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Lung Cancer Risk (lung + cancer_risk)
Selected AbstractsGenetic Predictor of Lung Cancer RiskCA: A CANCER JOURNAL FOR CLINICIANS, Issue 4 2008Article first published online: 31 DEC 200 No abstract is available for this article. [source] Lung cancer risk associated with occupational exposure to nickel, chromium VI, and cadmium in two population-based case,control studies in MontrealAMERICAN JOURNAL OF INDUSTRIAL MEDICINE, Issue 5 2010Rachelle Beveridge MSc Abstract Background Nickel, chromium VI, and cadmium have been identified as lung carcinogens in highly exposed cohorts. The purpose of this study was to examine the etiological link between lung cancer and these metals in occupations, that usually entail lower levels of exposure than those seen in historical cohorts. Methods Two population-based case,control studies were conducted in Montreal, from 1979 to 1986 and from 1996 to 2001, comprising 1,598 cases and 1,965 controls. A detailed job history was obtained to evaluate lifetime occupational exposure to many agents, including nickel, chromium VI, and cadmium compounds. Results Lung cancer odds ratios were increased only among former or non-smokers: 2.5 (95% CI: 1.3,4.7) for nickel exposure, 2.4 (95% CI: 1.2,4.8) for chromium VI, and 4.7 (95% CI: 1.5,14.3) for cadmium. The metals did not increase risk among smokers. Conclusions While excess risks due to these metal compounds were barely discernable among smokers, carcinogenic effects were seen among non-smokers. Am. J. Ind. Med. 53:476,485, 2010. © 2010 Wiley-Liss, Inc. [source] Polymorphisms in innate immunity genes and lung cancer risk in Xuanwei, China,ENVIRONMENTAL AND MOLECULAR MUTAGENESIS, Issue 4 2009Min Shen Abstract The high incidence of lung cancer in Xuanwei County, China has been attributed to exposure to indoor smoky coal emissions that contain polycyclic aromatic hydrocarbons (PAHs). The inflammatory response induced by coal smoke components may promote lung tumor development. We studied the association between single nucleotide polymorphisms (SNPs) in genes involved in innate immunity and lung cancer risk in a population-based case,control study (122 cases and 122 controls) in Xuanwei. A total of 1,360 tag SNPs in 149 gene regions were included in the analysis. FCER2 rs7249320 was the most significant SNP (OR: 0.30; 95% CI: 0.16,0.55; P: 0.0001; false discovery rate value, 0.13) for variant carriers. The gene regions ALOX12B/ALOX15B and KLK2 were associated with increased lung cancer risk globally (false discovery rate value <0.15). In addition, there were positive interactions between KLK15 rs3745523 and smoky coal use (OR: 9.40; Pinteraction = 0.07) and between FCER2 rs7249320 and KLK2 rs2739476 (OR: 10.77; Pinteraction = 0.003). Our results suggest that genetic polymorphisms in innate immunity genes may play a role in the genesis of lung cancer caused by PAH-containing coal smoke. Integrin/receptor and complement pathways as well as IgE regulation are particularly noteworthy. Environ. Mol. Mutagen., 2009. Published 2009 Wiley-Liss, Inc. [source] A variant of the Cockayne syndrome B gene ERCC6 confers risk of lung cancer,,HUMAN MUTATION, Issue 1 2008Zhongning Lin Abstract Cockayne syndrome B protein (ERCC6) plays an essential role in DNA repair. However, the Cockayne syndrome caused by the ERCC6 defect has not been linked to cancer predisposition; likely due to the fact that cells with severe disruption of the ERCC6 function are sensitive to lesion-induced apoptosis, thus reducing the chance of tumorigenesis. The biological function and cancer susceptibility of a common variant rs3793784:C>G (c.,6530C>G) in the ERCC6 was examined. We show that the c.,6530C allele has lower binding affinity of Sp1 by EMSA and displays a lower transcriptional activity in vitro and in vivo. We then examined the contribution of this polymorphism to the risk of lung cancer in a case,control study with 1,000 cases and 1,000 controls. The case,control analysis revealed a 1.76-fold (P= × 10,9) excess risk of developing lung cancer for the c.,6530CC carriers compared with noncarriers. The c.,6530CC interacts with smoking to intensify lung cancer risk, with the odds ratio (OR)=9 for developing lung cancer among heavy smokers. Our data constituted strong evidence that ERCC6 rs3793784:C>G alters its transcriptional activity and may confer personalized susceptibility to lung cancer. Hum Mutat 29(1), 113,122, 2008. Published 2007, Wiley-Liss, Inc. [source] Fruit and vegetable consumption and lung cancer risk: Updated information from the European Prospective Investigation into Cancer and Nutrition (EPIC)INTERNATIONAL JOURNAL OF CANCER, Issue 5 2007Jakob Linseisen Abstract The association of fruit and vegetable consumption and lung cancer incidence was evaluated using the most recent data from the European Prospective Investigation into Cancer and Nutrition (EPIC), applying a refined statistical approach (calibration) to account for measurement error potentially introduced by using food frequency questionnaire data. Between 1992 and 2000, detailed information on diet and life-style of 478,590 individuals participating in EPIC was collected. During a median follow-up of 6.4 years, 1,126 lung cancer cases were observed. Multivariate Cox proportional hazard models were applied for statistical evaluation. In the whole study population, fruit consumption was significantly inversely associated with lung cancer risk while no association was found for vegetable consumption. In current smokers, however, lung cancer risk significantly decreased with higher vegetable consumption; this association became more pronounced after calibration, the hazard ratio (HR) being 0.78 (95% CI 0.62,0.98) per 100 g increase in daily vegetable consumption. In comparison, the HR per 100 g fruit was 0.92 (0.85,0.99) in the entire cohort and 0.90 (0.81,0.99) in smokers. Exclusion of cases diagnosed during the first 2 years of follow-up strengthened these associations, the HR being 0.71 (0.55,0.94) for vegetables (smokers) and 0.86 (0.78,0.95) for fruit (entire cohort). Cancer incidence decreased with higher consumption of apples and pears (entire cohort) as well as root vegetables (smokers). In addition to an overall inverse association with fruit intake, the results of this evaluation add evidence for a significant inverse association of vegetable consumption and lung cancer incidence in smokers. © 2007 Wiley-Liss, Inc. [source] Dietary zinc, copper and selenium, and risk of lung cancerINTERNATIONAL JOURNAL OF CANCER, Issue 5 2007Somdat Mahabir Abstract Zinc, copper and selenium are important cofactors for several enzymes that play a role in maintaining DNA integrity. However, limited epidemiologic research on these dietary trace metals and lung cancer risk is available. In an ongoing study of 1,676 incident lung cancer cases and 1,676 matched healthy controls, we studied the associations between dietary zinc, copper and selenium and lung cancer risk. Using multiple logistic regression analysis, the odds ratios (OR) and 95% confidence intervals (CI) of lung cancer for all subjects by increasing quartiles of dietary zinc intake were 1.0, 0.80 (0.65,0.99), 0.64 (0.51,0.81), 0.57 (0.42,0.75), respectively (p trend = 0.0004); similar results were found for men. For dietary copper, the ORs and 95% CI for all subjects were 1.0, 0.59 (0.49,0.73), 0.51 (0.41,0.64), 0.34 (0.26,0.45), respectively (p trend < 0.0001); similar reductions in risk and trend were observed by gender. Dietary selenium intake was not associated with risk, except for a significant inverse trend (p = 0.04) in men. Protective trends (p < 0.05) against lung cancer with increased dietary zinc intake were also found for all ages, BMI > 25, current smokers, pack-years ,30, light drinkers and participants without emphysema. Increased dietary copper intake was associated with protective trends (p < 0.05) across all ages, BMI, smoking and vitamin/mineral supplement categories, pack-years ,30 and 30.1,51.75 and participants without emphysema. Our results suggest that dietary zinc and copper intakes are associated with reduced risk of lung cancer. Given the known limitations of case,control studies, these findings must be interpreted with caution and warrant further investigation. © 2006 Wiley-Liss, Inc. [source] Physical activity and lung cancer risk in the European Prospective Investigation into Cancer and Nutrition CohortINTERNATIONAL JOURNAL OF CANCER, Issue 10 2006Karen Steindorf Abstract Research conducted predominantly in male populations on physical activity and lung cancer has yielded inconsistent results. We examined this relationship among 416,277 men and women from the European Prospective Investigation into Cancer and Nutrition (EPIC). Detailed information on recent recreational, household and occupational physical activity, smoking habits and diet was assessed at baseline between 1992 and 2000. Relative risks (RR) were estimated using Cox regression. During 6.3 years of follow-up we identified 607 men and 476 women with incident lung cancer. We did not observe an inverse association between recent occupational, recreational or household physical activity and lung cancer risk in either males or females. However, we found some reduction in lung cancer risk associated with sports in males (adjusted RR = 0.71; 95% confidence interval 0.50,0.98; highest tertile vs. inactive group), cycling (RR = 0.73; 0.54,0.99) in females and non-occupational vigorous physical activity. For occupational physical activity, lung cancer risk was increased for unemployed men (adjusted RR = 1.57; 1.20,2.05) and men with standing occupations (RR = 1.35; 1.02,1.79) compared with sitting professions. There was no evidence of heterogeneity of physical activity associations across countries, or across any of the considered cofactors. For some histologic subtypes suggestive sex-specific reductions, limited by subgroup sizes, were observed, especially with vigorous physical activity. In total, our study shows no consistent protective associations of physical activity with lung cancer risk. It can be assumed that the elevated risks found for occupational physical activity are not produced mechanistically by physical activity itself but rather reflect exposure to occupation-related lung cancer risk factors. © 2006 Wiley-Liss, Inc. [source] CYP1A1 variants and smoking-related lung cancer in San Francisco bay area Latinos and African AmericansINTERNATIONAL JOURNAL OF CANCER, Issue 1 2005Margaret R. Wrensch Abstract We examined CYP1A1 T6235C (M1) and A4889G (M2) polymorphisms in San Francisco Bay Area African Americans and Latinos who were newly diagnosed with primary lung cancer from September 1998 to November 2002 and in age-gender-ethnicity frequency-matched controls. Owing mainly to rapid mortality of cases, overall percentages of cases genotyped were 26% and 32% for Latinos and African Americans, respectively. CYP1A1 variants were genotyped for Latinos (104 cases, 278 controls) and African Americans (226 cases, 551 controls). M1 and M2 frequencies in controls were 0.23 and 0.02 for African Americans and 0.38 and 0.29 for Latinos. In Latinos, the overall inverse odds ratio (OR) of 0.51 (95% CI = 0.32,0.81) for M1 variant genotype resulted from an inverse interaction with smoking. Nonsmokers with M1 genotype had a slight elevated OR (1.5; 0.59,3.7), but those with less than 30 or 30 or more pack-year history had 0.20 (0.06,0.70) and 0.21 (0.06,0.81) times (about 1/5) the odds expected if smoking and genotype were independent lung cancer risk factors. African Americans had interactions of similar magnitude that were not statistically significant. Results for M2 were very similar. Inverse interactions of CYP1A1 variants and smoking-associated lung cancer risk in Latinos might be causal, due to undetected bias or confounding, or represent a unique linkage disequilibrium between a new lung cancer locus and CYP1A1 in this highly admixed population. [source] Myeloperoxidase (MPO) genotype and lung cancer histologic types: The MPO ,463 A allele is associated with reduced risk for small cell lung cancer in smokersINTERNATIONAL JOURNAL OF CANCER, Issue 5 2002Heike Dally Abstract MPO participates in the metabolic activation of tobacco carcinogens such as PAHs. A frequent MPO ,463 G,A polymorphism in the promoter region reduces MPO transcription and has been correlated with >4-fold lower benzo[a]pyrene,DNA adduct levels in the skin of coal tar,treated patients. Four of 7 case-control studies found significantly reduced lung cancer risk associated with the A allele. Due to their different etiologies, we examined whether the MPO genotype affects histologic lung cancer types differentially. A case-control study was conducted in 625 ever-smoking lung cancer patients, including 228 adenocarcinomas, 224 SCCs, 135 SCLCs and 340 ever-smoking hospital controls. MPO genotyping was performed by capillary PCR followed by fluorescence-based melting curve analysis. Combining the MPO ,463 (G/A+A/A) genotypes, a protective effect approaching significance (OR = 0.75, 95% CI 0.55,1.01) was observed when comparing all lung cancer cases to controls. Among histologic types of lung cancer, a weak protective effect was found for both adenocarcinoma (OR = 0.81, CI 0.55,1.19) and SCC (OR = 0.82, CI 0.56,1.21); a stronger and significant effect was found for SCLC (OR = 0.58, CI 0.36,0.95; p = 0.029). Our results also suggest that the MPO genotype varies among inflammatory nonmalignant lung diseases. In conclusion, our results emphasize the need for a separate analysis of lung cancer histologic types and an adjustment for inflammatory nonmalignant lung diseases in future MPO-related studies. We confirm that the MPO ,463 A variant affords a protective effect against lung cancer risk in smokers, which was strongest for SCLC patients. © 2002 Wiley-Liss, Inc. [source] Polymorphisms in DNA repair genes XPD and XRCC1 and p53 mutations in lung carcinomas of never-smokersMOLECULAR CARCINOGENESIS, Issue 11 2006Wei-Min Gao Abstract The etiology of lung cancer in population with little or no tobacco exposure is not well understood. Individual genetic susceptibility factors have been suggested to contribute to lung cancer risk in this population. Mutations in the p53 tumor suppressor gene are implicated in the development of lung cancer as they are frequently found in lung tumors from both smokers and never-smokers. In order to determine whether genetic polymorphisms affecting DNA repair capacity modulate p53 mutations in lung tumors from never-smokers, we compared p53 mutations with genotypes of XPD 312, XPD 751, and XRCC1 399 in lung tumors from 43 lifetime never-smokers. p53 mutations were identified in 10 (23%) cases and consisted mostly of G/C to A/T transitions. No statistically significant association was found between p53 mutations and genotypes of XPD 312 or XPD 751. However, patients with the XRCC1 399 Gln allele, that results in a lower base excision repair capacity, were more likely to have p53 mutations, compared with patients the wild-type Arg allele (P,=,0.03). In addition, the p53 mutation frequency increased with an increasing number of combined genotypes associated with a lower DNA repair capacity of XPD 312, XPD 751, and XRCC1 399 (P,=,0.02). These results suggest that individuals who never smoked and had XRCC1 399 Gln allele may be at a greater risk of p53 mutations, especially if combined with the genotypes of XPD 312 and XPD 751 that may result in a lower DNA repair capacity. © 2006 Wiley-Liss, Inc. [source] Mortality among sheet metal workers participating in a medical screening programAMERICAN JOURNAL OF INDUSTRIAL MEDICINE, Issue 8 2009John Dement PhD Abstract Background The Sheet Metal Occupational Health Institute Trust (SMOHIT) was formed in 1985 to examine the health hazards of the sheet metal industry in the U.S. and Canada through an asbestos disease screening program. A study of mortality patterns among screening program participants was undertaken. Methods A cohort of 17,345 individuals with 20 or more years in the trade and who participated in the asbestos disease screening program were followed for vital status and causes of death between 1986 and 2004. Data from the screening program included chest X-ray results by International Labour Office (ILO) criteria and smoking history. Standardized mortality ratios (SMRs) by cause were generated using U.S. death rates and Cox proportional hazards models were used to investigate lung cancer risk relative to chest X-ray changes while controlling for smoking. Results A significantly reduced SMR of 0.83 (95% CI,=,0.80,0.85) was observed for all causes combined. Statistically significant excess mortality was observed for pleural cancers, mesothelioma, and asbestosis in the SMR analyses. Both lung cancer and COPD SMRs increased consistently and strongly with increasing ILO profusion score. In Cox models, which controlled for smoking, increased lung cancer risk was observed among workers with ILO scores of 0/1 (RR,=,1.17, 95% CI,=,0.89,1.54), with a strong trend for increasing lung cancer risk with increasing ILO profusion score >0/0. Conclusions Sheet metal workers are at increased risk for asbestos-related diseases. This study contributes to the literature demonstrating asbestos-related diseases among workers with largely indirect exposures and supports an increased lung cancer risk among workers with low ILO profusion scores. Am. J. Ind. Med. 52:603,613, 2009. © 2009 Wiley-Liss, Inc. [source] Identification of occupational cancer risk in British Columbia: A population-based case,control study of 2,998 lung cancers by histopathological subtypeAMERICAN JOURNAL OF INDUSTRIAL MEDICINE, Issue 3 2009Amy C. MacArthur MHSc Abstract Background Few studies have investigated occupational lung cancer risk in relation to specific histopathological subtypes. Methods A case,control study was conducted to evaluate the relationship between lung cancer and occupation/industry of employment by histopathological subtype. A total of 2,998 male cases and 10,223 cancer controls, diagnosed between 1983 and 1990, were identified through the British Columbia Cancer Registry. Matched on age and year of diagnosis, conditional logistic regression analyses were performed for two different estimates of exposure with adjustment for potentially important confounding variables, including tobacco smoking, alcohol consumption, marital status, educational attainment, and questionnaire respondent. Results For all lung cancers, an excess risk was observed for workers in the primary metal (OR,=,1.31, 95% CI, 1.01,1.71), mining (OR,=,1.53, 95% CI, 1.20,1.96), machining (OR,=,1.33, 95% CI, 1.09,1.63), transport (OR,=,1.50, 95% CI, 1.08,2.07), utility (OR,=,1.60, 95% CI, 1.22,2.09), and protective services (OR,=,1.27, 95% CI, 1.05,1.55) industries. Associations with histopathological subtypes included an increased risk of squamous cell carcinoma in construction trades (OR,=,1.25, 95% CI, 1.06,1.48), adenocarcinoma for professional workers in medicine and health (OR,=,1.73, 95% CI, 1.18,2.53), small cell carcinoma in railway (OR,=,1.62, 95% CI, 1.06,2.49), and truck transport industries (OR,=,1.51, 95% CI, 1.00,2.28), and large cell carcinoma for employment in the primary metal industry (OR,=,2.35, 95% CI, 1.11,4.96). Conclusions Our results point to excess lung cancer risk for occupations involving exposure to metals, polyaromatic hydrocarbons and asbestos, as well as several new histopathologic-specific associations that merit further investigation. Am. J. Ind. Med. 52:221,232, 2009. © 2008 Wiley-Liss, Inc. [source] Mortality of workers employed in shoe manufacturing: An update,AMERICAN JOURNAL OF INDUSTRIAL MEDICINE, Issue 7 2006Everett J. Lehman MS Abstract Background In the late 1970s, the National Institute for Occupational Safety and Health identified two shoe manufacturing facilities where workers experienced relatively "pure" exposures to toluene. A mortality study was conducted through December 31, 1982. An original study did not detect elevated leukemia mortality but did detect increased lung cancer mortality. The present study is an update of the mortality of the original cohort. Methods The study cohort consisted of workers employed 1 month or more between 1940 and 1979 at two Ohio shoe manufacturing plants. Vital status was ascertained through December 31, 1999. Results Seven thousand eight hundred twenty eight workers, contributing 300,777 person years, were available for analysis. An excess of lung cancer deaths persisted with additional years of follow-up (SMR,=,1.36, 95% confidence interval (CI),=,1.19,1.54). Trend tests did not indicate a positive trend between lung cancer risk and duration of employment. Mortality from leukemia was not significantly elevated in the updated analysis. Conclusions Results indicate a possible association between lung cancer mortality and exposure to chronic, low-levels of organic solvents. Although the strength of this conclusion was weakened by the lack of increasing lung cancer risk in relation to duration of employment, other studies have supported this association. Am. J. Ind. Med. 49:535,546, 2006. Published 2006 Wiley-Liss, Inc. [source] Association between asbestos exposure, cigarette smoking, myeloperoxidase (MPO) genotypes, and lung cancer riskAMERICAN JOURNAL OF INDUSTRIAL MEDICINE, Issue 1 2002Matthew B. Schabath MS Abstract Background As observed in tobacco-associated carcinogenesis, genetic factors such as the polymorphic metabolic/oxidative enzyme myeloperoxidase (MPO) could modulate individual susceptibility to asbestos-associated carcinogenesis. Methods RFLP-PCR analysis identified the MPO genotypes in 375 Caucasian lung cancer cases and 378 matched controls. An epidemiological interview elicited detailed information regarding smoking history and occupational history and exposures. Results Asbestos exposure was associated with a significantly elevated risk estimate (OR,=,1.45; 95% CI 1.04,2.02). On stratified analysis, we found the MPO genotypes modified the effect of asbestos exposure on lung cancer risk. Specifically, G/G carriers who were exposed to asbestos had an odds ratio (OR) of 1.72 (95% CI; 1.09,2.66), while A-allele carriers (G/A,+,A/A) exposed to asbestos exhibited a reduced OR of 0.89 (95% CI; 0.56,1.44). The OR was further reduced to 0.73 (0.49,1.06) for A-allele carriers not exposed to asbestos. A similar trend was observed for the joint effects between the MPO genotypes and pack-years smoking. Next, all three risk factors (MPO genotypes, asbestos exposure, and smoking) were analyzed simultaneously for joint effects. Heavy smokers with the G/G genotype and a history of asbestos exposure demonstrated a statistically significant elevated risk estimate (OR,=,2.19; 95% CI 1.16,4.11), while the A-allele carriers with the same exposure profile were at a lower risk for lung cancer (OR,=,1.18; 95% CI 0.58,2.38). The A-allele genotypes demonstrated similar protective effects for the other three exposure profiles. Conclusions For a similar level of exposure to established carcinogens, individuals with the MPO A-allele genotypes appear to have a reduced risk of lung cancer. Am. J. Ind. Med. 42:29,37, 2002. © 2002 Wiley-Liss, Inc. [source] Nested case-control study of lung cancer among pulp and paper workers in relation to exposure to dustsAMERICAN JOURNAL OF INDUSTRIAL MEDICINE, Issue 6 2001Irena Szadkowska-Sta, czyk MD Abstract Background Numerous studies have indicated an increased risk of lung cancer in pulp and paper industry workers. In a 1990 survey, standardized mortality ratio (SMR) was found to be 122 (95% CI:96,153) for lung cancer in Polish male workers in the pulp and paper industry, and 166 (95% CI:95,270) among workers engaged in paper production. Methods A nested case-control design within a cohort of pulp and paper workers was applied. Seventy-nine lung cancer cases and 237 "healthy" controls were selected from the cohort of 10,460 workers employed during the years 1968,1990, and observed until the end of 1995. Based on personnel files, occupational exposure was reconstructed by experts. Using a questionnaire, data on smoking habits were collected. ORs unadjusted and adjusted for smoking were calculated applying the model of conditional logistic regression. Results Occupational exposure to inorganic dusts (kaolin, lime, cement, brick, grindstone) adjusted for smoking was a significant lung cancer risk factor, with a 4.0-fold risk (95% CI:1.3,12.6), and a dose-response by cumulative dose index. Among organic dusts only wood dust increased albeit insignificantly the risk for those exposed (adjusted for smoking OR,=,2.1, 95% CI:0.9,4.9), but without dose-response relationship. Conclusions Exposure to occupational dust with relatively low content of silica, but at high concentrations may be considered as a factor increasing lung cancer risk. However, the observation made in this study should be viewed with caution as it was based on a small number of cases, and further evidence is needed to confirm or refute the authors' hypothesis. Am. J. Ind. Med. 39:547,556, 2001. © 2001 Wiley-Liss, Inc. [source] Chronic obstructive pulmonary disease and interstitial lung disease in patients with lung cancerRESPIROLOGY, Issue 3 2009Satoko MIZUNO ABSTRACT Background and objective: Although lung cancer is frequently accompanied by COPD and interstitial lung disease (ILD), the precise coincidence of these diseases with lung cancer is not well understood. The objectives of this study were to determine the prevalence of abnormal CT and spirometric findings suggestive of COPD or ILD in a population of patients with untreated lung cancer, and to estimate the lung cancer risk in this population. Methods: The study population consisted of 256 patients with untreated lung cancer and 947 subjects participating in a CT screening programme for lung cancer. Semi-quantitative analysis of low attenuation area (LAA), fibrosis and ground glass attenuation (GGA) on CT was performed by scoring. Gender- and age-matched subpopulations, with stratification by smoking status, were compared using the Mantel,Haenszel projection method. Results: Inter-observer consistency was excellent for LAA, but not as good for fibrosis or GGA scores. Pooled odds ratios for lung cancer risk using LAA, fibrosis, GGA scores and reduced FEV1/FVC and %VC were 3.63, 5.10, 2.71, 7.17 and 4.73, respectively (P < 0.0001 for all parameters). Multivariate regression analyses confirmed these results. Conclusion: Abnormal CT and spirometric parameters suggestive of COPD and ILD were strong risk factors for lung cancer, even after adjusting for gender, age and smoking status. [source] Hormone replacement therapy and lung cancer risk in ChineseCANCER, Issue 8 2007Kuan-Yu Chen MD Abstract BACKGROUND. The association between hormone replacement therapy (HRT) and a reduced lung cancer risk has been reported in previous studies. There is a high female to male ratio in Chinese lung cancer patients, and female patients have different clinicopathological characteristics compared with Western patient populations. The authors investigated whether HRT may reduce lung cancer risk in Taiwan. METHODS. The authors used a case-control study design to investigate 826 women with lung cancer and 531 healthy controls. Personal interviews based on a structured questionnaire were performed to collect information on HRT use of at least 3 months, age, ethnicity, active and passive smoking, exposure to air pollution, cooking or incense fumes, body mass index (BMI), menopause, and family history of cancers. RESULTS. HRT use was associated with reduced lung cancer risk with a multivariate, adjusted odds ratio of 0.70 (95% CI, 0.53,0.94; P = .019). HRT use was associated with reduced odds ratio of lung cancer in all subset analyses stratified by histology, active and passive cigarette smoking, BMI, history of incense burning, cooking, and motorcycle riding, as well as family history of certain cancers. CONCLUSIONS. This study confirmed that HRT is associated with a reduced lung cancer risk. The results appeared to be applicable to Chinese female population groups. Cancer 2007. © 2007 American Cancer Society. [source] Lack of Evidence of Association of p21WAF1/CIP1 Polymorphism with Lung Cancer Susceptibility and Prognosis in TaiwanCANCER SCIENCE, Issue 1 2000Chuen-Ming Shih An association between the Arg allele of the p21WAF1/CIP1 codon 31 polymorphism and lung cancer has been reported. However, the genotype distribution of the p21 codon 31 polymorphism, as well as the association of this polymorphism with lung cancer risk and prognosis, remain undefined in the Taiwanese population. Therefore, we investigated the genotype distribution of the p21 codon 31 polymorphism in 155 lung cancer patients and 189 non-cancer controls. The genotype frequencies in the Taiwanese non-cancer controls were 0.51 (Ser) and 0.49 (Arg). ,2 analysis indicated significant differences in Taiwanese genotype distribution of p21 from those reported for Swedes (P=0.001), Caucasians (P=0.001), Indians (P=0.001), and African-Americans (P=0.001). However, our data did not demonstrate an association of the Arg allele of the p21 polymorphism with lung cancer risk in Taiwan. Lung cancer patients with Ser/Arg and Arg/Arg genotypes were at a nonsignificant 1.15-fold increased risk of lung cancer when compared to individuals with the Ser/Ser genotype (95%CI, 0.70,1.86). In addition, although p21 is a downstream target of p53, we found no significant correlation of the p21 polymorphism with the p53 polymorphism and p53 gene mutation in lung cancer patients. We further investigated the association of the p21 polymorphism with prognosis in 154 lung cancer patients. Patients with the Ser/Ser genotype tended to have a poorer prognosis than those with the Ser/Arg and Arg/Arg genotypes (P=0.097, by the log rank test). Our data suggest that the p21 codon 31 polymorphism may not play a significant role in cancer susceptibility and the prognosis of lung cancer patients in Taiwan. [source] | |||||||||||||