Association of physical weight statuses defined by body mass index (BMI) with molecular subtypes of premenopausal breast cancer: a systematic review and meta-analysis

Li, Xuchu; Li, Jinping; Hu, Qirui; Zhang, Xu; Chen, Fang

doi:10.1007/s10549-023-07139-z

Cited by 2 publications

(1 citation statement)

References 82 publications

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“…Women with obesity are at risk for different subtypes of breast cancer depending on whether they have reached menopause. Premenopausal women with obesity are at an increased risk for triple negative breast cancer, which lacks expression of estrogen receptor (ER), progesterone receptor, and HER2 [9][10][11], while postmenopausal women with obesity have an increased risk for ER + breast cancer [12,13]. Women with obesity tend to develop more aggressive breast cancers regardless of Disclaimer/Publisher's Note: The statements, opinions, and data contained in all publications are solely those of the individual author(s) and contributor(s) and not of MDPI and/or the editor(s).…”

Section: Introductionmentioning

confidence: 99%

Obesity Induces DNA Damage in Mammary Epithelial Cells Which Is Exacerbated by Acrylamide Treatment Through CYP2E1-Mediated Oxidative Stress

Walton,

Kaplan,

Hrdlicka

et al. 2024

Preprint

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Obesity and environmental toxins are risk factors for breast cancer, however there is limited knowledge on how these risk factors interact to promote breast cancer. Acrylamide, a probable carcinogen and obesogen, is a biproduct in foods prevalent in the obesity-inducing Western diet. Acrylamide is metabolized by cytochrome P450 2E1 (CYP2E1) to the genotoxic epoxide, glycidamide, and is associated with increased risk for breast cancer. To investigate how acrylamide and obesity interact to increase breast cancer risk, female mice were fed a low-fat (LFD) or high-fat diet (HFD) and 0.7mM acrylamide-supplemented water or control water. While HFD significantly enhanced weight gain in mice, the addition of acrylamide did not significantly alter body weights compared to respective controls. Mammary epithelial cells from obese, acrylamide-treated mice had increased DNA strand breaks and oxidative DNA damage compared to all other groups. In vitro, glycidamide-treated COMMA-D cells showed significantly increased DNA strand breaks while acrylamide-treated cells demonstrated significantly higher levels of intracellular reactive oxygen species. Knockdown of CYP2E1 rescued the acrylamide-induced oxidative stress. These studies suggest that long-term acrylamide exposure through foods common in the Western diet may enhance DNA damage and CYP2E1-induced generation of oxidative stress in mammary epithelial cells, potentially enhancing obesity-induced breast cancer risk.

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Section: Introductionmentioning

confidence: 99%

Obesity Induces DNA Damage in Mammary Epithelial Cells Which Is Exacerbated by Acrylamide Treatment Through CYP2E1-Mediated Oxidative Stress

Walton,

Kaplan,

Hrdlicka

et al. 2024

Preprint

View full text Add to dashboard Cite

show abstract

Obesity Induces DNA Damage in Mammary Epithelial Cells Exacerbated by Acrylamide Treatment through CYP2E1-Mediated Oxidative Stress

Walton,

Kaplan,

Hrdlicka

et al. 2024

Toxics

View full text Add to dashboard Cite

Obesity and environmental toxins are risk factors for breast cancer; however, there is limited knowledge on how these risk factors interact to promote breast cancer. Acrylamide, a probable carcinogen and obesogen, is a by-product in foods prevalent in the obesity-inducing Western diet. Acrylamide is metabolized by cytochrome P450 2E1 (CYP2E1) to the genotoxic epoxide, glycidamide, and is associated with an increased risk for breast cancer. To investigate how acrylamide and obesity interact to increase breast cancer risk, female mice were fed a low-fat (LFD) or high-fat diet (HFD) and control water or water supplemented with acrylamide at levels similar to the average daily exposure in humans. While HFD significantly enhanced weight gain in mice, the addition of acrylamide did not significantly alter body weights compared to respective controls. Mammary epithelial cells from obese, acrylamide-treated mice had increased DNA strand breaks and oxidative DNA damage compared to all other groups. In vitro, glycidamide-treated COMMA-D cells showed significantly increased DNA strand breaks, while acrylamide-treated cells demonstrated significantly higher levels of intracellular reactive oxygen species. The knockdown of CYP2E1 rescued the acrylamide-induced oxidative stress. These studies suggest that long-term acrylamide exposure through foods common in the Western diet may enhance DNA damage and the CYP2E1-induced generation of oxidative stress in mammary epithelial cells, potentially enhancing obesity-induced breast cancer risk.

show abstract

Association of physical weight statuses defined by body mass index (BMI) with molecular subtypes of premenopausal breast cancer: a systematic review and meta-analysis

Cited by 2 publications

References 82 publications

Obesity Induces DNA Damage in Mammary Epithelial Cells Which Is Exacerbated by Acrylamide Treatment Through CYP2E1-Mediated Oxidative Stress

Obesity Induces DNA Damage in Mammary Epithelial Cells Which Is Exacerbated by Acrylamide Treatment Through CYP2E1-Mediated Oxidative Stress

Obesity Induces DNA Damage in Mammary Epithelial Cells Exacerbated by Acrylamide Treatment through CYP2E1-Mediated Oxidative Stress

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