The susceptibility to glioma is not well understood. It has been suggested that the X-ray cross complementing group 3 (XRCC3) gene influences the capacity to repair DNA damage, leading to increased glioma susceptibility. In this study, we evaluated the relationship between XRCC3 mutations and glioma risk. Genotypes were assessed in 389 Chinese glioma patients and 358 healthy controls. XRCC3 Thr241Met (rs861539) and 2 additional polymorphisms, rs3212112 (c.774+19T>G) and rs1799796 (c.562-14A>G), were directly sequenced.
Several studies have examined the association between excision repair cross-complementation group 1 (ERCC1) C8092A and ERCC2 Lys751Gln polymorphisms and glioma risk, but the results have been inconclusive. We conducted a meta-analysis of 12 studies to determine the association between ERCC1 rs3212986 and ERCC2 rs13181 genes and glioma susceptibility. We searched for relevant studies in both Chinese and English in PubMed, Web of Science, Cochrane Library, and EMBASE through January 1, 2014, and identified 3939 cases and 5407 controls.
Several previous studies indicated that genetic polymorphisms in inflammatory factor genes were associated with glioma risk. However, the relationship between the prostaglandin-endoperoxide synthase 2 (PTGS2) genetic polymorphism and glioma remains unclear in the Chinese population. We selected 199 histologically confirmed adult glioma patients and 199 cancer-free controls for the present study and analyzed the distribution of the PTGS2 genotypes and haplotypes.
Glioma is a term used to describe tumors derived from glial cells. These tumors are divided into subgroups based on the histological morphology and similarity of their differentiated glia cells. Traditionally, they are classified according to the World Health Organization and include astrocytomas, oligodendrogliomas, ependymomas, and oligoastrocytomas. Like most cancers, gliomas develop as a result of genetic changes that accumulate with tumor progression.
Several single-nucleotide polymorphisms (SNPs) in DNA repair gene have been shown to affect DNA repair and to modify susceptibility to cancer. In this study, to investigate the role of these SNPs in glioma, we examined the potential association of 14 SNPs in DNA repair genes with the glioma risk in a Chinese population. We included 326 glioma cases and 376 cancer-free controls. Genotyping of the 14 SNPs was performed on 384-well plates on the Sequenom MassARRAY platform. Of the 14 SNPs, rs1799782 and rs1799793 did not display the Hardy-Weinberg equilibrium in the control group.
We aimed to investigate the role of 4 single nucleotide polymorphisms of the xeroderma pigmentosum complementation group F (XPF) gene (rs3136038, rs1799798, rs1800067, and rs2276466) in glioma, and the roles of gene-gene interactions in the risk of developing this type of cancer. We collected samples from 225 glioma cases and 262 controls and genotyped the rs3136038, rs1799798, rs1800067, and rs2276466 polymorphisms using a 384-well plate format with the Sequenom MassARRAY platform.
Cytochalasin B (CB) is known to inhibit a number of cancer types, but its effects on gliomas are unknown. We examined the in vitro effects of CB on the proliferation of human glioma U251 cells, as well as determined its mechanism of action. Cell proliferation was determined using CCK-8. The effect of CB on U251 cell morphology was observed under a transmission electron microscope. Cell cycle distribution was assessed using propidium iodine and Giemsa staining, and cell apoptosis was determined by annexin V-fluorescein isothiocyanate/propidium iodide.
Studies of genetic mutations that have been used in predicting glioma prognosis have revealed a complex relationship between clinical and genetic factors. Epidermal growth factor (EGF) and the NAT2 gene play a central role in carcinogenesis. An adenine (A) to guanine (G) single nucleotide polymorphism at position 61 in the 5'-untranslated region (5'-UTR) of the EGF gene has been found to be associated with levels of EGF production, and the mutations in the NAT2 gene have been postulated as a risk factor for cancer.
Extracts of mistletoe (Viscum album) are intensively used in complementary medicine, but their mechanisms are not fully understood in most cases, and the effects on metabolism have not been investigated in detail. However, some biologically active natural products are well known to provoke unexpected cellular responses. They reduce overexpression of heat shock proteins (Hsps) in cancer cells. The aim of the current study was to determine whether methanolic extract of V.
GSTM1 (glutathione S-transferase mu 1) and GSTT1 (glutathione S-transferase theta 1) are critical enzymes for detoxification of endogenous and environmental carcinogens. Constitutive GST gene polymorphisms may be associated with increased risk for cancer development. We made an explorative study of a Brazilian population with malignant glioma to determine whether GSTM1 and GSTT1 genetic polymorphisms influence the response to intranasal administration of perillyl alcohol and the survival rate.