To maintain healthy skin tissue we produce stem cells that divide and mature into a multitude of specialist cell types. Cancer may result when this process goes wrong. A healthy balance between division and maturation is achieved with the help of transcriptional regulator proteins. The interplay between two such proteins, c-Myc and Sin3a, pushes stop and start buttons on genes in the stem cell. This image shows mouse skin that lacks Sin3a (viewed from below). Another protein (stained red) outlines the stalactite-like hair follicles. Without Sin3a immature stem cells (labelled green) build up, since they continue to divide rather than mature. This means they’re more likely to mutate and become cancerous. Understanding how c-Myc and Sin3a control the fate of skin cells helps explain how cancer arises, which is critical to the development of new therapeutic strategies.
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BPoD is also available in Catalan at www.bpod.cat with translations by the University of Valencia.