. Instead, the cells carried on dividing, increasing the risk of a melanoma forming.

This was because UV light triggers the release of a protein called KIT-ligand from surrounding hair follicles, which blocks the signal telling defective cells to shut down.

Meanwhile, the findings could have intriguing implications for the fast-growing science of senolytics – the development of drugs to clear senescent cells from the body.

While shut down, senescent cells are metabolically active but not ­functioning properly. As they accumulate in the body as we age, these cells are thought to drive the development of age-related illnesses, such as osteoarthritis and dementia.

‘Lots of research groups are now working on senolytics,’ says Professor Bennett. ‘If they are successful, then hair greying and hair loss are among the symptoms that might become treatable.’

Professor Desmond Tobin, a dermatological scientist at University College Dublin, says the findings from the Tokyo team need to be treated with caution.

He points out the study was ­carried out in mice – and the way hair grows in mice is fundamentally different from the process in humans. In mice, thousands of hair follicles grow in a synchronised wave every few weeks, meaning melanocyte stem cells divide far more frequently than in humans.

He adds: ‘The average age in humans for diagnosis of melanoma is between 60 and 70, long after most people show substantial hair greying.

‘Plus, melanoma of the scalp is ­relatively rare in humans – only about 2 to 5 per cent of all skin melanomas – and is usually confined to the outer layer of the skin, avoiding the hair follicles.

‘This highlights the unusual status of hair follicle melanocytes in the melanoma story,’ he adds.

Unlocking that mystery, he believes, could one day protect patients from melanoma.

Professor Bennett agrees: ‘The key processes of cell senescence work ­differently in mice and humans. It’s probably why mice typically live for about two years and humans can live to 80 or more.’