A research team in California has made a major breakthrough in potential cancer treatments by discovering a method to induce cell death.
Scientists from the University of California, Davis (UCD) have developed a way to destroy cells by using a crucial ‘timer bomb’ on the cells that line a tumor’s blood vessels.
These vessels regulate access to the tumor tissue, and until they open, cells intended to fight the cancer cannot reach the tumor.
Using the timer bomb technique, these barriers are triggered when the cell’s ‘death’ receptor, known as FAS or CD95, is activated.
Their findings, published on October 14 in Nature journal Cell Death & Differentiation, have been hailed as a significant advancement by the scientists involved.
“Previous efforts to target this receptor have been unsuccessful. But now that we’ve identified this epitope, there could be a therapeutic path forward to target Fas in tumors,” said Tushir-Singh, immunologist and senior author of the study.
The antibody that binds to this epitope (a specific part of the death receptor) essentially acts as the cell’s kill switch.
Once this immune checkpoint is triggered, other cancer treatments can be more effective, allowing them to target cancer cells more directly.
These targets, which are now more accessible, are often clumped together and hidden within the tumor.
“These are often called cold tumors because immune cells simply cannot penetrate the microenvironments to provide a therapeutic effect,” Tushir-Singh added.
“It doesn’t matter how well we engineer the immune receptor activating antibodies and T cells if they cannot get close to the tumor cells. Hence, we need to create spaces so T cells can infiltrate.”
UCD have mentioned that despite this breakthrough, cancer treatment will likely still rely on surgery, chemotherapy, and radiotherapy.
“These treatments may show effectiveness at first, but in some cases, cancers resistant to therapy tend to come back. Immunotherapies, like CAR T-cell-based treatments and immune checkpoint receptor molecule activating antibodies, have shown great potential in breaking this cycle,” the University stated.
At present, these therapies help only a very small number of patients, particularly those with solid tumors such as ovarian cancer, triple-negative breast cancer, lung cancer, and pancreatic cancer.
“Developing drugs that enhance death receptor activity could offer a critical weapon against tumors,” the University continued.
“However, despite some progress by drug companies in targeting Death Receptor-5, no Fas agonists have yet reached clinical trials. These findings could potentially change that.”