Scientists have discovered why a form of skin cancer called melanoma can be so malignant.
Skin cancer rates have been increasing across the UK
If not caught early the disease can spread through the body with an efficiency few other tumours possess.
Latest research suggests that, unlike other cancer cells, melanoma does not have to learn how to spread - it has that ability innately.
The research, by Whitehead Institute for Biomedical Research in the US, is published in Nature Genetics.
Lead researcher Professor Robert Weinberg said: "Other cancers need to learn how to spread, but not melanoma.
"Now, for the first time, we understand the genetic mechanism responsible for this."
The spread of disease to an unconnected body part - known as metastasis - is a highly inefficient, multi-step process that requires cancer cells to jump through many hoops.
The cells first must invade a nearby tissue, then make their way into the blood or lymphatic vessels.
Next they must migrate through the bloodstream to a distant site, exit the bloodstream, and establish new colonies.
Researchers have wondered why melanoma in particular is able to do this not only more efficiently than other cancers, but at a far earlier stage.
The latest study shows that as melanocytes - cells that protect the skin from sun damage by producing pigmentation - morph into cancer cells, they immediately reawaken a dormant cellular process that lets them travel swiftly throughout the body.
Central to this reawakened process is a gene called Slug which plays a key role in allowing cells to travel around the developing embryo in the womb.
Normally the gene is shut off in adult tissues, but the researchers found that when skin cells become malignant they reactivate Slug, and thus immediately acquire the ability to spread.
The researchers injected cancer-causing genes into normal human cells and then injected the resulting tumours under the skin of mice.
Mice injected with breast or connective tissue cancer cells developed tumours - but these did not spread.
But those injected with melanoma cells immediately developed invasive tumours throughout their body.
Detailed analysis showed that Slug was expressed in the melanoma cells.
When the gene was knocked out in melanoma cells, the cancer was unable to spread when introduced into a mouse.
Professor Weinberg said: "This work is a demonstration of the notion that certain embryonic genes normally involved in transferring cells from one part of the body to another are also involved in enabling cancer cells to spread."
The same team last year showed a similar embryonic gene, Twist, played a role in the spread of certain forms of breast cancer.
Dr Julie Sharp, senior cancer information officer at Cancer Research UK, said: "If scientists can target treatments to block the Slug gene, they might be able to prevent cancer spread and improve survival from this disease in the future," she said.
"It is also important to remember that the vast majority of melanomas are caused by UV damage from excess sun exposure."