Abstract
Identifying the mutant genes that are selected during carcinogenesis is key to identifying candidates for intervention and understanding the processes that promote transformation. Here we applied two selection metrics to study the dynamics of mutational selection in a mouse model of ultraviolet light driven skin carcinogenesis in which multiple synchronous tumors develop in each animal. Sequencing normal skin and tumors over a time course revealed two genetic routes to squamous carcinoma. Nonsynonymous Trp53 mutants were positively selected in both epidermis and tumors and present in 90% of tumors. The remaining tumors carried other oncogenic mutants, including activating Kras mutations. However, other positively selected mutant genes lost their competitive advantage in heavily mutated epidermis and in tumors. We found ten mutant genes under negative selection in normal skin, one of which was also negatively selected in tumors. In addition one gene was negatively selected in tumors but not normal skin. We conclude that analysing selection in normal tissue alongside tumors may resolve the dynamics of selection in carcinogenesis and refine the identification of cancer drivers.
| Original language | English |
|---|---|
| Article number | 127 |
| Pages (from-to) | 127 |
| Number of pages | 1 |
| Journal | Communications Biology |
| Volume | 9 |
| Issue number | 1 |
| Early online date | 12 Jan 2026 |
| DOIs | |
| Publication status | Published - 12 Jan 2026 |
UN SDGs
This output contributes to the following UN Sustainable Development Goals (SDGs)
-
SDG 3 Good Health and Well-being
Fields of science
- 302011 Dermatology
- 302 Clinical Medicine
- 301902 Immunology
Cite this
- APA
- Author
- BIBTEX
- Harvard
- Standard
- RIS
- Vancouver