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1.
Journal of Preventive Medicine ; (12): 649-652, 2019.
Article in Chinese | WPRIM | ID: wpr-815667

ABSTRACT

Objective@#To analyze the risk factors for lung cancer and to provide scientific evidence for prevention of lung cancer.@*Methods@#A total of 461 newly diagnosed patients with primary lung cancer from January 2015 to June 2017 in Shaoxing were selected as the case group. Six hundred healthy residents with the same residence,distribution of gender and age as the cases were selected as the control group by frequency matching method. A questionnaire survey was conducted to collect demographic characteristics,family history of major chronic diseases,disease history and behavioral factors. The method of case-control study and multivariate logistic regression model were used for statistical analysis of the risk factors for lung cancer.@*Results@# The results of multivariate logistic regression analysis showed that after adjusting for age and gender,family history of cancer(OR=6.606,95%CI:3.439-12.689),history of lung diseases(OR=2.836,95%CI:1.208-6.659),high level of stress(OR=2.485,95%CI:1.830-3.376),low consumption of fresh vegetables(OR=3.116,95%CI:2.470-3.930)and smoking(OR=6.029,95%CI:3.716-9.783)were risk factors for lung cancer;after adjusting for age,gender,family history of cancer,history of lung diseases,stress levels and consumption of fresh vegetables,quitting smoking for less than ten years was a risk factor for lung cancer(OR=4.751,95%CI:2.404-9.386)compared with quitting smoking for ten years or above.@*Conclusion@#Family history of cancer,history of lung diseases,high level of stress,low consumption of fresh vegetables and smoking were risk factors for lung cancer.

2.
Article | IMSEAR | ID: sea-199849

ABSTRACT

Background: Gemcitabine is a widely used cytotoxic drug in the treatment of a number of solid tumors, for instance, lung, pancreatic as well as breast cancer. As a consequence of the progressive genomic instability, the efficiency rates have eventually lowered. Genetic approach targeting one or several genes in drug targeting pathways facilitates substantially more valuable details in explaining the association between variants and also the efficacy of gemcitabine therapy. In addition, several researchers have reported ethnic discrepancies in clinical response to gemcitabine. Thus, the present study was aimed to establish the normative frequencies of genes associated with the metabolic pathway of Gemcitabine (RRM1 -37C>A (rs12806698), RRM1 -524T>C (rs11030918), CDA 79A>C (rs2072671) and CDA 435 C>T (rs1048977) in South Indian healthy population and compared with 1000 genome population. Additionally, the association of these SNPs with the risk of developing lung cancer was also evaluated.Methods: This study was carried out on 184 healthy subjects and 123 lung cancer patients of South Indian origin and genotyping was done using RT-PCR (Real Time Polymerase Chain Reaction). The frequencies of the above polymorphisms were in Hardy-Weinberg equilibrium (p >0 .05).Results: The minor allele frequencies of the SNPs RRM1 -37C>A (rs12806698), RRM1 -524T>C (rs11030918), CDA 79A>C (rs2072671) and CDA -435 C>T (rs1048977) were 31.3, 36.7, 24.5 and 22.0 respectively.Conclusions: There was a significant difference observed between the genotype and allele frequencies of south Indians with the 1000 genome populations. We also found that SNPs of RRM1 were significantly associated with lung cancer risk.

3.
Journal of Korean Medical Science ; : 1423-1428, 2015.
Article in English | WPRIM | ID: wpr-183079

ABSTRACT

Short telomeres are known as one of the risk factors for human cancers. The present study was conducted to evaluate the association between 6 polymorphisms, which were related with short telomere length in the Korean population, and lung cancer risk using 1,100 cases and 1,096 controls. Among the 6 polymorphisms, TERT rs2853669 was significantly associated with increased lung cancer risk under a recessive model (odds ratio [OR]=1.38, 95% confidence interval [CI]=1.05-1.81, P=0.02). The effect of rs2853669 on lung cancer risk was significant in younger individuals (OR=1.73, 95% CI=1.18-2.54, P=0.005) and adenocarcinoma (OR=1.50, 95% CI=1.07-2.07, P=0.02). Our results suggest that a common functional promoter polymorphism, TERT rs2853669, may influence both telomere length and lung cancer risk in the Korean population.


Subject(s)
Female , Humans , Male , Middle Aged , Adenocarcinoma/epidemiology , Case-Control Studies , Gene Frequency/genetics , Genetic Association Studies , Genetic Predisposition to Disease , Lung Neoplasms/epidemiology , Polymorphism, Single Nucleotide/genetics , Promoter Regions, Genetic/genetics , Republic of Korea/epidemiology , Telomerase/genetics , Telomere/physiology , Telomere Homeostasis/genetics
4.
Journal of Korean Medical Science ; : 221-226, 2015.
Article in English | WPRIM | ID: wpr-223791

ABSTRACT

The role of genetic polymorphisms of NAD(P)H:quinone oxidoreductase 1 (NQO1), which is known to be related to carcinogen metabolism and oxidative status, was evaluated for lung cancer development. The genotypes of two NQO1 polymorphisms, namely, IVS1-27C>G and Ex6+40C>T, were determined in 616 lung cancer cases and 616 lung cancer-free controls and haplotypes composed of the two polymorphisms were estimated. In the evaluation of the effect of the NQO1 genotypes or diplotypes, we did not find any significant association with lung cancer risk after adjusting for body mass index and smoking status. However, when we evaluated the effect of the NQO1 diplotypes for lung cancer risk in combination with smoking, smokers without the C-T/C-T diplotype showed a significantly increased risk of lung cancer compared with nonsmokers without the C-T/C-T diplotype (adjusted OR, 2.2; 95% CI, 1.67-3.02), and smokers with the C-T/C-T diplotype showed the highest OR of lung cancer (adjusted OR, 2.7; 95% CI, 1.78-4.21). Moreover, a trend test showed an additive interaction between smoking and the NQO1 C-T/C-T diplotype (P(trend) < 0.01). The additive effect of smoking and the NQO1 C-T/C-T diplotype was more apparent in squamous cell carcinoma, although this effect was statistically significant in all lung cancer cell types (all cell types, P(trend) < 0.05). This result suggests that haplotypes of the NQO1 gene play an important role in the development of lung cancer by interaction with smoking.


Subject(s)
Aged , Female , Humans , Male , Middle Aged , Carcinoma, Non-Small-Cell Lung/epidemiology , Genetic Predisposition to Disease , Haplotypes/genetics , Lung Neoplasms/epidemiology , NAD(P)H Dehydrogenase (Quinone)/genetics , Polymorphism, Single Nucleotide/genetics , Risk , Small Cell Lung Carcinoma/epidemiology , Smoking/adverse effects
5.
Environmental Health and Toxicology ; : e2013012-2013.
Article in English | WPRIM | ID: wpr-81332

ABSTRACT

OBJECTIVES: The role of genetic polymorphisms of tumor necrosis factor-alpha (TNF-alpha) for lung cancer development was evaluated. METHODS: Genotypes of the TNF-alpha polymorphisms, -1210C>T, -487A>G, -417A>G, IVS1+123G>A, and IVS3+51A>G, were determined in 616 lung cancer cases and 616 lung cancer-free controls. RESULTS: After adjusting for body mass index and smoking, each TNF-alpha genotype or haplotype composed of five TNF-alpha single nucleotide polymorphisms did not show an association with lung cancer risk (p>0.05). The statistical power was found to be 88.4%, 89.3%, 93.3%, 69.7%, and 93.9% for 1210C>T, -487A>G, -417A>G, IVS1+123G>A, and IVS3+51A>G, respectively. Furthermore, the effects of each SNP or haplotype on lung cancer risk were not found to be different according to the cell type of lung cancer (p>0.05). In the repeated analysis with only subjects without other diseases related to inflammation, there was also no association between polymorphisms or haplotypes of the TNF-alpha gene and lung cancer risk (p>0.05). CONCLUSIONS: This study found no association between common variants of the TNF-alpha gene and lung cancer risk.


Subject(s)
Body Mass Index , Genotype , Haplotypes , Inflammation , Lung Neoplasms , Lung , Polymorphism, Genetic , Polymorphism, Single Nucleotide , Smoke , Smoking , Tumor Necrosis Factor-alpha
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