Video: Related studypublished at about the same time as Wechsler-Reya et. al. Explains the hedgehog pathway, which P53 is located on.
P53 is an infamous process gene at the core of the development of tumors. When P53 functional, it pauses cell growth/division to verify that growth is necessary and that no mistakes were made in the process. Without this gene, cells can grow and divide uncontrolled, resulting in tumor cells. However, previous research shows that addressing P53 alone does not completely stop tumor growth.
In a new study, researchers at Sanford Burnham Prebys Medical Discovery Institute show that medulloblastoma, a brain cancer that affects children, deactivates P53 which deactivates other genes downstream. One of those genes produces major histocompatibility complex (MHC-I) proteins which are tagged onto cells to label them as cancerous. The immune system recognizes the MHC-I protein and destroys the cancerous cell. When MHC-I is deactivated, the immune system never receives a help signal, and the tumor can grow undetected.
Tumor necrosis factor (TNF) increases the production of MHC-I to overcome the cancer’s defense by labeling all tumor cells. The study, conducted in mice, showed that TNF was able to activate enough MHC-I to alert the immune system of the problem. Once the immune system is alert, T-cells kill the tumor.
Medulloblastoma requires an aggressive combination of surgery, chemotherapy, and radiation. On developing brains, this often results in chronic side effects like hormone imbalances, intellectual disabilities, and a predisposition to more cancer. Immunotherapy is a hopeful line of research for a more effective treatment with fewer and less severe side effects.
Sources: Sanford Burnham Prebys Medical Discovery Institute via EurekAlert!, Scheidt et. al, Wechsler-Reya et. al
