Many people instinctively turn to hair dye when they spot their first grey strands. However, an eye-opening new study reveals that these greys might actually signal the body’s clever mechanism for warding off cancer.

According to research published in Nature Cell Biology, grey hair is more than just an aging marker; it indicates that the body is actively combating cancer-causing mutations in scalp hair follicles.

These mutations have the potential to develop into malignant melanoma, the deadliest type of skin cancer.

Scientists suggest that by unraveling the workings of this natural defense, new preventative or treatment strategies for the disease—responsible for approximately 2,500 deaths in the UK each year—could be developed.

At the University of Tokyo, researchers conducted studies on mice and discovered that hair follicle cells known as melanocyte stem cells—which mature into melanocytes, the cells responsible for hair and skin pigmentation—initiate a self-destruct process upon detecting DNA damage that could lead to cancer, such as uncontrollable cell growth.

These stem cells enter a state of permanent shutdown, known as cell senescence, which effectively stops potential cancer in its tracks but results in the loss of hair color.

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.

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.

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

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?

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.

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

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.

H e 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.’