At the Weizmann Institute of Science, researchers have found that certain cells begin the body's programmed death sequence and then pause — surviving, multiplying, and rebuilding damaged tissue in the aftermath of injury. These so-called DARE cells reveal that the boundary between dying and living is not always a threshold crossed, but sometimes a threshold held. In this biological hesitation lies both a gift — the capacity to heal — and a shadow, for cancer may have learned to linger in that same suspended moment, evading the treatments designed to end it.
Scientists identify 'cheater cells' that survive death and regenerate tissue—and may explain cancer relapse
Cells that push the self-destruct button but survive anyway
Mark
So these DARE cells—they're dying but not actually dying. How does that help the body?
Mimi
They're part of how tissue repairs itself after injury. The cells start the death process, which sends out signals that tell neighboring cells to multiply and rebuild. But the DARE cells themselves survive and also multiply. It's like they're sacrificing themselves to trigger healing, except they don't actually sacrifice.
Luke
But we should be clear: this was observed in fruit fly larvae. The tissue regeneration happened in 48 hours in those experiments. We don't know yet if the same mechanism works the same way in human tissue or on the same timeline.
Mark
And the cancer connection—is that proven, or is it speculation?
Mimi
It's a reasonable concern based on what they found. The motor protein that keeps DARE cells alive has been linked to cancer growth before. So the pathway exists in cancer cells too. But whether cancer cells actually use this specific mechanism to survive treatment—that's the next question.
Luke
Right. They've identified a potential vulnerability and a potential escape route. They haven't shown that blocking this protein would actually stop cancer recurrence in humans, or that it wouldn't damage normal healing.
Mark
So this is foundational work, not a treatment yet.
Mimi
Exactly. It's the kind of discovery that opens a door. They've shown the mechanism exists and matters. Now researchers need to figure out how to use that knowledge without breaking something else.
Luke
And they need to test it in systems closer to human biology. Fruit flies are useful, but they're not us.
Mark
Fair. But the fact that they found this at all—that's significant?
Mimi
Very. Most people think of apoptosis as a simple on-off switch. This shows it's more nuanced. Cells can start the process and stop it. That changes how we think about cell death and survival.
The Pulse
- Cells that should die are choosing not to — and science is only now catching up to what that means for cancer survival and treatment resistance.
- In fruit fly experiments, DARE cells halted their own programmed death and then rapidly multiplied, regenerating nearly half of radiation-destroyed tissue within just 48 hours.
- A molecular motor protein is the key actor: it anchors the death-initiating enzyme to the cell membrane, preventing the final execution — and when researchers silenced it, regeneration collapsed entirely.
- The same protein has been found overactive in cancer cells, suggesting tumors may be hijacking a legitimate healing mechanism to survive chemotherapy and radiation.
- Scientists are now racing to determine whether blocking this protein in cancer cells could close the escape hatch — without dismantling the body's own capacity to repair itself.
At the Weizmann Institute of Science, researchers have found that certain cells begin the body's programmed death sequence and then pause — surviving, multiplying, and rebuilding damaged tissue in the aftermath of injury. These so-called DARE cells reveal that the boundary between dying and living is not always a threshold crossed, but sometimes a threshold held. In this biological hesitation lies both a gift — the capacity to heal — and a shadow, for cancer may have learned to linger in that same suspended moment, evading the treatments designed to end it.
Researchers at Israel's Weizmann Institute of Science have identified a class of cells that initiate the body's self-destruction sequence — and then stop. Named DARE cells, they begin apoptosis, the process by which the body eliminates damaged or unwanted cells, but halt before the process completes. Rather than dying, they survive, multiply, and rebuild. In experiments with radiation-damaged fruit fly larvae, DARE cells regenerated nearly half of destroyed tissue within 48 hours, findings published in Nature Communications that trace back to a curious 1970s observation: that irradiated fly larvae could still grow functional wings.
Using modern genetic tools, Dr. Tslil Braun and his team tracked which cells activated the early stages of death but persisted anyway. They also identified a second population — NARE cells — that aided repair without ever triggering apoptosis. But when DARE cells were removed from the system, the entire regenerative response failed, confirming their central role.
The mechanism depends on a molecular motor protein that anchors an initiator enzyme to the cell membrane, preventing the downstream enzymes that would actually destroy the cell from ever activating. The cell sends out distress signals that prompt neighbors to multiply and repair, while itself surviving the process it began. Silencing the motor protein caused DARE cells to die as expected — and tissue regeneration to fail.
Prof. Eli Arama, who leads Weizmann's molecular genetics department, noted that this same motor protein is overactive in cancer cells — a finding with direct implications. Cancer cells may be exploiting this natural survival mechanism to resist treatments designed to trigger apoptosis. A cell that can begin dying without finishing the process could theoretically withstand chemotherapy or radiation. The researchers' next challenge is determining whether blocking this protein in cancer could close that escape route — and whether doing so would leave the body's own healing capacity intact.
Researchers at Israel's Weizmann Institute of Science have identified a population of cells that begin dying but then stop themselves—and in doing so, may have stumbled onto an explanation for why some cancers survive treatment and return.
The discovery centers on what the team calls DARE cells, which initiate apoptosis, the body's programmed cell death process, but halt the sequence before it completes. In experiments with fruit fly larvae exposed to radiation damage, these cells not only survived but multiplied rapidly, regenerating nearly half of the destroyed tissue within 48 hours. The findings, published in Nature Communications, reveal a cellular survival trick that appears to serve a legitimate biological purpose: rebuilding tissue after injury. But that same mechanism, the researchers warn, could be the escape route cancer cells use to dodge treatment.
The work builds on a 1970s experiment in which radiation-damaged fly larvae regrew functional wings. Using modern genetic tools, Dr. Tslil Braun and his team at the institute tracked which cells activated the early stages of cell death but somehow persisted. "We set out to identify cells that push the self-destruct button but survive anyway," Braun said. What they found was a second population of cells, called NARE cells, that contributed to tissue repair without ever triggering apoptosis at all. The distinction mattered: when researchers removed the DARE cells, the entire regenerative response collapsed.
The mechanism turns on a molecular motor protein that appears to anchor the initiator caspase—an enzyme that starts the death process—to the cell membrane. This positioning prevents the activation of effector caspases, the enzymes responsible for actually destroying the cell. The cell begins to die, signals go out to neighboring cells to multiply and repair, but the dying cell itself survives. When the team silenced the motor protein in experiments, DARE cells died as they should have, and tissue regeneration failed. The system depends on this controlled interruption of death.
Prof. Eli Arama, who leads the molecular genetics department at Weizmann, noted that the same motor protein has been found overactive in cancer cells. The implication is direct: cancer cells may exploit this natural survival mechanism to resist apoptosis-inducing treatments. A cell that can initiate death but prevent its completion could theoretically withstand chemotherapy or radiation designed to kill it. Understanding how DARE cells manage this trick—and how to block it—could reshape how oncologists approach treatment resistance and cancer recurrence.
The research also illuminates compensatory proliferation, the biological process by which surviving cells multiply to replace those lost to injury. Signals from cells beginning apoptosis appear to activate DARE cells, triggering the rapid multiplication. This is not a flaw in the system; it is how the body heals. But cancer cells, which already ignore many of the body's normal constraints, may have learned to hijack this same signaling pathway. The next step for researchers will be determining whether blocking this motor protein in cancer cells could prevent them from evading treatment—and whether doing so would harm the body's legitimate regenerative capacity.
Notable Quotes
We set out to identify cells that push the self-destruct button but survive anyway— Dr. Tslil Braun, Weizmann Institute
Overactivation of the same protein had previously been associated with cancerous tumour growth, raising the possibility that cancer cells could exploit a similar mechanism to evade apoptosis— Prof. Eli Arama, Weizmann Institute
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