A group of Feinberg School of Medicine professors recently moved forward on experimentation regarding a potential method to kill cancer cells. The research opens doors for future cancer cell-specific treatments, as opposed to existing therapies which often affect healthy cells.

Feinberg Prof. Marcus Peter led the study, which was published last month in the scientific journal, Cell Reports. The study involved tests on lab mice and showed results supporting Peter’s theory that removing a protein, called CD95, and its ligand, CD95L, from tumor cells causes the cells to die.

CD95 has long been known by scientists as a protein that causes apoptosis, a form of programmed cell death that the mammalian immune system uses as a natural tumor defense mechanism. About a decade ago, Peter and his colleagues noticed that CD95 was expressed in most cancer cells. They discovered a previously overlooked additional role of CD95 — that it seemed to support the growth of malignant cells and stimulate various tumor-promoting activities.

It took the group about six years to confirm CD95, and its ligand CD95L, is necessary for cancer development. Using RNA interference technology, Peter and his team eliminated CD95 or CD95L from tumor cells, an experiment with results demonstrating that none of those cells could survive in the absence of either of the two proteins.

Peter coined the acronym DICE — Death Induced by CD95R/L Elimination — to describe the phenomenon.

In their most recently published paper, Peter and other members of his lab further verified their findings by generating two models of “knockout” mice — genetically engineered mice that have their CD95 receptor removed in specific tissues — that had ovarian and liver cancer. The researchers observed a substantial number of cancer cell deaths and none of the cancer cells formed lacked CD95 or CD95L completely, further reaffirming the DICE hypothesis.

Peter called DICE “a unique form of cell death difficult for cancer cells to become resistant against” because it simultaneously involves the activation of four known cell death pathways.

However, Peter said many challenges remain before DICE can be incorporated into actual cancer therapy.

Although DICE specifically targets cancer cells in mice, researchers are still unsure whether normal cells in cancer patients would be affected by such treatment, and are still testing the possible effects of DICE on potentially cancerous cells in the body.

“It is easy to kill cancer cells, but to selectively kill them, that is the difficulty,” he said.

The scientists must also determine how to best implement the CD95 removal process in a human body, Peter said.

Though many experiments are currently underway, it could take up to a decade before scientists are able to fully resolve the questions this study raises, he said.

“Cancer has proven to be much smarter than all of us, but let’s put it this way,” he said, “it would be fabulous if this research can make a dent.”

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