Equipping the Immune System to Fight Cancer
There are a number of innovative approaches to treating cancer, and one exciting area of research involves discovering new ways to boost anti-cancer mechanisms already present in the immune system. Researchers in the U.S. have now found a unique way to significantly increase the ability of certain immune cells to fight cancer. The study is detailed in an online issue of the Journal Investigative Dermatology.
Dr. Charles Dimitroff and research associates at Brigham and Women’s Hospital, have discovered that decreasing the creation of certain carbohydrates present in the cell surfaces of effector immune cells can greatly improve their ability to ward off cancer. These “effector” cells are part of the immune system and function to kill pathogens such as bacteria, viruses, and tumor cells. One of their most critical functions is to recognize their target.
Prior studies have already suggested that a protein known as Galectin-1 plays a major role in helping tumor cells evade destruction by the immune system by triggering cell-death in immune effector cells. It has also been documented that more aggressive and developed tumors express more Gal-1. These studies have gain interest in the research community who is now targeting this protein for both cancer diagnosis and treatment.
During the course of their study, Dimitroff and colleagues tested the concept that Gal-1 helps cancer cells to evade antitumor immune cells, and does so by binding with a family of carbohydrate molecules known as N-acetyllactosamines. To accomplish this task, they took lab mice with melanoma or lymphoma and treated them with a compound (peracetylated-4-fluro-glucosamine) that inhibits the production of N-acetyllactosamines.
The researchers then monitored what effect their test had on the mice’s tumors and immune system. They found that their suppressor compound (paeracetylated-4-fluro-glucosamine) stopped Gal-1 from triggering cell death in the immune system’s T cells and NK (natural killer) cells by decreasing the amount of N-acetyllactosamines expressed on their surfaces. The compound also assisted the immune cells in infiltrating the tumors and also promoted higher levels of tumor specific cells.
The authors conclude, “Collectively, our data suggest that metabolic lowering of Gal-1 binding N-acetyllactosamines may inhibit tumor growth by boosting antitumor immune cell levels, representing a promising approach for cancer immunotherapy.” Thus they hope their findings offer a new target for immune-system boosting cancer therapies.