Matthew Hangaur, lead author of the study and assistant professor of dermatology at the University of California, San Diego School of Medicine, explained:
"This discovery turns our understanding of cancer cell death upside down. Malignant cells that survive treatment receive a weak signal associated with cell death, and instead of killing them, this signal actually promotes the resumption of their growth. By blocking this signal, tumor recurrence can be reduced during treatment."
"In normal cells there is an enzyme called DFFB, which remains inactive as long as the cell is functioning normally. But when its function is disrupted and it needs to be eliminated, this enzyme turns into a destructive tool that cuts DNA into pieces to protect neighboring cells from damage."
In cancer cells that survive treatment, this enzyme is secreted in small quantities that do not cause significant damage to DNA, but are sufficient to generate a stress signal that inhibits the immune response and gives malignant cells a chance to grow and develop.
It is estimated that cancer causes one in six deaths worldwide. These deaths are mostly due to acquired resistance to treatment, which develops after an initial positive response. This resistance often results from mutations that accumulate gradually over months or years, similar to the mechanism of antibiotic resistance in bacteria. Addressing these mutations is challenging due to the limited range of available drugs. The newly discovered mechanism targets an early stage of resistance development, unrelated to genetic mutations, making it a promising target for future treatments.
August Williams, one of the study's participants from the Hangaur Laboratory, noted:
"Cancer cells use DNA 'destroyers' to resume growth after treatment. Our work has shown that non-mutagenic regeneration mechanisms can be activated at a very early stage and can be targeted by drugs, which may prolong remission and reduce the risk of disease recurrence."
The study was published in the journal Nature Cell Biology.
