Mathematical modelling shows how normal skin self-renewal processes impact skin cell evolution

What is it about?

All normal human tissues acquire mutations over time. Some of these mutations may be driver mutations that promote the development of cancer through increased proliferation and survival, while other mutations may be neutral passenger mutations that have no impact on cancer development. Currently, it is unclear how the normal self-renewal process of the skin called homeostasis impacts the development and evolution of gene mutations in cells. In this paper we used mathematical and computer modeling to demonstrate the impact of skin homeostasis on driver and passenger mutations. Skin cells undergo a normal life and death cycle of homeostasis. Cells in the lower basal layer proliferate, grow and move into the upper layers of the skin while undergoing cell differentiation and maturation. Eventually, the skin cells migrate into the uppermost layer of the skin where they form a protective barrier, die and are sloughed off. Homeostasis is typically maintained in the skin. Its thickness and growth do not significantly change over time, despite the accumulation of mutations. This is different from other tissue types that undergo increased growth and proliferation due to mutations. However, scientists are not sure how cell mutations in the skin evolve and form subclones, or groups of cells derived from a single parent cell, without impacting normal skin homeostasis.

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