Rihong Cong

Cigarette Smoking and the Risk of Endometrial Cancer: A Meta-Analysis

OBJECTIVE Epidemiologic findings are inconsistent concerning the association of endometrial cancer risk with cigarette smoking. We conducted a meta-analysis of epidemiologic studies to examine this relation. METHODS A systematic literature search up to June of 2007 was performed in MEDLINE and EMBASE. Study-specific risk estimates were pooled using a random-effects model. RESULTS Ten prospective and 24 case-control studies were included in the analysis of the effect of ever smoking. Ever smoking was statistically significantly associated with a reduced risk of endometrial cancer among prospective studies (relative risk 0.81; 95% confidence interval [CI], 0.74-0.88) and case-control studies (odds ratio 0.72; 95% CI, 0.66-0.79). The inverse association was significant among current and former smokers. Six prospective and 6 case-control studies were included in the quantitative analysis. We noted that an increase in smoking of 20 cigarettes per day was statistically significantly associated with 16% and 27% reduced risks of endometrial cancer in prospective and case-control studies, respectively. We also found that cigarette smoking was significantly associated with a decreased risk of endometrial cancer among postmenopausal women (relative risk 0.71; 95% CI, 0.65-0.78) but not among premenopausal women. In addition, the risk reduction seemed to be stronger among hormone replacement therapy users than nonusers. CONCLUSION Cigarette smoking was found to be significantly associated with a reduced risk of endometrial cancer, especially among postmenopausal women.

Hormone replacement therapy and ovarian cancer risk: A meta-analysis

OBJECTIVES Epidemiologic findings are inconsistent concerning the risk for ovarian cancer associated with hormone replacement therapy (HRT). We conducted a meta-analysis to summarize the available evidence from observational studies to examine this relation. METHODS We searched PUBMED and MEDLINE for relevant studies that were published from January 1, 1966, through May 1, 2007. Study-specific risk estimates were pooled by the use of a random-effects model. RESULTS Eight cohort (including 4715 cases and 1,555,374 participants) and 19 case-control studies (involving 8240 cases and 20,996 controls) were included. We found a summary relative risk (RR) of 1.24 (95% confidence interval [CI] 1.15-1.34) from cohort studies and a summary odds ratio [OR] of 1.19 (95%CI 1.02-1.40) from case-control studies for ever HRT use. However, the risk estimates of case-control studies might be upwardly biased. Summary risk estimates of four cohort and six case-control studies that distinguished estrogen replacement treatment (ERT) and estrogen-progestin replacement treatment (EPRT) from HRT both indicated that association was stronger among ERT user than EPRT user. Based on data abstracted from six case-control studies, duration of HRT use was not significant. The summary risk estimates for less than 5 years, 6-10, and more than 10 years use were 1.02, 1.13, and 1.21, respectively and 95%CI for each estimate crossed 1.0. CONCLUSION HRT use was associated with increased risk of ovarian cancer. These findings may expand the range of possible risks associated with HRT use. However, this positive association should also be considered in the context of HRTs other favorable effects on health.

Smoking and the Risk of Age-related Macular Degeneration: A Meta-Analysis

PURPOSE Some studies were undertaken to evaluate the association between cigarette smoking and age-related macular degeneration (AMD). This meta-analysis summarized the risk estimate of smoking and AMD and provided robust evidence for the association. METHODS Relevant studies were identified by searching PubMed and MEDLINE (from 1966 to June 2007) and reviewing the reference lists of key articles. The summary relative risk ratio (RR) or odds ratio (OR) and 95% confidence interval (CI) were calculated. Study-specific risk estimates were pooled using a random-effects model. RESULTS Five prospective cohort and eight case-control studies met our inclusion criteria. Ever smoking was statistically significant associated with increased risk of AMD among cohort studies (RR, 1.61; 95% CI, 1.01-2.57) or case-control studies (RR, 1.76; 95% CI, 1.56-1.99). Current smokers were at higher risk of AMD than past smokers. Both geographic atrophy (GA) and neovascular AMD (NV) are subtypes of AMD. A significant relationship was found between smoking and GA risk. Smoking increased the risk of NV, with marginal nonsignificance (RR, 1.47; 95% CI, 0.92-2.37) in cohort studies and significance in case-control studies (RR, 1.96; 95% CI, 1.69-2.27). CONCLUSIONS This meta-analysis indicated smoking, especially current smoking, was significantly associated with increased risks of AMD and its subtypes.

Gly82Ser Polymorphism of the Receptor for Advanced Glycation End Products Is Associated with an Increased Risk of Gastric Cancer in a Chinese Population

Purpose: It has been shown that the expression of the receptor for advanced glycation end products (RAGE) is closely associated with invasion and metastasis in gastric cancer. A Gly82Ser polymorphism in exon 3 of RAGE gene was identified and thought to have an effect on the functions of its protein. Therefore, the goal of the present study was to investigate whether the polymorphism is involved in the development or progression of gastric cancer. Experimental Design: In the hospital-based case-control study, the RAGE genotypes were determined using PCR-RFLP in 566 individuals (283 gastric cancer patients and 283 age- and sex-matched controls). Results: The distribution of genotype was significantly different between cases and controls (P = 0.038). Compared with the wild-type 82Gly/Gly carriers, subjects with the variant genotypes (82Gly/Ser and 82Ser/Ser) had a significantly higher risk of gastric cancer (adjusted odds ratio, 1.47; 95% confidence interval, 1.05-2.06). Moreover, the elevated gastric cancer risk was especially evident in younger individuals (ages ≤58 years), nonsmokers, and rural subjects. Further analyses revealed that the variant genotypes were associated with adjacent organ invasion in the subanalysis of gastric cancer patients. Conclusions: Our findings indicate that the RAGE Gly82Ser polymorphism may confer not only an increased risk of gastric cancer but also with invasion of gastric cancer in the Chinese population.

Genetic variant in glutathione peroxidase 1 gene is associated with an increased risk of coronary artery disease in a Chinese population

BACKGROUND Glutathione peroxidase 1 (GPX1), the key antioxidant enzyme in vascular endothelial cells, has been shown to exert a protective effect against the presence of coronary artery disease (CAD). The 198Pro/leu variant, located at codon 198 of GPX1 gene, has recently been linked to cardiovascular disease, but data were inconsistent. We investigated the association between the occurrence of CAD and the 198Pro/leu variant in a Chinese population. METHODS A total of 265 unrelated CAD patients and 265 age- and sex-matched control subjects were recruited in this study. The GPX1 198Pro/leu genotype was determined using polymerase chain reaction-restriction fragment length polymorphism. RESULTS Compared to the 198Pro/Pro carriers, subjects with the variant genotypes (198Pro/leu and 198Leu/leu) had a significantly higher risk of CAD (adjusted OR=2.02, 95%CI=1.27-3.22). In stratified analyses, the variant genotypes were significantly associated with increased CAD risk in subjects <64 y (adjusted OR=2.41, 95%CI=1.16-4.98), males (adjusted OR=1.86, 95%CI=1.09-3.18) and non-smokers (adjusted OR=2.40, 95%CI=1.15-5.01). However, no significant association was observed between this variant and the severity of CAD. CONCLUSION These data provide evidence that GPX1 198Pro/leu variant genotypes are significantly associated with CAD risk in this Chinese population.

Protective effect of an endothelial lipase gene variant on coronary artery disease in a Chinese population.

The aim of the present study was to assess the influence of the endothelial lipase (EL) gene 584C/T variant, which results in a change at codon 111 of the EL gene from threonine to isoleucine, on the risk of coronary artery disease (CAD) in a Chinese population. The study population consisted of 265 CAD patients and 265 age- and sex-matched control subjects. The T allele frequency was significantly lower among CAD patients than among control subjects (18.3% vs. 29.8%; P < 0.001). In both the CAD and control groups, the T allele carriers had higher high density lipoprotein cholesterol (HDL-C) levels than homozygote C allele carriers. In a multiple logistic regression model adjusted for age, sex, body mass index, smoking, hypertension, diabetes, hyperlipidemia, and low density lipoprotein cholesterol, a significantly decreased risk of developing CAD was found in subjects carrying a variant CT or TT genotype (odds ratio = 0.496, 95% confidence interval = 0.341–0.723; P < 0.001), and the significance persisted after further adjustment for HDL-C. In conclusion, our observation that the EL 584T allele was associated with protection from CAD in this Chinese population replicates the findings in a Japanese study, which found a similar association of this allele with acute myocardial infarction, independent of HDL-C levels.

A polymorphism in the resistin gene promoter and the risk of coronary artery disease in a Chinese population

Objective  Resistin, a novel adipocyte‐derived peptide, has been linked to the pathogenesis of atherosclerosis. Recently, –420C>G, a variant located in the promoter region of the resistin gene (RETN) was identified. The aim of this study was to investigate the association between this RETN–420C>G polymorphism and the risk of coronary artery disease (CAD).

Effect of Genistein on vasculogenic mimicry formation by human uveal melanoma cells

BackgroundVasculogenic mimicry (VM) was increasingly recognized as a form of aggressive melanoma acquiring blood supply. Genistein had attracted much attention as a potential anticancer agent. Therefore, we examined the effect of Genistein on VM in human uveal melanoma cells.MethodsVM structure was detected by periodic acid-Schiff (PAS) staining for uveal melanoma C918 cells cultured on the three-dimensional type I collagen gels after exposed to Genistein. We used reverse transcription polymerase chain reaction (RT-PCR) and Western Blot analysis to examine the effect of Genistein on vascular endothelial cadherin (VE-cadherin) mRNA and protein expression. The nude mice models of human uveal melanoma C918 cells were established to assess the number of VM using immunohistochemical and PAS double-staining.ResultsGenistein inhibited the survival of C918 cells in vitro. The ectopic model study showed that VM in tumor tissue sections were significantly reduced by Genistein in vivo. In vitro, the VM structure was found in control, 25 and 50 μM Genistein-treatment groups but not in 100 and 200 μM. RT-PCR and Western Blot showed that 100 and 200 μM concentration of Genistein could significantly decrease VE-cadherin mRNA and protein expression of C918 cells compared with control (P < 0.05). However, the 25 and 50 μM Genistein slightly decreased the VE-cadherin level in vitro (P > 0.05).ConclusionGenistein inhibits VM formation of uveal melanoma cells in vivo and in vitro. One possible underlying molecular mechanism by which Genistein could inhibit VM formation of uveal melanoma is related to down-regulation of VE-cadherin.

A polymorphism in the resistin gene promoter is related to increased C-reactive protein levels in patients with coronary artery disease.

BACKGROUND Resistin, a novel adipocyte-derived peptide, has been linked to inflammatory process and coronary artery disease (CAD). The -420C>G polymorphism located in the resistin gene (RETN) promoter has recently been suggested to play a potential role in proinflammatory conditions (e.g., atherogenesis). However, whether this polymorphism has any effect on the inflammatory process in patients with stable CAD is unclear. METHODS The RETN -420C>G polymorphism was determined by using PCR-restriction fragment length polymorphism. Plasma lipid profiles, glucose and high-sensitivity C-reactive protein (hs-CRP) were measured in fasting state. RESULTS Patients with variant genotypes (CG+GG) had significantly higher levels of hs-CRP than CC carriers (adjusted p<0.001). In addition, the variant genotypes were observed to be independently associated with higher hs-CRP levels (>3 mg/L, p=0.004). However, no association was found between this polymorphism and plasma lipids or glucose levels. CONCLUSION Our data suggest that the RETN -420C-to-G variant is associated with increased CRP levels in patients with stable CAD, suggesting that the RETN -420C>G polymorphism may be potentially involved in the inflammatory component of atherogenesis through an enhanced production of CRP.