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Final linear regression model relating DNA damage with consumption of macro and micronutrients and plasmatic variants

Final linear regression model relating DNA damage with consumption of macro and micronutrients and plasmatic variants

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Aims: To test if the level of oxidative stress is different in women with overweight and with metabolic syndrome. Study Design: Cross-sectional. Place and Duration of Study: Endocrinology Clinic of the Botucatu Medical School-UNESP, between March 2013 and March 2014. Methodology: Eighty women (31.15 ± 7.91 years old) attended at the Endocrinology C...

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... final linear regression model showed a positive association between the consumption of sodium and protein and DNA damage. On the other hand, polyunsaturated fat intake and plasma levels of α-carotene were negatively associated with DNA damage (Table 6). ...

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... In addition to fueling the growth of breast cancer, obesity has also been hypothesized to drive breast cancer initiation (Figure 1). A growing number of studies have highlighted an apparent genomic instability associated with obesity (91)(92)(93)(94). This is significant since genomic instability can lead to mutations that lead to tumorigenesis (95). ...
... For example, in one study DNA damage in peripheral blood lymphocytes was measured utilizing the comet assay that quantitates breaks in DNA. Both BMI and waist circumference were positively associated with DNA damage (94). Similar findings were made in an aging study, where obesity was a stronger predictor of skeletal muscle DNA damage compared to aging (96). ...
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Obesity is an established risk factor for breast cancer growth and progression. A number of advances have been made in recent years revealing new insights into this link. Early events in breast cancer development involve the neoplastic transformation of breast epithelial cells to cancer cells. In obesity, breast adipose tissue undergoes significant hormonal and inflammatory changes that create a mitogenic microenvironment. Many factors that are produced in obesity have also been shown to promote tumorigenesis. Given that breast epithelial cells are surrounded by adipose tissue, the crosstalk between the adipose compartment and breast epithelial cells is hypothesized to be a significant player in the initiation and progression of breast cancer in individuals with excess adiposity. The present review examines this crosstalk with a focus on obese breast adipose-derived estrogen, inflammatory mediators and adipokines, and how they are mechanistically linked to breast cancer risk and growth through stimulation of oxidative stress, DNA damage, and pro-oncogenic transcriptional programs. Pharmacological and lifestyle strategies targeting these factors and their downstream effects are evaluated for feasibility and efficacy in decreasing the risk of obesity-induced breast epithelial cell transformation and consequently, breast cancer development.