No abstract

Background The KIF5B-RET fusion gene is a novel oncogene that has been observed in a subset of lung cancers in recent years. However, the results of related epidemiological studies remain unclear. Thus, a meta-analysis was conducted to evaluate the correlation of KIF5B-RET expression based on RT-PCR detection with clinicopathological features and prognosis of lung cancer. Methods The PubMed, Google Scholar, Wiley Online, SpringerLink and Chinese National Knowledge Infrastructure databases were searched to identify the eligible studies. The association of the occurrence of KIF5B-RET fusion gene in lung cancer with age, gender, smoking status, histology type, differentiation and TNM stage was analyzed. HR, overall survival (OS) and progression-free survival (PFS) were used to describe the prognosis of patients with lung cancer. The OR and 95% CI were calculated to assess the correlations. Random- and fixed-effects models were used to analyze the data. Results A total of 13 studies, which included 8,859 lung cancer patients, were included in the study based on the inclusion criteria. A total of 121 patients with positive KIF5B-RET fusion gene status were detected, with a positive expression rate of 1.36%. KIF5B-RET fusion gene status was identified at significantly higher frequencies in female (OR=0.67, 95% CI=0.48–0.94) than male patients, and the same trend was found in young (<60 years) patients (OR=0.08, 95% CI=0.01–0.45) compared with old patients (≥60 years). No differences were found in the TNM stage, histology, differentiation and smoking. Based on the prognosis, no difference was found between the status of the positive and negative KIF5B-RET fusion genes in OS and PFS of patients. Conclusion The KIF5B-RET fusion gene occurred predominantly in young female patients with lung cancer. However, the relationship between the expression of the fusion gene and the prognosis of lung patients remains unclear.

No abstract

Background/Aims: Von Hippel-Lindau gene (VHL) has been reported as a tumor-suppressor gene in some cancers. However, the association between VHL promoter hypermethylation and renal cell carcinoma (RCC) remains to be clarified. We are the first to systematically integrate published papers to assess the role of hypermethylated VHL in RCC. Methods: The potential relevant papers were searched via PubMed, Embase, EBSCO, CNKI, and Wanfang databases. The overall odds ratio (OR) and corresponding 95% confidence interval (95% CI) were calculated to evaluate the relationship between VHL promoter hypermethylation and RCC. Results: Finally, a total of 1,998 RCC patients and 294 controls from 13 eligible articles were included in this meta-analysis. Under the fixed-effects model, the pooled OR from seven studies including 596 RCC and 294 nonmalignant samples showed that VHL promoter hypermethylation was significantly higher in cancer than in controls (OR = 7.93, 95% CI = 2.84- 22.15, P < 0.001). Subgroup analysis based on ethnic population and testing method revealed that hypermethylated VHL had a significantly similar OR value in different races and detection methodologies. No significant association was found between hypermethylated VHL and tumor grade, tumor stage, tumor size, histological types, and lymph node status in cancer (all P > 0.05). In the current study, there was no evidence of publication bias as determined by Egger's test (all P > 0.05). Conclusions: In the investigated patients, VHL promoter hypermethylation, which may play an important role in carcinogenesis of RCC, is significantly associated with an increased risk of RCC. However, VHL promoter hypermethylation is not correlated with specific clinicopathological characteristics. Additional future studies are needed to confirm our results.

An antisense strategy by targeting both bcr3/abl2 and VEGF was designed to suppress the growth of Philadephia 1 leukemia cells in vitro and in vivo in mice. In vitro, although bcr3/abl2 or VEGF antisense oligodeoxyribonucleotides (AS-ODNs) alone was able to inhibit the proliferation of K562 cells, the combination of bcr3/abl2 and VEGF AS-ODNs produced an additive inhibitory effect on the growth of K562 cells and significantly enhanced the sensibility of K562 cells to apoptosis-inducing stimuli including STI571. In vivo, the nude mice xenografted with K562 cells received intratumoral injections of bcr3/abl2 and VEGF AS-ODNs showed a significant reduction in leukemia tumor size and microvessel density and an increase of apoptosis in the tumors when compared to the mice that received an individual agent. These results demonstrate that targeting both bcr3/abl2 and VEGF can result in an additive tumor-suppressive action and may represent an excellent strategy to augment the efficacy of chemotherapy in CML.