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New research shows the presence of a particular gene can encourage tumor growth in wounded skin, indicating a need for further study on wound-treating ingredients.
Cancerous tumors sometimes form at the site of chronic wounds or injury, but the reason why is not entirely clear. Now researchers at Washington University School of Medicine in St. Louis have engineered mice with a persistent wound-like skin condition, and the mice are helping them understand the tumor-promoting effects of long-standing wounds and injuries.
"The chronic skin condition in the mice led to the growth of skin tumors," says Raphael Kopan, PhD, professor of developmental biology and of dermatology. "And what we learned from this process fit very well with the emerging realization that a tumor's surroundings play a critical role in its development."
Past clinical evidence has linked chronic skin wounds such as leg ulcers to an increased risk of skin cancer, and some scientists have suggested that chronic injury can predispose various organs to cancer.
In this study, published in Cancer Cell, the researchers found that the chronic skin condition led to secretion of molecules that activated dermal cells, increased the number of blood vessels and increased local inflammation, reinforcing the idea that wound repair mechanisms and inflammation are important agents in promoting cancer. The skin condition was engineered in the mice by inactivating a gene called Notch1 in patches of skin cells, leaving the rest of the skin intact. Notch1 is a master controller for normal skin development and was thought to suppress tumor growth in skin cells in which it resides.