Brief discussion on the research overview of glioma

Brief discussion on the research overview of glioma

What kind of tumor disease is glioma? Glioma originates from the brain's glial cells and is one of the most common intracranial tumors. It is also a disease caused by the interaction of congenital genetic high-risk factors and environmental carcinogenic factors. Let me briefly talk about the relevant research overview of glioma.

Like other tumors (diseases), gliomas are caused by the interaction of congenital genetic high-risk factors and environmental carcinogenic factors. 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 brain gliomas than the general population. In addition, some environmental carcinogenic factors may also be related to the occurrence of gliomas. Studies have shown that electromagnetic radiation, such as the use of mobile phones, may be related to the occurrence of gliomas. However, there is currently no evidence that there is an inevitable 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 very 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 manifested by slow cell division and proliferation; while high-grade gliomas are manifested by high-speed cell division and proliferation, accompanied by neovascularization, hypoxia and necrosis of the tumor. Correspondingly, low-grade gliomas often do not have the activation and high expression of molecular channels 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 (turningover) under normal physiological conditions, there will still be certain cell divisions in the central organs of the brain under specific periods and conditions. For example, in childhood, there is neuronal division. Therefore, in childhood, the incidence of neuronal tumors, such as medulloblastoma, is higher than that in adults. However, this does not mean that if cell division occurs, there is the possibility of tumor canceration. Because, in most cases, mutations (spontaneous mutations) that occur during cell proliferation can be corrected by the "maintaining stability" 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 small probability accidental event. Low-grade gliomas may "accumulate" new mutations during cell proliferation, thereby transforming them into high-grade gliomas (malignant transformation). In order to systematically understand the molecular etiology of gliomas, the United States launched the molecular gene atlas project (cancermolecular atlas) of gliomas in 2008. By sequencing the DNA of gliomas, it was found that on average each glioblastoma has up to 5 molecular mutations. Among them, the NF gene is the most commonly mutated tumor suppressor gene; EGFR is the most common proto-oncogene. These molecular mutations drive the expression of various signal pathways and constitute the molecular basis for the occurrence and development of gliomas.

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