Clinical significance of micro ribonucleic acid (miR)-24 and miR-101 were investigated by evaluating the expression of miR-24 and miR-101 in the tissues of patients with advanced gastric cancer. A total of 247 gastric cancer tissue specimens and 150 cancer-adjacent normal tissues (>5 cm away from the tumor) from patients with advanced gastric cancer who underwent surgical resection in the Surgical Oncology Department of Tianjin Union Medical Centre (Tianjin, China) from April 2013 to May 2016 were collected. The expression of miR-24 and miR-101 in gastric cancer and cancer-adjacent normal tissues were detected via reverse transcription-quantitative polymerase chain reaction (RT-qPCR), and the correlation of the levels of miR-24 and miR-101 in gastric cancer tissues with their clinical and pathological features were explored. The expression level of miR-24 in gastric cancer tissues was significantly higher than that in cancer-adjacent normal tissues (t=10.26, p<0.01), while the expression level of miR-101 was significantly lower (t=13.940, p<0.01). The expression of miR-24 and miR-101 in gastric cancer was correlated with the pathological differentiation degree of the tumor, lymph node metastasis and depth of infiltration (p<0.05). The multivariate Cox regression analysis revealed that miR-24 and miR-101 were independent prognostic factors affecting the overall survival of patients (p<0.01). The results indicated that the expression of miR-24 is upregulated and that of miR-101 is downregulated in gastric cancer tissues. miR-24 and miR-101 may promote the occurrence, development, infiltration and metastasis of gastric cancer, and can be indicators for the prognosis of patients with gastric cancer.
Temozolomide (TMZ) is a novel cytotoxic alkylating agent for chemotherapy of malignant gliomas. However, intrinsic or acquired resistance to TMZ often defines poor efficacy of chemotherapy in malignant gliomas. A growing number of studies indicate that expression of O 6 -methylguanine-DNA methyltransferase (MGMT) is one of the principal mechanisms responsible for this chemoresistance. In the present study, we evaluated the relationship between expression of MGMT and resistance to TMZ. We generated a TMZ-resistant cell line, U251/TR, by stepwise (8 months) exposure of parental U251 cells to TMZ. The resistance to TMZ was quantified using SRB assay. MGMT expression was evaluated at mRNA (RT-PCR) and protein (Western blot) levels. U251/TR cells showed increased (* sevenfold) resistance to TMZ. The MGMT expression (both mRNA and protein) was significantly (P \ 0.01) increased in U251/TR cells compared with parental U251 cells. Further, MGMT expression fluctuated during exposure of U251/TR cells to TMZ. The resistance of U251/TR cells to TMZ could be overcome by application of elevated doses of TMZ when MGMT expression was at the lowest level. In conclusion, our results demonstrate that the primary mechanism responsible for resistance of U251/TR cells to TMZ is associated with increased expression of MGMT. Resistance of malignant gliomas to TMZ can be overcome by synchronizing metronomic TMZ regimen with MGMT expression.
BackgroundIntraventricular glioblastoma multiforme (GBM) is extremely rare, especially in the trigone region. This report presents a case of trigone ventricular GBM with trapped temporal horn (TTH).Case presentationA 59-year-old woman was admitted to our department with a 1-month history of rapidly progressive headache, nausea, and weakness in the right lower extremity. Head non-contrast computed tomography and enhanced magnetic resonance imaging (MRI) revealed a trigone ventricular mass lesion with TTH and heterogeneous enhancement. The lesion was found 18 months ago as a small asymptomatic tumor mimicking ependymoma. This neoplasm was removed subtotally through the right parieto-occipital approach guided by neuroendoscopy. A ventriculoperitoneal shunt was subsequently performed to relieve TTH. The final pathological diagnosis was GBM. Unfortunately, 36 days after the first surgery, the patient died due to her family’s decision to refuse therapy.ConclusionThis rare case shows that GBM should be considered in the differential diagnosis of trigonal tumors. In this case, the tumor possibly originated from the neural stem cells in the subventricular zone. Patients with intraventricular GBM have a worse prognosis, and careful follow-up and early surgery for small intraventricular tumors are necessary, even for those with ependymoma-like radiological findings.
Aldo-keto reductase family 1 member B1 (AKR1B1) plays a vital role in tumor development and is involved in the tumor immune process. However, its role in glioma cell is poorly studied. This study’s aim was to assess the role of AKR1B1 in glioma through bioinformatics analysis. The AKR1B1 expression data and corresponding clinical data of glioma were collected from the Cancer Genome Atlas (TCGA) database. The R packages were used for data integration, extraction, analysis, and visualization. According to the median value of the risk score, all patients were divided into high-risk and low-risk groups to draw the Kaplan–Meier (KM) survival curves and to explore the level of immune infiltration. The expression of AKR1B1 was significantly elevated in glioma tissues compared to normal tissues ( P < 0.001). The high expression of AKR1B1 was significantly associated with WHO grade ( P < 0.001), IDH status ( P < 0.001), 1p/19q codeletion ( P < 0.001), primary therapy outcome ( P = 0.004), and age ( P < 0.05). Kaplan–Meier survival analysis found that OS (HR = 3.75, P < 0.001), DSS (HR = 3.85, P < 0.001), and PFI (HR = 2.76, P < 0.001) were lower in patients with glioma with high AKR1B1 expression than in the group with low AKR1B1 expression. Based on GESA, six pathways (including interferon gamma signaling, signaling by interleukins, cell cycle checkpoints, cytokine receptor interaction, cell adhesion molecules (CAMs), and cell surface interactions) at the vascular wall were identified as significantly different between the two groups. Moreover, highly expressed AKR1B1 was associated with immune cell infiltration. AKR1B1 plays a key role in glioma progression and prognosis and, therefore, serves as a potential biomarker for prediction of patients’ survival.
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