The deadly mutation that allows cancer to exceed the human immune system

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New research from the comprehensive UC Davis Cancer Center has revealed an evolutionary change that may explain why some human immune cells are less effective in fighting solid tumors compared to non -human monkeys. This insight can lead to more powerful cancer treatments.

The study was published in Nature Communications. It revealed a small genetic difference in an immune protein called Fas Ligand (FASL) between humans and non -human monkeys. This genetic mutation makes the FASL protein vulnerable to obese by plasin, which is a tumor -related enzyme. This weakness appears unique to humans and is not found in non -human mainly, such as chimpanzees.

“Perhaps the evolutionary mutation in FASL has contributed to the size of the largest brain in humans,” said Jojunder Toser-Seng, a great author of the study and associate professor in the Department of Microbiology and Medical Immunology. “But in the context of cancer, it was a favorable comparison because the mutation gives some tumors a way to remove parts of our immune system.”

The tumor environment neutralizes the main immune protein

FASL is the immune cell membrane protein leads to the death of the programmed cell called the program of programmed cells. Stimulant immune cells, including CAR-T cells made from the patient’s immune system, use programmed cells to kill cancer cells.

The UC Davis team discovered that in human genes, changing evolutionary amino acids – Serene instead of the Bollein in Place 153 – makes the FASL more vulnerable to cutting and not activating it by plasin.

Plasmine is a brutase enzyme that often rises in aggressive solid tumors such as triple negative breast cancer, colon cancer and ovarian cancer.

This means that even when human immune cells are activated and ready to attack cancer cells, one of the main weapons of death – FASL – can be neglected through the tumor environment, which reduces the effectiveness of immune treatments.

Results may help clarify the cause of Car-T and T-CEL in blood cancers, but they are often short in solid tumors. Blood cancers often do not rely on plasin for their spread, while tumors such as ovarian cancer depend greatly on the plasmin to spread cancer.

Plastic inhibitors may enhance immunotherapy

Miscellaneous, the study also showed that the Blazine or FASL banning of the division can restore its cancer -full strength. This discovery may open new doors to improve immunotherapy.

By combining current treatments and plasma inhibitors or antibodies specially designed to protect FASL, scientists may be able to enhance immune responses in patients with solid tumors.

“Humans have a much higher cancer rate than chimpanzees and other monkeys. There are many that we do not know and they can still learn from the main and progress to improve immunotherapy for human cancer,” said Toser-Seng. “Regardless, this is a big step towards allocating and enhancing immunotherapy to positive plasma cancer that was difficult to treat.”

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