Tel Aviv [Israel], January 18 (ANI/TPS): For the first time, scientists have identified the specific cells that allow severely damaged tissue to regenerate after widespread destruction, a discovery that could change how cancer relapse is prevented, researchers at the Weizmann Institute of Science told The Press Service of Israel.
Their study, recently published in the peer-reviewed Nature Communications, focuses on a phenomenon known for decades as "compensatory proliferation" -- the ability of tissue to regrow after radiation wipes out large numbers of cells. The effect was first observed in the 1970s in fruit flies, but until now, scientists did not know which cells were responsible or how the process worked at a molecular level.
Professor Eli Arama from the Department of Molecular Genetics at the Weizmann Institute, who supervised the study, told TPS-IL that while the phenomenon itself was not new, seeing the process unfold at the cellular level was unprecedented.
"The phenomenon was identified 50 years ago. It was understood that not all cells die after radiation. Some survive, divide, and recreate the tissue. But no one actually saw these cells. We were able to identify them for the first time," he said.
Using advanced genetic tools and live tracking in fruit fly tissue, the researchers discovered a small population of cells that activate the early stages of the cellular self-destruct program, known as apoptosis, but then stop short of dying. These cells survive radiation, multiply rapidly, and drive the rebuilding of the damaged tissue.
"They became visible about 24 hours after radiation, and within the following 24 hours the entire tissue is rebuilt," Arama explained.
At the heart of the discovery are caspases, enzymes best known for executing cell death. The study found that in these regeneration-driving cells, caspases are activated but then restrained, allowing the cells to survive while still triggering signals that promote growth in neighboring cells. The result is a tightly controlled burst of regeneration, rather than uncontrolled growth.
This balance is critical, and it may help explain a troubling pattern seen in cancer treatment. Tumors that return after radiation therapy are often more aggressive and resistant to further treatment. According to the researchers, the same survival mechanism that enables healthy tissue to regenerate may also be exploited by cancer cells.
"Cancer appears to use a similar mechanism. But now that we understand the mechanism that allows these cells to survive, we may be able to manipulate it so they do not," Arama said.
According to a statement by the Weizmann Institute, the implications extend well beyond basic biology. By learning how to selectively block survival in cancer cells, scientists hope to improve radiation therapy outcomes.
At the same time, the findings could guide new strategies in regenerative medicine, accelerating healing after injury or surgery. In particular, the research raises the potential of improving healing for burns, surgical recovery, and organ injuries, while enhancing lab-grown tissues and organ transplants.
Moreover, by activating or mimicking the tissue "resurrection" pathways, it may be possible to slow or reverse damage in cases of degenerative diseases such as Alzheimer's and Parkinson's.
"That is why understanding this mechanism is so important," Arama said, "with the hope that in the coming years it can be applied clinically." (ANI/TPS)