How 'undead' cells trigger cancer-promoting inflammation
Researchers have discovered that cellular senescence, a state where damaged cells stop dividing, occurs in distinct stages rather than all at once. This finding suggests that it may be possible to suppress the harmful, inflammation-causing signals of these 'undead' cells without reversing their growth arrest.
Why it matters
This research could lead to more effective cancer therapies that minimize chronic inflammation and improve patient outcomes.
by Katherine Fenz, Rockefeller University
This article has been reviewed according to Science X's editorial process and policies . Editors have highlighted the following attributes while ensuring the content's credibility:
Add as preferred source CDK4/6i and doxorubicin both induce senescence features with distinct levels of DNA damage and p53 activation. Credit: Life Science Alliance (2026). DOI: 10.26508/lsa.202603790 Stopping tumor growth is only half the battle. Rather than killing tumor cells, many cancer therapies can only push them into cellular senescence, a state in which cells stop dividing but do not die. These "undead" cells continue to release signals that reshape the tumor environment. Some of these signals help the immune system clear damaged cells. But others fuel chronic inflammation that can encourage tumor growth.
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