The Study Of Glioma IDH1Gene Mutation And Glioma Cell Proliferation And Tumor Size

Objective: IDH1mutation detection of human glioma specimens, and establish astable animal model of human glioma, different time points observe tumor size,microangiopathy, and Ki-67antigen detection to explore how glioma IDH1genemutation impact the size of glioma tumor and cell proliferation, lay the foundation forclinical applicationsMethods: Collecting the Xinjiang Uygur Autonomous Region people’s Hospital ofNeurosurgery surgically excised and the pathology report confirmed glioma tumorsamples,using PCR method detected IDH1gene mutation, and immunohistochemicaldetected microvessel density (MVD), Ki-67antigen expression, mutation and nonmutation cell in glioma specimens was cell culture, using stereotactic, theself-cultured glioma cells were seeded in Adult male Wistar rat brain, making ratglioma model. The120male wistar rats were randomly divided into surgicalgroup(N=60), the sham group (N=30,) control group (N=30). surgical group wasdivided into two groups(N=30),were transplanted human glioma mutant and wild-typecells, sham group were transplanted saline, and the control group receivedconventional breeding.The wistar rats were normal feeding, imaging examinationafter1W,2W,3W modeling and recording tumor size, after three weeks later take therats brain, HE staining, glial fibrillary acidic protein (GFAP) immunofluorescencestaining, microvessel density (MVD) and Ki-67antigen detection.Results:1. Animal experiments show that the mutant group glioma tumor size was nosignificant difference between the wild-type group, the tumor size were197.55±18.84and205.51±20.84,and no significant difference in the growth rate. The antigen Ki-67expression of IDH1mutation group were significantly lower than those wild-typeglioma, the difference was statistically significant (P<0.05), the microvessel densityin IDH1mutation group were significantly lower than those wild-type glioma（P<0.05）, showed the gene mutation IDH1could reduced the cell’s proliferativeactivity. The antigen Ki-67expression in IDH1mutation group were significantlylower than those wild-type glioma, the difference was statistically significant(t=2.134，P=0.039).the Ki-67labeling index in the mutation group and wild-typeglioma group were21.19%±11.49%and14.44%±8.23%. The microvessel density inIDH1mutation group were significantly lower than those wild-type glioma (t=2.328，P=0.025), the microvessel density were40.54±12.11and31.11±13.47. low-gradegliomas Ki-67and microvessel density (MVD) expression were significantly lowerthan high-grade gliomas (t=9.138, P <0.001; t=-8.369, P <0.001), low gradegliomas (WHO I grade, II grade) and high-grade gliomas (WHO III grade, IV grade) Ki-67expression were8.36%±2.84%and25.55%±7.53%,and its vascular densitycounts23.94±8.03and45.54±8.19,Both expression increased with the grade ofgliomas, animal experiments consistent with human tumor samples assay results.Conclusions: Glioma,s IDH1gene mutation had no significant effect on tumor growthand size, but its impact on the proliferation of tumor cells. The mutation affecttumor’s energy metabolism, and energy metabolism decreased cell proliferationactivity, so that a large number of cells in a dormant stage, resulting in neovascularendothelial cells divide slowly and reduce the number of neoplastic blood vessels,malignancy and metastasis was inhibited, suppressed for IDH1gene mutation prolongsurvival mechanism provides a new theoretical basis.