Stories about: skin cancer

Give me some skin (or not)

GROWTH CONTROL: Under conditions of low cell density (top image), Yap1, shown in green, is concentrated in cell nuclei, where it turns on growth-promoting genes. Under conditions of cell crowding (bottom image), Yap1 is kept out of cell nuclei (black areas) and is unable to act. Instead it's spread throughout the cell cytoplasm.

Generating new skin for burn victims and treating skin cancer are two sides of the same coin, according to a new study, which also reveals an inborn “crowd control” mechanism that flips the coin. Healthy people have a switch that senses how tightly cells are packed in the “neighborhood,” and turns growth-promoting genes on or off as needed in epidermal (skin-forming) stem cells.

Fernando Camargo, a researcher in the Children’s Hospital Boston Stem Cell Program, has worked out how this switch works and why it’s stuck “on” in cancers like squamous cell carcinoma, the second most common skin cancer. That could be a fresh clue to treating these cancers.

And as Camargo’s team demonstrated in mice, tinkering with that same switch could grow new skin when it’s needed, to heal a burn or ulcer.

Camargo, born in Peru and named a Pew Scholar last year at the age of 33, has been interested in understanding what maintains organs at a specific size. How do our skin and kidneys and livers “know” when it’s time to stop growing?

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