Researchers from the University of Texas opened immunoregulator that defines the progression of glioblastomas.
The results of pre-clinical research conducted Shulin Li, MD, professor of pediatrics, and Amy Heymberger, MD, Professor of Neurosurgery, published in Nature Communications on 25 January.
"The progression of brain tumors associated with activation of oncogene and inactivation of tumor suppressor gene, but genetic and epigenetic mutations are not the only cause of the progression of glioblastoma, - says Lee -. Some immune regulators can do the same and are key regulators of cancer, especially in certain tissues and the environment. "
Glioblastoma, unlike melanoma and lung cancer, Does not cause a strong immune response of T-cells, and immunotherapy are still not as strong in the fight against it. Results of the study show that FGL2 (fibrinogen-like protein 2), which is known to suppress the immune system, is highly expressed in glioblastoma. Researchers have shown that inactivation, or "knock-out» FGL2 from tumor cells can eliminate the progression of tumors in mice. This will help to identify the causes of disease progression.
The first author, PhD Joon Yang, showed that e L2, is present in the tumor cells, controls a specialized group of dendritic cells which activate the T cells. FGL2 CD103 prevents movement of the population of dendritic cells that are needed for starting tumor T-cells which kill tumor. The study also found that the dendritic cells have to find a way to the microenvironment of the tumor in the central nervous center to activate T cells.
"This study is important because it shows that the immune system needs to interact in the CNS and in the tumor to be effective Previously it was believed that this interaction is necessary only in specialized immune organs such as the lymph nodes, -. Says Heymberger. - It also shows a new mechanism of immunosuppression which has not been described previously and also confirms how FGL2 important for the disease ".
Command also analyzed cases Atlas of glioblastoma cancer genome and found that lower levels of protein expression FGL2 in combination with high levels of GM-CSF or IFN, T-cell activator are associated with a prolonged survival of patients with glioblastoma.
Lee and Heymberger actively working on therapeutic strategies aimed at FGL2.