Tek bir kanser geni hücreleri farklı yazgılara sürüklüyor

Cellular senescence is often described as a protective state in which damaged cells stop dividing, but research from NYU Abu Dhabi shows that the outcome is not uniform. Using a zebrafish model of liver cancer, the team activated a cancer-causing gene and tracked the earliest responses of precancerous cells. Some cells entered terminal senescence and could no longer form tumours. Others appeared senescent at first but later resumed division, meaning they could still contribute to cancer. This distinction also affected treatment. A commonly used senolytic drug, designed to eliminate senescent cells, worked against only some of the precancerous cell groups. The result is relevant because chemotherapy frequently pushes cancer cells into senescence without necessarily destroying them. Treating all such cells as biologically identical could therefore leave behind populations capable of renewed growth. The researchers argue that future cancer strategies should identify which form of senescence a cell has acquired and match treatment to its specific behaviour.