• Asian Pacific Journal of Cancer Prevention
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• 제14권1호
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• pp.595-598
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• 2013

Background: Lung cancer is the leading cause of cancer death worldwide Therefore, identification of genetic as well as environmental factors is very important in developing novel methods of lung cancer prevention. However, this is a multi-layered problem. Therefore a lung cancer risk prediction system is here proposed which is easy, cost effective and time saving. Materials and Methods: Initially 400 cancer and non-cancer patients' data were collected from different diagnostic centres, pre-processed and clustered using a K-means clustering algorithm for identifying relevant and non-relevant data. Next significant frequent patterns are discovered using AprioriTid and a decision tree algorithm. Results: Finally using the significant pattern prediction tools for a lung cancer prediction system were developed. This lung cancer risk prediction system should prove helpful in detection of a person's predisposition for lung cancer. Conclusions: Most of people of Bangladesh do not even know they have lung cancer and the majority of cases are diagnosed at late stages when cure is impossible. Therefore early prediction of lung cancer should play a pivotal role in the diagnosis process and for an effective preventive strategy.

• Genomics & Informatics
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• 제8권4호
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• pp.194-200
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• 2010

The PIK3CA gene, oncogenic gene located on human chromosome 3q26.3, is an important regulator of cell proliferation, death, motility and invasion. To evaluate the role of PIK3CA gene in the risk of Korean lung cancer, genotypes of the PIK3CA polymorphisms (rs11709323, rs2699895, rs3729679, rs17849074 and rs1356413) were determined in 423 lung cancer patients and 443 normal controls. Statistical analyses revealed that the genotypes and haplotypes in the PIK3CA gene were not significantly associated with the risk of lung cancer in the Korean population, suggesting that these PIK3CA polymorphisms do not contribute to the genetic susceptibility to lung cancer in the Korean population.

• Journal of Preventive Medicine and Public Health
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• 제53권6호
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• pp.476-486
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• 2020

Objectives: The objective of this study was to estimate the risk of lung cancer in relation to angiotensin II receptor blocker (ARB) use among patients with hypertension from the Korean National Health Insurance Service-National Health Screening Cohort. Methods: We conducted a retrospective cohort study of patients with hypertension who started to take antihypertensive medications and had a treatment period of at least 6 months. We calculated the weighted hazard ratios (HRs) and their 95% confidence intervals (CIs) of lung cancer associated with ARB use compared with calcium channel blocker (CCB) use using inverse probability treatment weighting. Results: Among a total of 60 469 subjects with a median follow-up time of 7.8 years, 476 cases of lung cancer were identified. ARB use had a protective effect on lung cancer compared with CCB use (HR, 0.75; 95% CI, 0.59 to 0.96). Consistent findings were found in analyses considering patients who changed or discontinued their medication (HR, 0.50; 95% CI, 0.32 to 0.77), as well as for women (HR, 0.56; 95% CI, 0.34 to 0.93), patients without chronic obstructive pulmonary disease (HR, 0.75; 95% CI, 0.56 to 1.00), never-smokers (HR, 0.64; 95% CI, 0.42 to 0.99), and non-drinkers (HR, 0.69; 95% CI, 0.49 to 0.97). In analyses with different comparison antihypertensive medications, the overall protective effects of ARBs on lung cancer risk remained consistent. Conclusions: The results of the present study suggest that ARBs could decrease the risk of lung cancer. More evidence is needed to establish the causal effect of ARBs on the incidence of lung cancer.

• Asian Pacific Journal of Cancer Prevention
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• 제15권16호
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• pp.6863-6869
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• 2014

Objectives: Several preclinical and observational studies have shown that anti-diabetic medications (ADMs) may modify the risk of lung cancer. We performed a systematic review and meta-analysis evaluating the effect of metformin, sulfonylureas (SUs), thiazolidinediones (TZDs), and insulin on the risk of lung cancer in patients with diabetes mellitus (DM). Materials and Methods: We conducted a systematic search of Pubmed and Web of Science, up to August 20, 2013. We also searched the Conference Proceedings Citation Index (CPCI) and China National Knowledge Infrastructure (CNKI) for abstracts from major meetings. Fixed or random effect pooled measures were selected based on heterogeneity among studies, which was evaluated using Q test and the I2 of Higgins and Thompson. Meta-regression was used to explore the sources of between-study heterogeneity. Publication bias was analyzed by Begg's funnel plot and Egger's regression test. Associations were assessed by odds ratios (ORs) with 95% confidence intervals (CIs). Results: A total of 15 studies (11 cohort, 4 case-control) were included in this meta-analysis. In observational studies no significant association between metformin (n=11 studies; adjusted OR=0.99, 95%CI: 0.87-1.12), SUs (n=5 studies; adjusted OR=0.98, 95%CI: 0.79-1.22), or TZDs (n=7 studies; adjusted OR=0.92, 95%CI: 0.75-1.13), insulin (n=6 studies; adjusted OR=1.13, 95%CI: 0.79-1.62) use and risk of developing lung cancer was noted. There was considerable inherent heterogeneity between studies not explained by study design, setting, or location. Conclusions: Meta-analysis of existing studies does not support a protective or harmful association between ADMs use and risk of lung cancer in patients with DM. There was considerable heterogeneity across studies, and future, well-designed, prospective studies would be required for better understanding of any association.

• Safety and Health at Work
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• 제12권2호
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• pp.174-183
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• 2021

Background: Toluene diisocyanate (TDI) is a highly reactive chemical that causes sensitization and has also been associated with increased lung cancer. A risk assessment was conducted based on occupational epidemiologic estimates for several health outcomes. Methods: Exposure and outcome details were extracted from published studies and a NIOSH Health Hazard Evaluation for new onset asthma, pulmonary function measurements, symptom prevalence, and mortality from lung cancer and respiratory disease. Summary exposure-response estimates were calculated taking into account relative precision and possible survivor selection effects. Attributable incidence of sensitization was estimated as were annual proportional losses of pulmonary function. Excess lifetime risks and benchmark doses were calculated. Results: Respiratory outcomes exhibited strong survivor bias. Asthma/sensitization exposure response decreased with increasing facility-average TDI air concentration as did TDI-associated pulmonary impairment. In a mortality cohort where mean employment duration was less than 1 year, survivor bias pre-empted estimation of lung cancer and respiratory disease exposure response. Conclusion: Controlling for survivor bias and assuming a linear dose-response with facility-average TDI concentrations, excess lifetime risks exceeding one per thousand occurred at about 2 ppt TDI for sensitization and respiratory impairment. Under alternate assumptions regarding stationary and cumulative effects, one per thousand excess risks were estimated at TDI concentrations of 10 - 30 ppt. The unexplained reported excess mortality from lung cancer and other lung diseases, if attributable to TDI or associated emissions, could represent a lifetime risk comparable to that of sensitization.

• Asian Pacific Journal of Cancer Prevention
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• 제13권9호
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• pp.4465-4468
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• 2012

Objective: The conclusions of published reports on the relationship between the glutathione S-transferase M3 (GSTM3) A/B gene polymorphism and the risk of lung cancer are still debated. This meta-analysis was performed to evaluate the association between GSTM3 and the risk of lung cancer. Methods: Association investigations were identified from PubMed, Embase, and Cochrane Library, and eligible studies were included and synthesized using a meta-analysis method. Results: Eight reports were included into this meta-analysis for the association of GSTM3 A/B gene polymorphism and lung cancer susceptibility, covering 1,854 patients with lung cancer and 1,926 controls. No association between the GSTM3 A/B gene polymorphism and lung cancer was found in this meta-analysis (B allele: OR = 1.25, 95% CI: 0.89-1.76, P = 0.20; BB genotype: OR = 1.53, 95% CI: 0.71-3.32, P = 0.28; AA genotype: OR = 0.85, 95% CI: 0.59-1.23, P = 0.39). Conclusions: The GSTM3 A/B gene polymorphism is not associated with lung cancer susceptibility. However, more studies on the relationship between GSTM3 A/B gene polymorphism and the risk of lung cancer should be performed in the future.

• 보험의학회지
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• 제31권1호
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• pp.34-36
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• 2012

Lung cancer such as small cell lung cancer(SCLC) and non small cell lung cancer(NSCLC) have high mortality rate, so, we insurance doctors have little interest in their risk. But nowadays there's a lot of development in targeted therapy of NSCLC. Screening by CT scanning and early resection strategy also shows better prognosis. It is helpful for underwriters and insurance doctors to review the current development of targeted therapy of NSCLC and estimation of extra-risk of early lung cancer. The preferred treatment option for patients whose tumors contain EGFR-activating mutations are one of the EGFR-directed tyrosine kinase inhibitors, such as gefitinib or erlotinib. In patients with NSCLC whose tumors harboured an ALK rearrangement, there was 61% objective response rate to crizotinib in the phase 1 study. The median survival progression-free survival was 10 months. Mortality analysis of early lung cancer who were detected by CT screening, MR of 105% and EDR of 1‰ were calculated.

• Asian Pacific Journal of Cancer Prevention
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• 제15권15호
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• pp.6333-6337
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• 2014

Background: In this case-control study, we aimed to investigate the relationship between the methylenetetrahydrofolate reductase (MTHFR) C677T polymorphism and lung cancer. Materials and Methods: Total 200 individuals including 100 patients with lung cancer and 100 controls were analyzed. Genotyping of MTHFR C677T was performed using PCR and RFLP methods. Results: The majority of the patients were men and 90% were smokers. We found that the risk ratio for development of LC was 13-times higher in smokers compared with non-smokers between patient and control groups in our study (OR:13.5, 95%CI:6.27-29.04, p:0.0001). Besides, the risk ratio for development of LC was nine times higher in individuals with cancer history in their family than those without cancer history (OR:9.65, 95%CI: 2.79-33.36; p:0.0001). When genotype distributions and allele frequencies were analyzed in the study groups, no significant difference was apparent (${\chi}^2$:0.53, p=0.76). In addition, no correlation between genotypes of MTHFRC677T polymorphism and histological type of LC was found (${\chi}^2$:0.99, p=0.60). Conclusions: These results suggest that there was no association between the MTHFR C677T polymorphism and lung cancer in the Turkish population.

• Asian Pacific Journal of Cancer Prevention
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• 제15권5호
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• pp.1993-1999
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• 2014

Background: This study aimed to explore the role of XRCC1 (Arg399Gln) and XPD (Lys751Gln) gene polymorphisms, lifestyle and environmental factors as well as their possible interactions in propensity to develop lung cancer in a population with high incidence from North East India. Materials and Methods: A total of 272 lung cancer cases and 544 controls were collected and XRCC1 (Arg399Gln) and XPD (Lys751Gln) genotypes were analyzed using a polymerase chain reaction based restriction fragment length polymorphism assay. Conditional multiple logistic regression analysis was used to calculate adjusted odds ratios and 95% confidence intervals after adjusting for confounding factors. Results: The combined Gln/Gln genotype of XRCC1 and XPD genes (OR=2.78, CI=1.05-7.38; p=0.040) was significantly associated with increased risk for lung cancer. Interaction of XRCC1Gln/Gln genotype with exposure of wood combustion (OR=2.56, CI=1.16-5.66; p=0.020), exposure of cooking oil fumes (OR=3.45, CI=1.39-8.58; p=0.008) and tobacco smoking (OR=2.54, CI=1.21-5.32; p=0.014) and interaction of XPD with betel quid chewing (OR=2.31, CI=1.23-4.32; p=0.009) and tobacco smoking (OR=2.13, CI=1.12-4.05; p=0.022) were found to be significantly associated with increased risk for lung cancer. Conclusions: Gln/Gln alleles of both XRCC1 and XPD genes appear to amplify the effects of household exposure, smoking and betel quid chewing on lung cancer risk in the study population.

• Asian Pacific Journal of Cancer Prevention
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• 제15권24호
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• pp.10653-10658
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• 2015

Background: A very high incidence of lung cancer is observed in Mizoram and Manipur, North East India. We conducted a population based case control study to establish associations of p53 codon 72 polymorphisms and interactions with environmental factors for this high incidence. Material and Methods: A total of 272 lung cancer cases and 544 controls matched for age (${\pm}5years$), sex and ethnicity were collected and p53 codon 72 polymorphism genotypes were analyzed using a polymerase chain based restriction fragment length polymorphism assay. We used conditional multiple logistic regression analysis to calculate adjusted odds ratios and 95% confidence intervals after adjusting for confounding factors. Results: p53 Pro/Pro genotype was significantly associated with increased risk of lung cancer in the study population (adjusted OR=2.14, CI=1.35-3.38, p=0.001). Interactions of the p53 Pro/Pro genotype with exposure to wood smoke (adjusted OR=3.60, CI=1.85-6.98, p<0.001) and cooking oil fumes (adjusted OR=3.27, CI=1.55-6.87, p=0.002), betel quid chewing (adjusted OR=3.85, CI=1.96-7.55, p<0.001), tobacco smoking (adjusted OR=4.42, CI=2.27-8.63, p<0.001) and alcohol consumption (adjusted OR=3.31, CI=1.10-10.03, p=0.034) were significant regarding the increased risk of lung cancer in the study population. Conclusions: The present study provided preliminary evidence that a p53 codon 72 polymorphism may effect lung cancer risk in the study population, interacting synergistically with environmental factors.