International Agency for Research on Cancer

About: International Agency for Research on Cancer is a government organization based out in Lyon, France. It is known for research contribution in the topics: Cancer & Population. The organization has 2989 authors who have published 9010 publications receiving 929752 citations. The organization is also known as: IARC.

Meta- and pooled analyses of the effects of glutathione S-transferase M1 polymorphisms and smoking on lung cancer risk

Abstract: Susceptibility to lung cancer may in part be attributable to inter-individual variability in metabolic activation or detoxification of tobacco carcinogens. The glutathione S-transferase M1 (GSTM1) genetic polymorphism has been extensively studied in this context; two recent meta-analyses of case-control studies suggested an association between GSTM1 deletion and lung cancer. At least 15 studies have been published after these overviews. We undertook a new meta-analysis to summarize the results of 43 published case-control studies including >18 000 individuals. A slight excess of risk of lung cancer for individuals with the GSTM1 null genotype was found (odds ratio (OR) = 1.17, 95% confidence interval (CI) 1.07-1.27). No evidence of publication bias was found (P = 0.4), however, it is not easy to estimate the extent of such bias and we cannot rule out some degree of publication bias in our results. A pooled analysis of the original data of about 9500 subjects involved in 21 case-control studies from the International Collaborative Study on Genetic Susceptibility to Environmental Carcinogens (GSEC) data set was performed to assess the role of GSTM1 genotype as a modifier of the effect of smoking on lung cancer risk with adequate power. Analyses revealed no evidence of increased risk of lung cancer among carriers of the GSTM1 null genotype (age-, gender- and center-adjusted OR = 1.08, 95% CI 0.98-1.18) and no evidence of interaction between GSTM1 genotype and either smoking status or cumulative tobacco consumption.

Opium, tobacco, and alcohol use in relation to oesophageal squamous cell carcinoma in a high-risk area of Iran

Abstract: The very high incidence of oesophageal squamous cell carcinoma (ESCC) in Golestan Province in northeastern Iran was suggested by studies in the 1970s as partly due to opium use, which is not uncommon in this area, but based on limited numbers. From December 2003 to June 2007, we administered a validated structured questionnaire to 300 ESCC cases and 571 controls, matched on neighbourhood of residence, age (±2 years), and sex. We used conditional logistic regression models to calculate odds ratios (ORs) and 95% confidence intervals (95% CIs) adjusted for potential confounders. Compared with those who used neither tobacco nor opium, risk of ESCC was increased in those who used tobacco only (OR, 95% CI: 1.70, 1.05–2.73), in those who used opium only (2.12, 1.21–3.74), and in those who used both tobacco and opium (2.35, 1.50–3.67). All forms of tobacco use (cigarettes, hookah, and nass) were associated with higher ESCC risk. Similarly, use of both crude opium and other forms of opium were associated with higher risk. Alcohol consumption was seen in only 2% of the cases and 2% of the controls, and was not associated with ESCC risk.

PTEN (MMAC1) mutations are frequent in primary glioblastomas (de novo) but not in secondary glioblastomas.

Abstract: Loss of heterozygosity (LOH) on chromosome 10 is the most frequent genetic alteration associated with the evolution of malignant astrocytic tumors and it may involve several loci. The tumor suppressor gene PTEN (MMAC1) on chromosome 10q23 is mutated in approximately 30% of glioblastomas (WHO Grade IV). In this study, we assessed the frequency of PTEN mutations in primary glioblastomas, which developed clinically de novo, and in secondary glioblastomas, which evolved from low-grade (WHO Grade II) or anaplastic astrocytomas (WHO Grade III). Nine of 28 (32%) primary glioblastomas contained a PTEN mutation and an additional case showed a homozygous PTEN deletion. This indicates that after overexpression/amplification of the EGF receptor, loss of PTEN function is the most common alteration in primary glioblastomas. In this series, 5 of 28 (18%) primary glioblastomas showed both a PTEN mutation and EGFR amplification. In contrast, only 1 of 25 (4%) secondary glioblastomas contained a PTEN mutation, and none of them showed a homozygous PTEN deletion. The secondary glioblastoma with a PTEN mutation developed from an anaplastic astrocytoma that already carried the mutation. The observation that secondary glioblastomas have a p53 mutation as a genetic hallmark but rarely contain a PTEN mutation supports the concept that primary and secondary glioblastomas develop differently on a genetic level.

Evaluation of under- and overreporting of energy intake in the 24-hour diet recalls in the European Prospective Investigation into Cancer and Nutrition (EPIC)

Abstract: Objective: To evaluate under- and overreporting and their determinants in the EPIC :24-hour diet recall (24-HDR) measurements collected in the European Prospective Investigation into Cancer and Nutrition (EPIC). Design: Cross-sectional analysis. 24-HDR measurements were obtained by means of a standardised computerised interview program (EPIC-SOFT). The ratio of reported energy intake (EI) to estimated basal metabolic rate (BMR) was used-to ascertain the magnitude, impact and determinants of misreporting. Goldberg's cut-off points were used to identify participants with physiologically extreme low or high energy intake. At the aggregate level the value of 1.55 for physical activity level (PAL) was chosen as reference. At the individual level we used multivariate statistical techniques to identify factors that could explain EI/BMR variability. Analyses were performed by adjusting for weight, height, age at recall, special diet, smoking status, day of recall (weekday vs. weekend day) and physical activity. Setting: Twenty-seven redefined centres in the 10 countries participating in the EPIC project. Subjects: in total, 35955 men and women, aged 35-74 years, participating in the nested EPIC calibration sub-studies. Results: While overreporting has only a minor impact, the percentage of subjects identified as extreme underreporters was 13.8% and 10.3% in women and men, respectively. Mean EI/BMR values in men and women were 1.44 and 1.36 including all subjects, and 1.50 and 1.44 after exclusion of misreporters. After exclusion of misreporters, adjusted EI/BMR means were consistently less than 10% different from the expected value of 1.55 for PAL (except for women in Greece and in the UK), with overall differences equal to 4.0% and 7.4% for men and women, respectively. We modelled the probability of being an underreporter in association with several individual characteristics. After adjustment for age, height, special diet,- smoking status, day of recall and physical activity at work logistic regression analyses resulted in an odds ratio (OR) of being an underreporter for the highest vs. the lowest quartile of body mass index (BMI) of 3.52 (95% confidence interval (CI) 2.91-4.26) in men and 4.80 (95% CI 4.11-5.61) in women, indicating that overweight subjects are significantly more likely to underestimate energy intake than subjects in the bottom BMI category. Older people were less likely to underestimate energy intake: ORs were 0.58 (95% CI 0.45-0.77) and 0.74 (95% CI 0.63-0.88) for age (greater than or equal to 65 years vs. < 50 years). Special diet and day of the week showed strong effects. Conclusion: EI tends to be underestimated in the vast majority of the EPIC centres, although to varying degrees; at the aggregate level most centres were below the expected reference value of 1.55. Underreporting seems to be more prevalent among women than men in the EPIC calibration sample. The hypothesis that BMI (or weight) and age are causally related to underreporting seems to be confirmed in the present work. This introduces further complexity in the within-group (centre or country) and between-group calibration of dietary questionnaire measurements to deattenuate the diet-disease relationship. (Less)