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Scientists have identified a protein that plays a key role in the spread of a deadly type of skin cancer. It is hoped the discovery will lead to new treatments to block the progression of squamous cell carcinoma.

The protein, collagen VII, normally helps hold the skin intact but it is also needed by cancer cells to spread to other parts of the body.

Details of the Stanford University research are published in Science.

The study does show a number of important interactions between skin cells and the matrix that underlies the skin

Professor Alan Storey the researchers focused on collagen VII because it was already linked to a condition closely associated with squamous cell carcinoma.

Around two-thirds of children with recessive dystrophic epidermolysis (RDEB) - a blistering skin disorder - go on to develop the cancer.

RDEB is caused by gene mutations which lead either to an altered version of collagen VII, or a complete absence of the protein.

The Stanford team found that a key fragment of collagen VII is required for skin cancer cells to break free from the neighbouring skin tissue and spread.

They pinpointed the crucial sequence by studying skin samples from 12 children with RDEB.

The researchers used laboratory tools to activate molecular switches that normally turn skin cells cancerous.

However, four of the 12 samples never turned cancerous, no matter what cancer-promoting molecular switches the researchers had flicked.

Analysis showed the cancer-resistant skin cells were from children who lacked the collagen VII protein altogether.

Fragment .

The remaining cancer-prone samples all contained just a fragment of the protein.

Both types of mutations leave the children equally prone to RDEB - but only those cells that contained a portion of the collagen VII protein were susceptible to cancer.

When the researchers added the fragment to RDEB cells that lacked it, they were able to trigger the development of cancer.

And when they blocked production of the key fragment using an antibody, it was impossible to induce cancer.

Tests on mice produced similar results.

Lead researcher Professor Paul Khavari stressed more work was needed as cancer processes are very different in humans and mice.

Professor Alan Storey, of the Cancer Research UK Skin Tumour Laboratory, said the research was interesting but relied on small samples.

It might also be difficult to draw general conclusions from a very tightly focused study.

He added: "The study does show a number of important interactions between skin cells and the matrix that underlies the skin."