Childhood Gliomas

The incidence of childhood glioma is becoming higher and higher. It is actually a very common genetic disease. Therefore, you can do a prenatal check-up when you are pregnant. This way you can prevent the fetus in your womb from developing this disease. If it has already occurred, surgical treatment must be used. Only in this way can the disease be prevented from worsening again and better treated.

Some known genetic diseases, such as neurofibromatosis (type I) and tuberculous sclerosis, are genetic susceptibility factors for brain gliomas. Patients with these diseases have a much higher chance of developing glioma than the general population. In addition, some environmental carcinogenic factors may also be related to the occurrence of glioma.

Studies have shown that electromagnetic radiation, such as the use of mobile phones, may be associated with the development of gliomas. However, there is currently no evidence to show that there is a causal relationship between the two. Although most glioblastoma patients have had macrophage virus infection and evidence of macrophage virus infection has been found in the vast majority of glioblastoma pathological specimens, it is not clear whether there is a causal relationship between the two.

The molecular changes corresponding to the clinical and cytopathological manifestations of gliomas of different grades are also different. For example, low-grade gliomas are mainly characterized by slow cell division and proliferation, while high-grade gliomas are characterized by rapid cell division and proliferation accompanied by neovascularization, as well as tumor hypoxia and necrosis. Correspondingly, low-grade gliomas often lack the activation and high expression of molecular pathways such as HIF-1 and VEGF at the molecular level.

It is worth noting that although the brain is considered to be an organ in which cells hardly divide and proliferate (turning over) under normal physiological conditions, the central organs of the brain will still undergo a certain amount of cell division under specific periods and conditions. For example, during childhood, there is the division of neurons. Therefore, tumors of neuronal origin, such as medulloblastoma, occur more frequently in childhood than in adulthood. However, this does not mean that if cell division occurs, there is a possibility of tumor transformation. Because, in most cases, mutations (spontaneous mutations) that occur during cell proliferation can be corrected by the "stability maintenance" function of cell molecules; if they cannot be corrected, the cells will initiate the apoptosis pathway, causing the mutated cells to die spontaneously.

It can be seen that the occurrence of glioma is a low-probability accidental event. During the process of cell proliferation, low-grade gliomas may "accumulate" new mutations, causing them to transform into high-grade gliomas (malignant transformation). In order to systematically understand the molecular etiology of glioma, by sequencing the DNA of glioma, it was found that on average each glioblastoma had up to 5 molecular mutations. Among them, NF gene is the most commonly mutated tumor suppressor gene; EGFR is the most common oncogene. These molecular mutations drive the expression of various signaling pathways and constitute the molecular basis for the occurrence and development of gliomas.