Introduction: Primary tumours associated with nerve cells are exceptionally rare whereupon the majority of these tumours present as benign.
Neurons develop oncogenic mutations less than their supporting neuroglias which are transformed into glioma tumours.
Methods and materials: Using a multi-faceted approach, search strategies were generated using specific keywords and performed on selected
scientific databases. Literature searches were performed and a shortlist of seven publications was generated following a strict criteria based
Results: Reduced number of proliferating cells: Early cell cycle exit results in the inability for nerve cells to regenerate as well as preventing
malignancies from developing as no DNA is required to replicate. Additionally, post-mitotic Neurons have the ability to re-enter the cell cycle
without producing two daughter cells to repair damaged DNA.
Tumour suppressor proteins: A high abundancy of PTEN and TP53 are present in the CNS and PNS (higher than most other areas of the
body). These act as protective mechanisms for detection of damaged DNA to mark cells for immediate apoptosis.
Inhospitable environment created by the lymphatic system: An extensive network of lymphatic vessels channel tumour cell dissemination to
cervical lymph nodes. This stimulates immune responses by the high abundancy of dendritic cells and the destruction of tumour cells.
Immunity in the nervous system: Natural Killer (NK) cells, seen in high abundancy in the CNS, are the most effective response factors against
tumours and viral infections. NK cells express a large range of cellular receptors to tumour ligands which stimulates NK mediated cytotoxicity.
Hereditary: Li-Fraumeni syndrome, Cowden syndrome and neurofibromatosis 1 syndrome represent three genetic conditions with associated
high risks of developing tumors such as glioblastoma, schwannoma and astrocytoma.
Geographic location: There is a correlation between countries with high Human Development Index (HDI) and the incidence and mortality of
Conclusions and future directions: Mutations are rare in nerve cells due to their inability to proliferate and regenerate. Mutated nerve cells are
marked for DNA damage repair or apoptosis preventing passing on of oncogenic mutations. The high abundancy and range of immune cells
surveilling the nervous system and lymphatic system mark cancerous growths for degradation. Germline mutations account for a small
proportion of nerve cell tumors.