• Asian Pacific Journal of Cancer Prevention
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• 제16권5호
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• pp.1759-1764
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• 2015

Purpose: To establish the concept of lung cancer hazard assessment theoretical models, evaluating the degree of lung cancer risk of Beijing for regional population lung cancer hazard assessment to provide a basis for technical support. Materials and Methods: ISO standards were used to classify stratified analysis for the entire population, life cycle, processes and socioeconomic management. Associated risk factors were evaluated as lung cancer hazard risk assessment first class indicators. Study design: Using the above materials, indicators were given the weight coefficients, building lung cancer risk assessment theoretical models. Regional data for Beijing were entered into the theoretical model to calculate the parameters of each indicator and evaluate the degree of local lung cancer risk. Results: Adopting the concept of lung cancer hazard assessment and theoretical models for regional populations, we established a lung cancer hazard risk assessment system, including 2 first indicators, 8 secondary indicators and 18 third indicators. All indicators were given weight coefficients and used as information sources. Score of hazard for lung cancer was 84.4 in Beijing. Conclusions: Comprehensively and systematically building a lung cancer risk assessment theoretical model for regional populations in conceivable, evaluating the degree of lung cancer risk of Beijing, providing technical support and scientific basis for interventions for prevention.

• Journal of Preventive Medicine and Public Health
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• 제48권6호
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• pp.280-286
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• 2015

Objectives: Approximately 10% to 15% of lung cancer cases occur in never-smokers. Hormonal factors have been suggested to lead to an elevated risk of lung cancer in women. This systematic review (SR) aimed to investigate the association between hormonal replacement therapy (HRT) and the risk of lung cancer in women using cohort studies. Methods: We first obtained previous SR articles on this topic. Based on these studies we made a list of refereed, cited, and related articles using the PubMed and Scopus databases. All cohort studies that evaluated the relative risk of HRT exposure on lung cancer occurrence in women were selected. Estimate of summary effect size (sES) with 95% confidence intervals (CIs) were calculated. Results: A total of 14 cohort studies were finally selected. A random effect model was applied due to heterogeneity (I-squared, 64.3%). The sES of the 14 articles evaluating the impact of HRT exposure on lung cancer occurrence in women indicated no statistically significant increase in lung cancer risk (sES, 0.99; 95% CI, 0.90 to 1.09). Conclusions: These results showed that HRT history had no effect on the risk of lung cancer in women, even though the sES of case-control studies described in previous SR articles indicated that HRT had a protective effect against lung cancer. It is necessary to conduct a pooled analysis of cohort studies.

• Environmental Analysis Health and Toxicology
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• 제28권
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• pp.12.1-12.5
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• 2013

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.

• Asian Pacific Journal of Cancer Prevention
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• 제15권7호
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• pp.3071-3074
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• 2014

Background: To investigate the related risk factors of postoperative nosocomial pneumonia (POP) in patients withI-IIIa lung cancer. Methods: Medical records of 511 patients who underwent resection for lung cancer between January 2012 to December 2012 were retrospectively reviewed. Risk factors of postoperative pneumonia were identified and evaluated by univariate and multivariate analyses. Results: The incidence of postoperative pneumonia in these lung cancer patients was 2.9% (15 cases). Compared with 496 patients who had no pneumonia infection after operation, older age (>60), histopathological type of squamous cell carcinoma and longer surgery time (>3h) were significant risk factors by univariate analysis. Other potential risk factors such as alcohol consumption, history of smoking, hypersensitivity, hypertension, diabetes mellitus and so on were not showed such significance in this study. Further, the multivariate analysis revealed that old age (>60 years) (OR 5.813, p=0.018) and histopathological type of squamous cell carcinoma (OR 5.831, p<0.001) were also statistically significant independent risk factors for postoperative pneumonia. Conclusions: This study demonstrated that being old aged (>60 years) and having squamous cell carcinoma histopathological type might be important factors in determining the risk of postoperative pneumonia in lung cancer patients after surgery.

• Asian Pacific Journal of Cancer Prevention
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• 제15권23호
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• pp.10539-10542
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• 2015

A method to predict the risk of lung cancer is proposed, based on two feature selection algorithms: Fisher and ReliefF, and BP Neural Networks. An appropriate quantity of risk factors was chosen for lung cancer risk prediction. The process featured two steps, firstly choosing the risk factors by combining two feature selection algorithms, then providing the predictive value by neural network. Based on the method framework, an algorithm LCRP (lung cancer risk prediction) is presented, to reduce the amount of risk factors collected in practical applications. The proposed method is suitable for health monitoring and self-testing. Experiments showed it can actually provide satisfactory accuracy under low dimensions of risk factors.

• Asian Pacific Journal of Cancer Prevention
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• 제16권7호
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• pp.2713-2717
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• 2015

Background: Possible associations between the single nucleotide polymorphism (SNP) rs8034191 in the aminoglycosidephosphotransferase domain containing 1 (AGPHD1) gene and lung cancer risk have been studied by many researchers but the results have been contradictory. Materials and Methods: A computerized search for publications on rs8034191 and lung cancer risk was performed. Odds ratios (ORs) with 95% confidence intervals (CIs) were calculated to assess the association between rs8034191 and lung cancer risk with 13 selected case-control studies. Sensitivity analysis, test of heterogeneity, cumulative meta-analysis, and assessment of bias were also performed. Results: A significant association between rs8034191 and lung cancer susceptibility was found using the dominant genetic model (OR=1.344, 95% CI: 1.285-1.406), the additive genetic model (OR=1.613, 95% CI: 1.503-1.730), and the recessive genetic model (OR=1.408, 95% CI: 1.319-1.503). Moreover, an increased lung cancer risk was found with all genetic models after stratification of ethnicity. Conclusions: The association between rs8034191 and lung cancer risk was significant using multiple genetic models, suggesting that rs8034191 is a risk factor for lung cancer. Further functional studies of this polymorphism and lung cancer risk are warranted.

• Asian Pacific Journal of Cancer Prevention
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• 제16권15호
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• pp.6685-6690
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• 2015

Background: Genetic studies have shown a possible relationship between the rs16969968 polymorphism in CHRNA5 and the risk of lung cancer. However, the results have been conflicting. Thus we rigorously conducted a meta-analysis to clarify any association. Materials and Methods: A total of 10 case-control studies involving 17,962 lung cancer cases and 77,216 control subjects were analysed. Odds ratios (ORs) with 95% confidence intervals (CIs) were used to measure the strength of the association. Results: We found the CHRNA5 rs16969968 polymorphism to be associated with the risk of lung cancer (AA vs GG: OR=1.60, 95%CI=1.51-1.71). On stratified analysis by smoking status, a statistically significant increased risk was observed in the smoking group (AA vs GG: OR=1.80, 95%CI=1.61-2.01). However, this polymorphism was not associated with lung cancer risk in Asians (AA vs GG: OR=0.95, 95%CI=0.35-2.59), whereas it was linked to increased risk of lung cancer among Caucasians (AA vs GG: OR=1.65, 95%CI=1.55-1.76). Conclusions: Our meta-analysis provided statistical evidence for a strong association between rs16969968 polymorphism and the risk of lung cancer, especially in smokers and Caucasians. Application of this relationship may contribute to identification of individuals at high risk of lung cancer and indicate a chemoprevention target.

• Asian Pacific Journal of Cancer Prevention
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• 제14권3호
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• pp.1937-1943
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• 2013

Altered expression or function of manganese superoxide dismutase (MnSOD) has been shown to be associated with cancer risk but assessment of gene polymorphisms has resulted in inconclusive data. Here a search of published data was made and 22 studies were recruited, covering 20,025 case and control subjects, for meta-analyses of the association of MnSOD polymorphisms with the risk of prostate, esophageal, and lung cancers. The data on 12 studies of prostate cancer (including 4,182 cases and 6,885 controls) showed a statistically significant association with the risk of development in co-dominant models and dominant models, but not in the recessive model. Subgroup analysis showed there was no statistically significant association of MnSOD polymorphisms with aggressive or nonaggressive prostate cancer in different genetic models. In addition, the data on four studies of esophageal cancer containing 620 cases and 909 controls showed a statistically significant association between MnSOD polymorphisms and risk in all comparison models. In contrast, the data on six studies of lung cancer with 3,375 cases and 4,050 controls showed that MnSOD polymorphisms were significantly associated with the decreased risk of lung cancer in the homozygote and dominant models, but not the heterozygote model. A subgroup analysis of the combination of MnSOD polymorphisms with tobacco smokers did not show any significant association with lung cancer risk, histological type, or clinical stage of lung cancer. The data from the current study indicated that the Ala allele MnSOD polymorphism is associated with increased risk of prostate and esophageal cancers, but with decreased risk of lung cancer. The underlying molecular mechanisms warrant further investigation.

• Nuclear Engineering and Technology
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• 제40권7호
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• pp.539-550
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• 2008

Lung cancer is the most prevalent global cancer, ${\sim}90%$ of which is caused by cigarette smoking. The LNT hypothesis has been inappropriately applied to estimate lung cancer risk due to ionizing radiation. A threshold of ${\sim}1\;Gy$ for lung cancer has been observed in never smokers. Lung cancer risk among nuclear workers, radiologists and diagnostically exposed patients was typically reduced by ${\sim}40%$ following exposure to <100 mSv low LET radiation. The consistency and magnitude of reduced lung cancer in nuclear workers and occurrence of reduced lung cancer in exposed non-worker populations could not be explained by the HWE. Ecologic studies of indoor radon showed highly significant reductions in lung cancer risk. A similar reduction in lung cancer was seen in a recent well designed case-control study of indoor radon, indicating that exposure to radon at the EPA action level is associated with a decrease of ${\sim}60%$ in lung cancer. A cumulative whole-body dose of ${\sim}1\;Gy$ gamma rays is associated with a marked decrease in smoking-induced lung cancer in plutonium workers. Low dose, low LET radiation appears to increase apoptosis mediated removal of $\alpha$-particle and cigarette smoke transformed pulmonary cells before they can develop into lung cancer.

• Tuberculosis and Respiratory Diseases
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• 제69권1호
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• pp.1-15
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• 2010

Lung cancer remains the most common cause of cancer death in the United States and worldwide. About 80~90% of cases are smoking-related and smoking cessation programs are of great importance in reducing lung cancer risk. However, the lifetime risk for lung cancer remains elevated even in ex-smokers. Chemoprevention holds the promise to further reduce this risk and thus to decrease lung cancer incidence and mortality. Over the last decades, most chemoprevention trials for lung cancer have yielded negative outcomes. Population-based studies suggest that high intake of certain foods such as soy, red wine or green vegetables may be associated with decreased cancer risk. Because of these observations and their general safety, a plethora of natural compounds is currently being studied for the chemoprevention of cancer. In this review we discuss promising in vitro and in vivo data of novel natural compounds, their interference with molecular mechanisms responsible for lung cancer development and potential implications for their further preclinical and clinical investigation.