Scientists have identified a cancer “master switch” that could open the door to revolutionary new treatments.

Activating a specific gene common to fruit flies, mice and humans may allow cancer to be “switched off”, say researchers.

Although the work is at an early stage, it has enormous implications for treating and curing cancers by snuffing out the very root of tumour formation.

The discovery outlined in two scientific papers relates to eye tumours in flies and bowel cancers in mice and humans.

But other “master switches” common to different species may exist for other cancers. All belong to a gene family vital to differentiation, the process by which cells acquire specialist roles in the body. Cancer cells, by definition, have no function and are less differentiated than normal cells.

The new research published in the online journal PLoS Biology focuses on the ATOH1 gene in mice and humans and its fruit fly equivalent, Ato. Both belong to the Atonal group of genes, conserved across a wide stretch of evolution, which are thought to be key differentiation controllers.

Scientists showed that ATOH1 suppressed bowel cancer in both mice and humans, while Ato prevented eye tumours developing in fruit flies. Switching off the gene triggered the growth of cancers in flies, mice and humans.

Laboratory experiments showed that loss of ATOH1 not only led to the growth of bowel cancer, but also Merkel cell carcinoma (MCC) — a rare but deadly form of skin cancer. Re-activating the gene in laboratory-grown cancer cells caused the tumours to stop dividing and commit suicide.

Separate teams of scientists led by Dr Wouter Bossuyt, from the VIB biotechnology institute and K.U. Leuven School of Medicine in Belgium, carried out the research.

The authors wrote: “We suggest that Ato/ATOH1, and similar genes, are important brakes on malignant transformation.”

Cells begin differentiating in the womb. In an adult, almost every cell is highly specialised and assigned a particular job. Cancer reverses the process, causing cells to become less differentiated. ATOH1 appears to switch on the last step in the specialisation of cells. Removing or de-activating it reverses differentiation, leading to cancer. Re-activating it engages the process again.

Dr Bossuyt and his colleagues raised the possibility of other “master switch” genes affecting other cancers. There was already evidence that related genes might play a role in the early stages of breast cancer development.

Dr Joanna Owens, from the charity Cancer Research UK, said: “This is an exciting addition to what we already know about the key molecular triggers for cancer formation. If we can understand more about these crucial events, we can find new ways to put the brakes on cancer.”