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| 32. |
- Kjaerheim, K, et al.
(författare)
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Variation in Nordic Work-Related Cancer Risks after Adjustment for Alcohol and Tobacco
- 2018
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Ingår i: International journal of environmental research and public health. - : MDPI AG. - 1660-4601. ; 15:12
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Tidskriftsartikel (refereegranskat)abstract
- Background: Alcohol and tobacco strongly increases the risk of cancers of the tongue, mouth, pharynx, larynx, and oesophagus, and are also established risk factors for cancer of the liver, colon, and rectum. It is well documented that these habits are unequally distributed among occupational groups. Most occupational cohort studies lack information on these potentially important confounders, and may therefore be prone to bias. Aim: The aim of the study is to present Nordic standardized incidence ratios (SIRs) for alcohol and tobacco related cancer by occupation, after adjustment for alcohol and tobacco, and to compare to the unadjusted SIRs. Material and Methods: The study is based on the Nordic Occupational Cancer (NOCCA) database. We used confirmatory factor analysis models for simultaneous analysis of the cancer sites related to alcohol and tobacco, to obtain factors that allow for computation of adjusted expected numbers from the reference rates. We then calculated adjusted SIRs for the relevant cancer sites for each occupation. Results: For some occupations and cancers, the changes of risk estimates were striking, from significantly high to significantly low and vice versa. Among Nordic farmers, unadjusted SIRs for cancer of the mouth and oesophagus were 0.56 (95% confidence interval (CI) 0.51–0.61) and 0.67 (CI 0.63–0.70), respectively. After adjustment, estimates changed to 1.10 (CI 1.01–1.21) and 1.16 (CI 1.10–1.22). Unadjusted SIR for pharynx cancer among wood workers was 0.83 (CI 0.75–0.91), adjusted SIR was 1.14 (CI 1.03–1.25). For larynx cancer, results in the opposite direction were seen: unadjusted SIR for economically inactive was 1.38 (CI 1.31–1.46) while the adjusted SIR was 0.91 (CI 0.86–0.96). Conclusions: Adjustment for the latent indicators of alcohol and tobacco consumption changed risk estimates for several occupations, gave a less confounded description of risk, and may guide in the identification of true risk factors.
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| 33. |
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| 34. |
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| 35. |
- Law, Philip J., et al.
(författare)
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Association analyses identify 31 new risk loci for colorectal cancer susceptibility
- 2019
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Ingår i: Nature Communications. - : Springer Science and Business Media LLC. - 2041-1723. ; 10
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Tidskriftsartikel (refereegranskat)abstract
- Colorectal cancer (CRC) is a leading cause of cancer-related death worldwide, and has a strong heritable basis. We report a genome-wide association analysis of 34,627 CRC cases and 71,379 controls of European ancestry that identifies SNPs at 31 new CRC risk loci. We also identify eight independent risk SNPs at the new and previously reported European CRC loci, and a further nine CRC SNPs at loci previously only identified in Asian populations. We use in situ promoter capture Hi-C (CHi-C), gene expression, and in silico annotation methods to identify likely target genes of CRC SNPs. Whilst these new SNP associations implicate target genes that are enriched for known CRC pathways such as Wnt and BMP, they also highlight novel pathways with no prior links to colorectal tumourigenesis. These findings provide further insight into CRC susceptibility and enhance the prospects of applying genetic risk scores to personalised screening and prevention.
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| 36. |
- Luostarinen, T, et al.
(författare)
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Joint effects of different human papillomaviruses and Chlamydia trachomatis infections on risk of squamous cell carcinoma of the cervix uteri
- 2004
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Ingår i: European Journal of Cancer. - : Elsevier BV. - 1879-0852 .- 0959-8049. ; 40:7, s. 1058-1065
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Tidskriftsartikel (refereegranskat)abstract
- This case-control study based in Nordic serum banks evaluated the joint effects of infections with genital human papillomavirus (HPV) types, and Chlamydia trachomatis in the aetiology of cervical squamous cell carcinoma. Through a linkage with the cancer registries, 144 cases were identified and 420 controls matched to them. Exposure to past infections was defined by the presence of specific IgG antibodies. The odds ratio (OR) for the second-order interaction of HPV16, HPV6/11 and C. trachomatis was small (1.0) compared to the expected multiplicative OR, 57, and the additive OR, 11. The interactions were not materially different among HPV16 DNA-positive squamous cell carcinomas. When HPV16 was replaced with HPV18/33 in the analysis of second-order interactions with HPV6/11 and C. trachomatis, there was no evidence of interaction, the joint effect being close to the expected additive OR. Possible explanations for the observed antagonism include misclassification, selection bias or a true biological phenomenon with HPV6/11 and C. trachomatis exposures antagonizing the carcinogenic effects of HPV16. (C) 2004 Elsevier Ltd. All rights reserved.
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