Quantitative assessment of the relationship between RASSF1A gene promoter methylation and bladder cancer (PRISMA).

BACKGROUND: Methylation of the Ras-association domain family 1 isoform A (RASSF1A) gene promoter region is thought to participate in the initiation and development of many different cancers. However, in bladder cancer the role of RASSF1A methylation was unclear. To evaluate the relationship between RASSF1A methylation and bladder cancer, a quantitative assessment of an independent meta-analysis was performed. In addition, a DNA methylation microarray database from the cancer genome atlas (TCGA) project was used to validate the results of the meta-analysis. METHODS: We searched published articles from computerized databases, and DNA methylation data were extracted from TCGA project. All data were analyzed by R software. RESULTS: The results of the meta-analysis indicated that the frequency of RASSF1A gene methylation in bladder cancer patients is significantly higher than in healthy controls. The hazard ratio (HR) was 2.24 (95% CI = [1.45; 3.48], P = 0.0003) for overall survival (OS), and the RASSF1A gene promoter methylation status was strongly associated with the TNM stage and differentiation grade of the tumor. The similar results were also found by the data from TCGA project. CONCLUSION: There was a significant relationship between the methylation of the RASSF1A gene promoter and bladder cancer. Therefore, RASSF1A gene promoter methylation will be a potential biomarker for the clinical diagnosis of bladder cancer.

Effect of hydrothorax EGFR gene mutation and EGFR-TKI targeted therapy on advanced non-small cell lung cancer patients.

Lung cancer is a malignancy with the highest incidence of morbidity and mortality worldwide. The lack of effective detection methods leads to the ineffectiveness of convetional therapy. The aim of the current study was to analyze the hydrothorax epidermal growth factor receptor (EGFR) mutation in patients with advanced non-small lung cancer (NSCLC) and malignant pleural effusion. A new method for clinical treatment was developed through a comparison of the difference of EGFR tyrosine kinase inhibitor (EGFR-TKI)-targeted therapy. Between January 2013 and January 2015, 68 cases diagnosed with advanced non-small lung cancer and malignant pleural effusion, were enrolled in the study. Previous first-line chemotherapeutic treatment schemes had been unsuccessful. EGFR 19 and EGFR 21 sites were detected for all the patients. Platinum-based drugs were provided for patients with wild-type EGFR. These patients served as the control group and underwent four cycles of treatments, with each cycle lasting 3 weeks. TKI medicine Gefitinib (Iressa™) was administered to patients with mutant EGFR tid, po, for a duration of 4-8 months. These patients served as the experimental group. There were 41 cases of EGFR mutations, of which 13 cases had EGFR 19 site mutations, 16 cases EGFR 21 site mutations, and the remaining 12 cases had 2 site mutations. EGFR mutations were not significant for gender, age, tumor type, stage and diameter (P>0.05). The results showed that the six-month survival rate, progression-free survival time (PFS), objective response rate (RP) and disease control rate (DCR) in the experimental group were higher than those in the control group. The drug side-effects in the experimental group indicated no statistical differences compared to the control group (P>0.05). The incidence of EGFR mutation was higher in patients with advanced non-small lung cancer and malignant pleural effusion. Targeted therapy improved the survival rate and was deemed to be a safe and effective method for patients with EGFR mutations.