The murine skin is an excellent model organ to study the cellular and molecular interplay in tissue homeostasis and cancer formation, as the skin is one of the best-studied adult stem cell systems and cancer is believed to arise from deregulated stem and progenitor populations. Stem cells of the skin’s epithelium are located in distinct niches of the hair follicle, the sebaceous gland, and the interfollicular epidermis and their respective progeny are normally restricted to defined areas. However, injuries like acute wounds disturb the balance of homeostasis and allow stem cell progeny to repopulate new areas. Cancer also disturbs – or needs a disturbed – homeostasis, thus it is not surprising that wound healing and cancer formation are closely linked processes.
To build a comprehensive picture of skin homeostasis and cancer initiation we are addressing three different yet tightly linked key questions:
1. What is the cellular plasticity and diversity of epithelial (stem) cells in skin homeostasis?
2. How does wound healing concert reprogramming of epithelial (stem) cells?
3. What roles do (stem cell) niches play during tissue maintenance and cancer initiation?
We use a broad range of methods, such as lineage-tracing mouse models, single-cell transcriptomics, single-molecule FISH, and computational analyses to unravel stem cell diversity and plasticity in adult tissue maintenance, and to reveal how wound repair and stem cell reprogramming influence the development of non-melanoma skin cancer.
© 2016 kasper lab