A team of researchers at Texas A&M University have found a mechanism within the body that hides cancer cells from the immune system. When the immune system is unable to detect a problem, it has nothing telling it to defeat corrupt cells, leading to the formation of tumors.
When the immune system is functioning normally, it will recognize and destroy cancer cells making it impossible for them to continue to develop and spread throughout the body. Researchers now understand exactly why the process sometimes doesn’t work accordingly. When cancer cells are capable of blocking a gene known as NLRC5, they can successfully hide from the immune system and start to multiply rapidly. This development in potential future cancer treatment has been outlined in the Proceedings of the National Academy of Sciences (or PNAS) journal.
Koichi Kobayashi, M.D., Ph.D, lead author of the PNAS article as well as professor at the Texas A&M College of Medicine says researchers have found what they are calling a “major mechanism” of how cancer cells are able to escape from the body’s immune system and start building tumors. NLRC5 was found to be an important biomarker for the survival of cancer patients as well as therapeutic response. This biomarker may quickly become a new target for future treatments of the disease.
Kobayashi says cancer cells are born due to a change in genetics, which may appear in the form of mutations or a rearrangement of chromosomes. This is why all cancer cells have new and ‘foreign’ genes which hold T-cells that normally would be detected by the body as tumor antigens. He states this anti-tumor system is very efficient.
A few years ago, the team of researchers made a discovery about NLRC5, finding that it actually regulates major histocompatibility complex (or MHC) class I genes. These particular genes code for molecules on the outermost layer of cells that contain foreign protein fragments that have occupied the cell. The fragments send a signal to the cytotoxic T cells, causing the immune system to immediately take action against the foreign substance.
The most important new information provided during the latest study is that the system described above should technically work in getting rid of cancer cells. However, this is not always the case, as the NLRC5 gene can be disabled. According to Sayuri Yoshihama, M.D., Ph.D., when the presence of the MHC class I antigen does not work, cancer cells are not removed by T cells. The first author of the new study says both the function and expression of NLRC5 is compromised within cancer cells by a variety of mechanisms.
Biopsy samples taken from 7,747 cancer patients in The Cancer Genome Atlas (or TCGA) database show the expression of NLRC5 has a very high correlation to survival of cancer patients. Those with greater expressions will live longer in most instances. Kobayashi says this information is important in predicting not only how long cancer patients may have to live but also what forms of treatment may be most beneficial to them.
The team is currently spending their time researching the role of NLRC5 and hopes to use this data to develop technologies that will be able to be used to quickly pinpoint the best treatment plans for individual cancer sufferers. This will help minimize cost for treatment as well as provide help before cancer spreads beyond control.
Researchers hope they can find a way to regulate NLRC5’s activation and expression level in order to create a new form of cancer treatment. Kobayashi anticipates that within the matter of a few years the team will be able to pinpoint potential drugs that can increase NLRC5 levels to assist the immune system in the fight against cancer.