ArticleAnnals of epidemiology2015
Genetic polymorphisms in DNA repair and oxidative stress pathways may modify the association between body size and postmenopausal breast cancer.
Article in Annals of epidemiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
5 citing papers in PubMed, 9 citations in OpenAlex.
- Article
- Large-scale exome sequence analysis identifies sex- and age-specific determinants of obesity.Cell genomics · 2023Article
- Disadvantaged neighborhoods and racial disparity in breast cancer outcomes: the biological link.Cancer causes & control : CCC · 2019Review
- Visceral Adipose Tissue Modulates Radiosensitivity in Oesophageal Adenocarcinoma.International journal of medical sciences · 2019Article
- Polycyclic aromatic hydrocarbons and postmenopausal breast cancer: An evaluation of effect measure modification by body mass index and weight change.Environmental research · 2017Article
Corrections and comments
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Authors and funding
15 authors at 7 institutions in 2 countries.
Funding
Abstract
purposeObesity is associated with increased bioavailability of estrogen, hyperinsulinemia, and chronic inflammation, all of which may promote tumor growth. Given DNA repair and oxidative stress pathways may work together with these mechanisms to influence carcinogenesis, we hypothesized that genetic variation in these pathways may modify the obesity-postmenopausal breast cancer (BC) association.
methodsResources from a population-based case-control study (990 cases and 970 controls) were used to construct logistic regression models. Body mass index (BMI, weight [kilogram]/height [square meter]) was assessed 1 year before reference date. We characterized interactions between BMI and 29 genetic polymorphisms in oxidative stress and DNA repair pathways.
resultsAge-adjusted odds ratios (95% confidence intervals) for postmenopausal BC were 1.24 (1.00-1.52) and 1.35 (1.09-1.71) for 25 ≥ BMI < 30 and BMI ≥ 30 kg/m(2), respectively. We observed multiplicative interactions (P ≤ .05) for eight gene polymorphisms in DNA repair and oxidative stress pathways. For example, among MPO variant allele carriers, obesity was associated with a twofold increased risk of postmenopausal BC (2.13 [1.35-3.36]); however, in wild-type homozygotes, the relationship was less pronounced (1.33 [0.93-1.89]). Our findings were no longer significant after Bonferroni correction.
conclusionsObesity may be particularly deleterious for postmenopausal BC development in the presence of biologically plausible DNA repair or oxidative stress genotypes.
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