Educational inequalities in quantity, duration and type of tobacco consumption among lung cancer patients in Asturias: epidemiological analyses.

Socioeconomic inequalities cause different tobacco consumption patterns. The purpose of this study was to examine the relationship between educational level and smoking behaviour, including type of tobacco consumption, in lung cancer patients. To this end, epidemiological analyses of 801 lung cancer patients recruited for a case-control study in four public hospitals in Asturias, Spain, between October 2000 and April 2006 were carried out. Smoking behaviour and educational level data were obtained through personal interview. Analyses indicated that the probability of heavy smoking among low educational-level patients was approximately twice as high as for high educational-level patients (RRR>31.2 packs/years=2.04; CI 95%=1.15-3.62; RRR>52packs/years=2.14; CI 95%=0.98-4.64). Low-educated patients were more than three times as likely to be long-time smokers (RRR>40 years=3.30; CI 95%=1.43-7.62). The probability of smoking exclusively black tobacco was almost four times greater in low educational-level patients (RRRblack only=3.72; CI 95%=1.23-11.19). The results show that there are broad educational inequalities with regard to the quantity, duration and type of tobacco consumption among lung cancer patients in Northern Spain.

Educational inequalities in quantity, duration and type of tobacco consumption among lung cancer patients in Asturias: epidemiological analyses / Desigualdades educativas según la cantidad, duración y tipo de tabaco consumido en pacientes con cáncer de pulmón en Asturias: análisis epidemiológicos

Socioeconomic inequalities cause different tobacco consumption patterns. The purpose of this study was to examine the relationship between educational level and smoking behaviour, including type of tobacco consumption, in lung cancer patients. To this end, epidemiological analyses of 801 lung cancer patients recruited for a case-control study in four public hospitals in Asturias, Spain, between October 2000 and April 2006 were carried out. Smoking behaviour and educational level data were obtained through personal interview. Analyses indicated that the probability of heavy smoking among low educational-level patients was approximately twice as high as for high educational-level patients (RRR>31.2packs/years = 2.04; CI 95%= 1.15-3.62; RRR>52packs/years= 2.14; CI 95%= 0.98-4.64). Low-educated patients were more than three times as likely to be long-time smokers (RRR>40years= 3.30; CI 95%= 1.43-7.62). The probability of smoking exclusively black tobacco was almost four times greater in low educational-level patients (RRRblack only= 3.72; CI 95%= 1.23-11.19). The results show that there are broad educational inequalities with regard to the quantity, duration and type of tobacco consumption among lung cancer patients in Northern Spain(AU)

Las desigualdades socioeconómicas causan diferentes patrones de consumo tabáquico. El objetivo de este estudio fue examinar la relación entre el nivel educativo y el hábito tabáquico en pacientes con cáncer de pulmón. Para ello se llevaron a cabo análisis epidemiológicos en 801 casos de cáncer de pulmón reclutados en un estudio caso-control de Asturias, entre octubre de 2000 y abril de 2006. Los datos relativos al hábito tabáquico y al nivel educativo fueron obtenidos mediante entrevista personal. La probabilidad de ser gran fumador entre pacientes de bajo nivel educativo es aproximadamente dos veces mayor que en pacientes con nivel educativo alto (RRR>31,2paquetes-año = 2,04; IC95% = 1,15-3,62; RRR>52paquetes-año= 2,14; IC95%= 0.98-4.64). Los pacientes con bajo nivel educativo fumaban durante más tiempo (RRR>40años= 3,30; IC95%= 1,43-7,62) y tenían cuatro veces más probabilidades de fumar exclusivamente tabaco negro (RRRsolo tabaco negro= 3,72; IC95%= 1,23-11,19). Los resultados indican que existen grandes desigualdades educativas en relación a la cantidad, duración y tipo de tabaco consumido entre los pacientes de cáncer de pulmón en Asturias(AU)

Polymorphism +17 C/G in matrix metalloprotease MMP8 decreases lung cancer risk.

BACKGROUND: Matrix metalloproteases (MMPs) constitute a family of enzymes capable of degrading different components of the extracellular matrix and are implicated in the invasion of tumor cells through the basement membrane. Polymorphisms in MMP genes may result in changes in the expression of MMPs being associated with the development and progression of cancer. We have investigated the association between three polymorphisms (-1607 1G/2G, +17 C/G and -77 A/G) in the human collagenases MMP1, MMP8 and MMP13 and the risk of development or progression of lung cancer. METHODS: A hospital-based case-control study was designed including 501 lung cancer patients and 510 controls matched. Genotypes were determined by PCR-RFLP. Results were analyzed using unconditional logistic regression, Cox's proportional hazard regression, and the Kaplan-Meier method. RESULTS: The MMP1 and MMP13 promoter polymorphisms were not associated with lung cancer risk, while the C/G polymorphism in MMP8 was associated with a statistically significant decreased risk of developing lung cancer (ORadj = 0.65; 95%CI = 0.45-0.93). The Kaplan-Meier analysis showed that the polymorphisms in MMP1, MMP8 and MMP13 not seem to modify the overall survival. Multivariate analysis revealed that MMP1, MMP8 and MMP13 polymorphisms are not independent prognostic factors for overall survival. CONCLUSION: This study suggests that the polymorphism in MMP8 is associated with a decreased lung cancer risk, which can be used as a prognostic marker in lung cancer.

The TP53 Arg72Pro polymorphism and lung cancer risk in a population of Northern Spain.

SUMMARY: Polymorphisms in tumor suppressor genes might contribute to the individual susceptibility to develop different types of cancer. Alterations in genes involved in cell cycle regulation and apoptosis, as tumor suppressor gene TP53, can lead to malignant transformations increasing the risk of developing cancer. We have investigated effects of polymorphism Arg72Pro on lung cancer risk, focusing on smoking and histology. Our study is a hospital-based case-control study designed with 589 lung cancer patients mainly with squamous cell carcinoma (215), adenocarcinoma (156) and small cell carcinoma (90), and 582 control subjects, matched in ethnicity, age and gender. Genotypes were determined by PCR-RFLP and the results were analysed using multivariate unconditional logistic regression, adjusted for age, gender and smoking status. The analysis showed a statistically significant increase of lung cancer risk in Pro carriers (Arg/Pro and Pro/Pro) (adjusted OR=1.32; 95% CI=1.03-1.69), especially for ever smokers (adjusted OR=1.34; 95% CI=1.04-1.73), heavy smokers (adjusted OR=1.48; 95% CI=1.01-2.16) and smokers of exclusively black tobacco (adjusted OR=1.45; 95% CI=1.04-2.00). Moreover, Pro carriers present an increased risk of developing small cell lung cancer (adjusted OR=1.70; 95% CI=1.07-2.69) and cancer in stage IV for NSCLC (adjusted OR=1.56; 95% CI=1.07-2.27). Our results suggest that polymorphism Arg72Pro in tumor suppressor gene TP53 increases the risk of lung cancer. The effect is especially strong for small cell lung cancer (SCLC) and heavy smokers.

Polymorphisms in XPC, XPD, XRCC1, and XRCC3 DNA repair genes and lung cancer risk in a population of northern Spain.

BACKGROUND: Polymorphisms in DNA repair genes have been associated to repair DNA lesions, and might contribute to the individual susceptibility to develop different types of cancer. Nucleotide excision repair (NER), base excision repair (BER), and double-strand break repair (DSBR) are the main DNA repair pathways. We investigated the relationship between polymorphisms in two NER genes, XPC (poly (AT) insertion/deletion: PAT-/+) and XPD (Asp312Asn and Lys751Gln), the BER gene XRCC1 (Arg399Gln), and the DSBR gene XRCC3 (Thr241Met) and the risk of developing lung cancer. METHODS: A hospital-based case-control study was designed with 516 lung cancer patients and 533 control subjects, matched on ethnicity, age, and gender. Genotypes were determined by PCR-RFLP and the results were analysed using multivariate unconditional logistic regression, adjusting for age, gender and pack-years. RESULTS: Borderline association was found for XPC and XPD NER genes polymorphisms, while no association was observed for polymorphisms in BER and DSBR genes. XPC PAT+/+ genotype was associated with no statistically significant increased risk among ever smokers (OR = 1.40; 95%CI = 0.94-2.08), squamous cell carcinoma (OR = 1.44; 95%CI = 0.85-2.44), and adenocarcinoma (OR = 1.72; 95%CI = 0.97-3.04). XPD variant genotypes (312Asn/Asn and 751Gln/Gln) presented a not statistically significant risk of developing lung cancer (OR = 1.52; 95%CI = 0.91-2.51; OR = 1.38; 95%CI = 0.85-2.25, respectively), especially among ever smokers (OR = 1.58; 95%CI = 0.96-2.60), heavy smokers (OR = 2.07; 95%CI = 0.74-5.75), and adenocarcinoma (OR = 1.88; 95%CI = 0.97-3.63). On the other hand, individuals homozygous for the XRCC1 399Gln allele presented no risk of developing lung cancer (OR = 0.87; 95%CI = 0.57-1.31) except for individuals carriers of 399Gln/Gln genotype and without family history of cancer (OR = 0.57; 95%CI = 0.33-0.98) and no association was found between XRCC3 Thr241Met polymorphism and lung cancer risk (OR = 0.92; 95%CI = 0.56-1.50), except for the 241Met/Met genotype and squamous cell carcinoma risk (OR = 0.47; 95%CI = 0.23-1.00). CONCLUSION: In conclusion, we analysed the association between XPC, XPD, XRCC1, and XRCC3 polymorphisms and the individual susceptibility to develop lung cancer in the Spanish population, specifically with a highly tobacco exposed population. We attempt to contribute to the discovery of which biomarkers of DNA repair capacity are useful for screening this high-risk population for primary preventing and early detection of lung cancer.

Poly (AT) polymorphism in intron 11 of the XPC DNA repair gene enhances the risk of lung cancer.

Reduced DNA repair capacity due to inherited polymorphisms may increase the susceptibility to smoking-related cancers. In this report, we investigate the relationship between xeroderma pigmentosum complementary group C poly (AT) insertion/deletion polymorphism (XPC-PAT) of the XPC gene and lung cancer risk in a hospital-based case-control study of 359 newly diagnosed lung cancer patients and 375 control subjects matched on age, sex, and catchment area. The XPC genotype was determined by PCR-RFLP, and the results were analyzed using logistic regression, adjusting for relevant covariates. We found that the frequency of the PAT+/+ genotype was higher in the cases (20.6%) than in the controls (14.1%; P = 0.057) and that the PAT+/+ subjects were at significantly increased risk for lung cancer [adjusted odds ratio (OR), 1.60; 95% confidence interval (95% CI), 1.01-2.55]. Stratified analysis revealed that the risk was higher in former smokers (OR, 2.15; 95% CI, 1.07-4.31) and older people (OR, 2.76; 95% CI, 1.02-7.51), although this probably occurs due to 63.4% of cases older than 73 years being ex-smokers. When stratified by histologic type, the variant genotype was associated with statistically significant increased risk for squamous cell carcinoma (OR, 1.93; 95% CI, 1.06-3.51). In conclusion, our findings support the hypothesis that PAT and intron 11 C/A XPC polymorphisms are linked in the Spanish population and may contribute to the risk of developing lung cancer probably due to a higher frequency of deletion of exon 12 and reduced DNA repair capacity of the XPC protein.