Background: Stroke is one of the leading causes of death and disability for adult men and women worldwide, and a number of studies have explored the influences of smoking on stroke. However, few studies have discussed the relationship between stroke and smoking with consideration of the following factors: sex, the number of cigarettes smoked per day, stroke subtype, and the follow-up duration. Consequently, we aimed to extend previous work by using a systematic review to explore the relationship between stroke and cigarette smoking in reference to the above factors. Methods: A systematic review was conducted using the PubMed, Embase, and Cochrane Central Register databases and the following search criteria: [“stroke” (MeSH) and “smoking” (MeSH)]. All analyses were conducted with Stata, and funnel plots and Egger regression asymmetry tests were used to assess publication bias. Results: The meta-analysis included 14 studies involving 303134 subjects. According to the meta-analysis, smokers had an overall increased risk of stroke compared with nonsmokers, with a pooled odds ratio (OR) of 1.61 (95% confidence interval [CI]: 1.34–1.93, P < .001). A subgroup analysis conducted based on smoking status revealed ORs of 1.92 (95% CI: 1.49–2.48) for current smokers and 1.30 (95% CI: 0.93–1.81) for former smokers. In addition, the relationship between stroke of any type and smoking status was also statistically significant; current smokers had an increased risk of stoke compared with nonsmokers (OR: 1.46, 95% CI: 1.04–2.07, P < .001), which was influenced by sex (men: OR: 1.54, 95% CI: 1.11–2.13, P = .002; women: OR: 1.88, 95% CI: 1.45–2.44, P < .023). From the analysis, we also observed that passive smoking increased the overall risk of stroke by 45% (OR: 1.45, 95% CI: 1.0–2.11, P < .05). Based on the dose-response meta-analysis, the risk of stroke increased by 12% for each increment of 5 cigarettes per day.

Pancreatic cancer is one of the leading causes of cancer-related deaths worldwide and is characterized by highly hypoxic tumor microenvironment. Hypoxia-inducible factor-1 alpha (HIF-1α) is a major regulator of cellular response to changes in oxygen concentration, supporting the adaptation of tumor cells to hypoxia in an oxygen-deficient tumor microenvironment. Numerous studies revealed the central role of HIF-1α in the carcinogenesis and progression of pancreatic cancer. This article reviewed the molecular mechanisms of how HIF-1α regulated tumorigenesis and progression of pancreatic cancer and suggested that targeting HIF-1α and its signaling pathways could be promising therapeutics for pancreatic cancer.

Human Hox genes (Homeobox) have crucial roles in development and differentiation, regulating numerous processes including apoptosis, receptor signalling, differentiation, motility and angiogenesis. Aberrant expression of Hoxc6 gene has been reported in several tumor tissues and cancer cell lines. The prognostic significance of Hoxc6 in gastric cancer remains largely unknown.This study was aimed to investigate the clinical significance of Hoxc6 in gastric cancer.Total RNA of paired tissue samples (n=25) and a tissue microarray containing 161 paired tissues from patients with gastric cancers at different stages were collected. Quantitative real-time PCR and immunochemistry assay were carried out to investigate the expression of Hoxc6.Hoxc6 mRNA was increased in gastric cancer tissues ( 16 of 25) compared with the adjacent normal mucosa (P<0.05). Immunohistochemical detection showed that expression of Hoxc6 was associated with the depth of tumor invasion (P<0.05). Patients with higher expression levels of Hoxc6 had a shorter overall survival rate (P<0.05).Hoxc6 might contribute to the progression of gastric carcinogenesis and may be a significant predictor of poor survival in patients with gastric cancer after curative operations.

No abstract