Skin cancers in which the upper layers of the skin grow uncontrollably - known as epithelial tumours - are maintained by special cancer stem cells. A paper in Nature has identified how the cells in these tumours signal to one another in order to keep the population of rogue stem cells topped up.
Joerg Huelsken and colleagues studied this type of skin cancer in mice. They found that transplanting material derived from the cancer stem cells to a cancer-free mouse caused identical cancer development in the recipient. And they pinpoint a protein known as beta-catenin as being crucial for sustaining these cancer stem cells - in genetically engineered animals without the protein - the tumours shrink because there is no longer a signal to tell the cells to keep renewing themselves.
The team's discovery may open up a possible route to treating this type of skin cancer in humans. They show that squamous cell carcinomas - the human equivalent of the mouse tumours - also rely on beta-catenin. As the stem cells responsible for renewing normal skin do not depend on beta-catenin, targeting this molecule could help wipe out the cancer stem cells in a malignant tumour.
Joerg Huelsken (Ecole Polytechnique Federale de Lausanne, Switzerland)
(C) Nature press release.
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