Research shows that cancer can fool immune cells, which normally repair the body, into actually helping develop the disease.
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Cancer is a tricky disease, and a recent study from the Icahn School of Medicine at Mount Sinai shows just how cunning the disease can be. Research shows that cancer can fool immune cells, which normally repair the body, into actually helping develop the disease.
The research, which was published in Nature, showed that early-stage lung cancer tumors can co-opt the immune cells, known as tissue-resident macrophages. The trickery actually helps the cancer tumor invade the tissue inside the lungs.
The Mount Sinai researchers mapped out how these macrophages are supposed to help become hurtful. The co-opting of the cells allows the tumor to hide from the immune system and then expand into deadlier stages of cancer.
The scientific team from Mount Sinai studied tissue samples from lung cancer tumors and surrounding lung tissue in 35 patients. The goal was to determine the role of macrophages in the development of cancerous tumors.
The research team wanted to learn the macrophage microenvironment to understand the key players that drive tumor growth in cancer, which can ultimately be targeted with immunotherapeutics. However, the Mount Sinai team was quick to note that therapeutically modifying macrophages has proven difficult.
Miriam Merad, the lead author of the study and Director of the Precision Immunology Institute at the Icahn School of Medicine at Mount Sinai, said the findings are essential for Mount Sinai’s future. The medical school has a robust lung cancer screening program capable of identifying early lung cancer lesions in patients before they become fully invasive.
For this research, Merad and her team developed a comprehensive study that started when patients entered surgery to have their lesions removed. Then, the samples of the tumors and surrounding tissue were analyzed on a cellular level to map out the immune system components they contained.
Following the analyses, the researchers found the macrophages that the cancer had co-opted. Those findings identify a potential target for drug developers. Additionally, the research team discovered the co-opting process that allows the cancer cells to trick the macrophages in mice, which will help in that drug development process.
“These findings will help devise immunoprevention strategies to prevent tumor progression in patients at risk by reprogramming macrophages and killing the tumor without surgery,” said Merad, who is also the Director of the Human Immune Monitoring Center and a member of the Institute of Thoracic Oncology and The Tisch Cancer Institute at Mount Sinai. Knowing how to attack the cancer at an early stage could have huge impacts on the number of patients relapsing and their overall survival, Merad added.
