Ben-Gurion University team finds a molecular switch that helps tumors survive chemotherapy

Researchers at Ben-Gurion University of the Negev in Beersheba have identified a switch inside human cells that decides whether a cell under severe stress fights to survive or triggers its own programmed death. The university announced the study on 24 September 2026, and it was published in the journal Redox Biology. Because chemotherapy works by pushing cancer cells into exactly this kind of stress, the finding helps explain why some tumors shrug off treatment.

The work centers on two proteins, DNAJB12 and DNAJB14, which sit in the membrane of the endoplasmic reticulum, the compartment where cells fold newly made proteins. Under moderate stress the pair act as guardians: they open an emergency route that lets certain proteins leak out of the endoplasmic reticulum into the surrounding cell fluid, where those proteins disable the machinery of cell death. The team showed that this 'reflux' keeps damaged cancer cells alive after drug treatment.

Under heavier stress, rising levels of the antioxidant glutathione break the chemical bonds that hold the two guardians together, and the cell destroys them. With the guardians gone, a protein called BIK builds up and recruits the proteins BAX and BAK to the membrane, setting off self-destruction. The researchers describe the cell's internal chemical balance as acting like a scale that tips the cell toward survival or death. They found the same cascade at work in heart cells starved of oxygen and then reoxygenated, a model of heart-attack injury.

The study was led by Dr. Aeid Igbaria of BGU's Department of Life Sciences, with co-lead authors Laila Abu Madegam and Noa Gavriel and researcher Raifu Tolulope Adebisi. It was funded by the Israel Science Foundation and the Israel Cancer Research Fund. In an interview with The Times of Israel, Igbaria said his lab's interest began with glioblastoma, an aggressive brain cancer, and that the results could matter most for solid tumors. The findings are laboratory work in human cell lines, so any drug that targets the switch is still some way off.