Gene acts as stop signal for skin cancer
MONASH (AUS) — The discovery of a gene that stops a common form of skin cancer from developing could make new cancer treatments and prevention available to the public in five years, researchers say.
Until now, the genetic basis of squamous cell cancer (SCC) has not been well understood, with surgical treatments the only option.
Researchers say they discovered that a gene with an important role in a fetus’s skin development is missing in adult SCC tumor cells. Although they initially focused on skin cancer, the protective gene is also lost in SCC that arises in other tissues, including head and neck cancers—which are often associated with poor outcomes.
Findings are reported in the journal Cancer Cell.
“Virtually every SCC tumor we looked at had almost undetectable levels of this particular gene, so its absence is a very profound driver of these cancers,” says Stephen Jane, professor at Monash University.
The gene was found to knock out the signal to stop skin cells from growing—without it, the cells keep increasing in number and eventually form a cancer.
Identifying this driver of cancer in skin and other organs provides a clear direction for developing strategies for both prevention and treatment in the relatively near future, Jane says.
“Our research indicates that drugs already in clinical trials for other cancers may actually be effective in treating SCC—they just need to be applied to skin or head and neck cancers. This means that a number of the usual hurdles in getting therapies to trial have already been cleared, so patients could be reaping the benefits of this research in under five years.”
“It’s a similar case with prevention. There are strategies by which we could increase the expression of this gene that will likely afford some protection from skin cancer, for example in the form of a supplement in sun-cream. The molecules that would increase this expression are very well validated, so there would be few barriers to applying them in clinical trials.”
Researchers from Harvard University, the Polish Academy of Sciences, Royal Melbourne Hospital, Walter and Eliza Hall Institute, and the Peter MacCallum Cancer Center contributed to the research.
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