How does melanoma trick the host's immune system to increase its tolerance to chemotherapy?

  The complex human immune system has developed into an effective protective system that can resist the development of many diseases (such as cancer). These diseases can use a surveillance process called "immune surveillance" to identify and destroy cancer cells. I will. The immune system may exhibit another personality that promotes tumor formation and development rather than destroying cancer cells. This dual behavior makes the diagnosis of prognostic markers and drug development very difficult. In fact, one of the challenges facing oncology researchers is how to develop better and more effective immunotherapy. In the latest research report published in the International Journal of Natural Medicine, "Intermediate Factors Recombine the Microenvironment of Melanoma to a Pathogen and Immune Resistance", scientists from the Spanish National Cancer Center and other institutions have demonstrated how melanoma cells affect the host Immune system. Detecting or discovering that the host’s immune system does not attack melanoma cells and make them allies. Related research results have important clinical significance and are expected to be applied to other cancer research.

  In 2017, researchers discovered through research that a protein called MIDKINE plays a very important role in the metastasis of melanoma. Therefore, protein activation can determine the possibility of tumor metastasis. In fact, this is the early stage of melanoma. Due to the high possibility of metastasis, the researchers analyzed the expression of MIDKINE protein in the new animal model, and high levels of MIDKINE expression are directly related to its high translocation, thereby blocking the function of MIDKINE. I found. It can inhibit the spread of cancer cells; in this study, researchers have made new discoveries. In short, we have discovered a new role for MIDKINE protein in the host immune system. It does not attack melanoma cells, does not promote inflammation and promotes inflammation. The growth of melanoma. Next, the researchers analyzed the databases of six independent studies and found a group of genes directly related to MIDKINE protein expression in patients who did not respond to immunotherapy or developed drug resistance. The researchers tested these observations on animal models. Soengas researchers say that blocking the expression of the MIDKINE protein will cause two important immune cells (macrophages and T lymphocytes) to resume normal operation. Start tumor onset. This means that the treatment of patients with melanoma requires dual treatment, which is to step on the brake pedal on the immune response. In other words, the use of immune checkpoint inhibitors is obviously not enough, and MIDKINE protein is also sufficient. It must be suppressed so that the body's immune defense system can return to normal functions. At the same time, we are also studying other types of tumors, such as glioma, lung cancer and kidney cancer. We believe these findings may have a significant impact on the future treatment of many diseases.

  In recent years, researchers and clinicians have made a lot of efforts on how to strengthen the body's immune cells to fight cancer. However, in some cases, immunotherapy is very successful, but this method is still very successful and needs further development. For example, in fact, immunotherapy seems to be less successful in the treatment of pancreatic cancer. In the treatment of melanoma, about 60% of patients respond to the treatment. According to the tumor's response to immunotherapy, tumors are classified as "hot" or "cold". Some types of "heat" do not fully respond to treatment. This is a fact that researchers cannot explain. The research in this article expects that the results will help researchers explain why this phenomenon occurs, and may help improve the effectiveness of immunotherapy in the treatment of these tumors.