A joint Hungarian research team has made a startling discovery that could reshape the way we understand cancer treatment. Scientists from the HUN-REN Centre for Natural Sciences and the National Institute of Oncology have revealed how certain cancer cells can survive chemotherapy by entering a dormant, ‘zombie-like’ state—only to later reawaken and trigger tumour regrowth.
For decades, scientists believed that therapy-induced senescence (TIS)—a process in which damaged cancer cells stop dividing—was an irreversible step toward cellular death. However, using a novel single-cell sequencing technique, the Hungarian team mapped these senescent cells and found that they are far more resilient than previously thought. According to a statement by the HUN-REN Hungarian Research Network, the findings show that cells in this dormant state can eventually escape, resume division, and reignite the cancer. Shockingly, these cells showed resistance to nearly half of the FDA-approved breast cancer drugs tested, turning what was once considered a death sentence for cancer cells into a survival strategy.
Published in the journal Molecular Cancer, the research is both a scientific breakthrough and a cautionary tale. It warns that treating TIS as a therapeutic endpoint could be dangerous, as surviving cells may not only restart the tumour but also develop resistance to various forms of treatment, including immunotherapy. ‘This is a truly paradoxical situation,’ lead author of the study Eszter Bajtai said, who spent six years on the project. ‘What we thought was our ally in stopping cancer may actually be a hidden enemy. In our experiments, tumour cells in TIS almost always escaped it within a few months—it was both thrilling and terrifying.’ The study also found that these ‘zombie cells’ suppress immune responses. Normally, senescent cells trigger immune attacks that help remove them. However, TIS tumour cells activate specific signalling pathways and produce proteins that block this immune clearance, allowing them to persist in the body undetected.
‘The discovery of this darker side of TIS required broad collaboration,’ Dr József Tóvári, head of the Experimental Pharmacology Department at the National Institute of Oncology, noted. The research involved multiple Hungarian institutions, including HUN-REN TTK, the HUN-REN Centre for Energy Research, the University of Szeged, and two national labs focused on drug development and tumour biology.
Dr András Füredi of HUN-REN TTK highlighted the broader implications: ‘This resistance mechanism may explain why some tumours recur even decades after seemingly successful treatment. It gives cancer cells a kind of shield against most conventional therapies.’
He added that overcoming this challenge will require radically new approaches. Encouragingly, the team has already identified the key elements of the TIS mechanism, which they hope to exploit in developing new therapeutic strategies in the coming months.
As cancer treatment continues to evolve, this discovery may mark a turning point, forcing researchers and clinicians to rethink how therapy-induced cell dormancy is understood and addressed in future cancer care.
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