Overview
- A Nature paper published 27 July 2026 reports experiments in which researchers bred four genetically diverse mouse strains, gave each animal a single dose of the liver carcinogen diethylnitrosamine (DEN), and sequenced nearly 600 tumours to track how cancers formed and evolved.
- The team found that tumours in all strains almost always acquired a driver mutation that activated the MAPK signalling pathway, showing a common route to cancer despite different genetic backgrounds.
- The specific driver mutations, the activity of other cancer pathways, and the tendency for tumours to undergo whole‑genome duplication varied strongly by inherited genetic background.
- Researchers say the results imply that prevention, screening and responses to DNA‑damaging cancer therapies may need to account for inherited genetic diversity, but they stress that human studies are required before clinical changes.
- The experiments used a controlled mouse system to remove environmental confounders, relied mainly on funding from Cancer Research UK, the Medical Research Council, the European Research Council and Wellcome, and leave open how closely the mouse findings map onto human populations.