Cancer treatment: Researchers zero in on a new approach to immunotherapy

Researchers at the University of Michigan carried out a study that found disrupting the interaction between cancer cells and some immune cells is more effective in destroying cancer cells in the body than the current immunotherapy treatments.

The findings of the study were published in the journal JCI Insight. For the study, the researchers studied cell lines and animal models. They zeroed in on a protein called CD6 as a target for a new approach to immunotherapy.

According to the study, only around one-third of patients with cancer eventually benefit from currently available immune checkpoint inhibitors.

"I'm interested in how cancer cells interact with certain immune cells to control the immune response to cancer, and how the immune system interacts with organs and tissues to cause autoimmune diseases," said study senior author David Fox, M.D., a rheumatologist and cancer researcher at the University of Michigan Rogel Cancer Center.

He questioned: "How can researchers intervene to alter these interactions and simultaneously destroy cancers while preventing autoimmunity?"

The new study claimed to offer a successful treatment in combatting human breast cancer, lung cancer, and prostate cancer in cell lines. This suggested that the anti-CD6 antibody, known as UMCD6, could help treat a wide range of cancer types.

For the experiment, the researchers grafted human breast cancer cells into immunocompromised mice. They then took a follow-up with transferring human immune cells into the mice.

When given an injection of UMCD6, the tumours almost completely disappeared in just one week, compared to mice treated without UMCD6, authors of the study stated.

The ability of UMCD6 to prevent and treat autoimmune diseases makes the potential implications for cancer immunotherapy especially intriguing, they added.

The researchers observed that when treated with UMCD6, the mice showed striking reductions in disease activity, autoimmunity, and organ damage in mice.

"When UMCD6 binds to CD6 on these specific immune cells, it creates a CD6 cluster that dives into the interior of the cell, allowing no CD6 to remain on the cell surface," said Fox.

He added: "This causes the killer T cells to seek out and destroy the cancer cells much more aggressively. At the same time, removing CD6 from the surface of CD4 cells, with the same UMCD6 antibody, controls, and limits the activity of the CD4 cells, which are the cells that instigate autoimmune diseases."

"Until now, we haven't been able to get immune cells to kill cancer cells without triggering an immune response that can be harmful to patients. What we've created here completely challenges prevailing concepts," he further said.

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