Four molecular markers of glioma

The initial IDH mutation was closely related to the formation of low-level glioma, followed by 1p/19q co-miss, TERT mutation or P53 and ATRX mutation;- From the article chapter
(Ruff: Ruff: Ruff: Ruff: Ruff: Ruff MW, et alNeuro-oncology2019 Feb 13doi: 10.1212/WNL.000000000000007126) Michael WRuff of the Mayo Clinic in Rochster, Minnesota, USA, and others systematically describe four genetic markers that affect the pathogenesis and therapeutic effects of gliomas (Table 1), published online in February 2019 in The Oncologymain features of table 14 genetic markersNote:MGMT:oxygen (6) - methyl oatin-DNA-methyl transferase;IDH:isotrecic acid dehydrogenase;TMs:tumor-related microtubase; TMZ: tamamine; PCV: methylzine, lomoxine and changchun neonicotinoid combination therapy; TERT: telomerase anti-transcriptase; D2-HG: D-2-hydroxyl dystril acid However, when glioma cells express MGMT, MGMT inhibits the effects of antikane-based chemotherapy drugs such as TMZ The expression of MGMT gene promoter methylation reduced MGMT enzyme, which reduced the effect of MGMT inhibiting alkaneagents such as TMZ, and the glioma of MGMT gene promoter methylation had better therapeutic sensitivity to TMZ chemotherapy In clinical practice, neuro-oncologists can predict the sensitivity of radiation and chemotherapy by evaluating the condition of glioma MGMT promoter methylation, and even have a guiding effect on the treatment of some elderly patients Given TMZ's poor efficacy in the absence of MGMT promoter methylation, the idea that no TMZ clinical trial sits in patients with MGMT promoter methylation is generally accepted 2016 edition of who central nervous system tumor classification standards will be combined with IDH mutation into the diagnostic indicators, so glioma is divided into two categories, such as GBM is divided into "IDH wild type" and "IDH mutant type", to emphasize the unique pathophysiological mechanism of IDH mutant tumorand and responsiveness to treatment IDH-1 is a cytoplasmic NADP-dependent enzyme involved in cell metabolism, and most mutations in gliomas are IDH-1 mutations After the IDH-1 mutation, tumor metabolites D2-HG are produced within cells, and D2-HG has inhibitory effects on a variety of enzymes in cells, the most critical of which is DNA demethylase Inhibition of DNA demethylase is an increase in DNA methylation, including methylation (G-CIMP phenotypes) on CpG Island CpG Island methylation interferes with the formation of the three-stage structure of DNA by blocking the binding sites of CTCF insulator proteins CTCF binds to interference, which destroys the formation of chromatin rings, and the physical separation of DNA is destroyed and gathered with different genes This newly discovered tumor mechanism illustrates the effects of IDH-1 mutations in the onset of glioma, and shows that it is associated with better prognosis and greater sensitivity to radiation chemotherapy The tumor with the IDH-1 mutation has homologous recombination defects, which are characterized by cell metabolism and alkane-type chemotherapy to aggravate DNA damage 2016 edition of who central nervous system tumor classification standards define 1p/19q co-missing gliomas as less protoscoccal glioblastoma Compared with patients with no 1p/19q total missing tumors, 1p/19q total loss of tumor was always accompanied by IDH mutation, and the prognosis and treatment response was good 1p/19q total deletion inhibits the formation of tumor-related microtubas (TMs) and increases sensitivity to chemotherapy; 1p/19q co-missing tumors do not have the ability to form TMs, which are shorter and more fragile even if TMs are present TERT is a telomere-extended nucleotide reverse transcriptase that is usually inhibited in post-natal somatic cells Mutation activation of terT promoters causes telomeres to extend, causing cells to remain biochemical The out-of-control expression of TERT in somatic cells plays an important role in the formation of gliomas, most commonly GBM the current hypothesis of the pathogenesis of glioma is that the initial IDH mutation is closely related to the formation of low-level glioma, followed by 1p/19q co-miss, TERT mutation or P53 and ATRX mutation; A model for the incidence of gliomas and the mechanisms affecting treatment tolerance and the sensitivity mechanisms of radiation chemotherapy as the understanding of glioma continues to deepen, the prognosis of patients can be more accurately evaluated when making clinically selected treatment decisions Further study of the pathogenesis of glioma will help improve the quality of life of patients with recurrent gliomas, reduce the side effects of treatment, and achieve the goal of final cure.