The etiology and prevention of breast cancer

Cavalieri, Ercole L.; Rogan, Eleanor G.

doi:10.1016/j.ddmec.2013.02.001

Cited by 13 publications

(12 citation statements)

References 107 publications

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“…Several mechanisms have been postulated regarding the etiology and progression of breast cancer (2). Among these mechanisms, chronic inflammation is widely recognized to play a crucial role in cancer development, progression, and risk of recurrence due to its effects on carcinogenesis and the tumor microenvironment (3).…”

Section: Introductionmentioning

confidence: 99%

The Effect of Exercise Training on Mediators of Inflammation in Breast Cancer Survivors: A Systematic Review with Meta-analysis

Meneses-Echávez

Correa-Bautista

González‐Jiménez

et al. 2016

Cancer Epidemiology, Biomarkers &Amp; Prevention

125

104

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Several sources of evidence indicate that exercise during and after breast cancer could positively modulate the tumor microenvironment. This meta-analysis aimed to determine the effects of exercise training on mediators of inflammation in breast cancer survivors. We searched for randomized controlled trials published from January 1990 to March 2014. An inverse variance method of meta-analysis was performed using a random effects model in the presence of statistical heterogeneity. Eight high-quality trials (n ¼ 478) were included. Exercise improved the serum concentrations of IL6 [weighted mean difference (WMD) ¼ À0.55 pg/mL; 95% confidence interval (CI), À1.02 to À0.09], TNFa (WMD ¼ À0.64 pg/mL; 95% CI, À1.21 to À0.06), IL8 (MD ¼ À0.49 pg/mL; 95% CI, À0.89 to À0.09), and IL2 (WMD ¼ 1.03 pg/mL; 95% CI, 0.40 to 1.67). No significant differences were found in the serum concentrations of C-reactive protein (WMD ¼ À0.15; 95% CI, À0.56 to 0.25) or IL10 (WMD ¼ 0.41; 95% CI, À0.18 to 1.02). Exercise training positively modulates chronic low-grade inflammation in women with breast cancer, which may impact upon carcinogenic mechanisms and the tumor microenvironment. These findings align with the other positive effects of exercise for breast cancer survivors, reinforcing the appropriateness of exercise prescription in this population.

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Section: Introductionmentioning

confidence: 99%

The Effect of Exercise Training on Mediators of Inflammation in Breast Cancer Survivors: A Systematic Review with Meta-analysis

Meneses-Echávez

Correa-Bautista

González‐Jiménez

et al. 2016

Cancer Epidemiology, Biomarkers &Amp; Prevention

125

104

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“…Unbalanced estrogen metabolism is a critical factor in cancer initiation. The discovery that specific oxidative metabolites of estrogens, the catechol estrogen quinones, react with DNA supports the hypothesis that estrogens can become endogenous carcinogens by generating the mutations leading to the initiation of cancer [11–14]. This paradigm indicates that specific, critical mutations produce abnormal cell proliferation leading to cancer, rather than ER‐mediated abnormal cell proliferation that generates random mutations [1, 6–10].…”

Section: Mechanism Of Metabolic Activation Of Estrogens To Initiate Cmentioning

confidence: 99%

Depurinating estrogen‐DNA adducts, generators of cancer initiation: their minimization leads to cancer prevention

Cavalieri

Rogan

2016

Clinical & Translational Med

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Estrogens can initiate cancer by reacting with DNA. Specific metabolites of endogenous estrogens, the catechol estrogen-3,4-quinones, react with DNA to form depurinating estrogen-DNA adducts. Loss of these adducts leaves apurinic sites in the DNA, generating mutations that can lead to the initiation of cancer. A variety of endogenous and exogenous factors can disrupt estrogen homeostasis, which is the normal balance between estrogen activating and protective enzymes. In fact, if estrogen metabolism becomes unbalanced and generates excessive catechol estrogen 3,4-quinones, formation of depurinating estrogen-DNA adducts increases and the risk of initiating cancer is greater. The levels of depurinating estrogen-DNA adducts are high in women diagnosed with breast cancer and those at high risk for the disease. High levels of depurinating estrogen-DNA adducts before the presence of breast cancer indicates that adduct formation is a critical factor in breast cancer initiation. Women with thyroid or ovarian cancer also have high levels of estrogen-DNA adducts, as do men with prostate cancer or non-Hodgkin lymphoma. Depurinating estrogen-DNA adducts are initiators of many prevalent types of human cancer. These findings and other discoveries led to the recognition that reducing the levels of estrogen-DNA adducts could prevent the initiation of human cancer. The dietary supplements N -acetylcysteine and resveratrol inhibit formation of estrogen-DNA adducts in cultured human breast cells and in women. These results suggest that the two supplements offer an approach to reducing the risk of developing various prevalent types of human cancer. Graphical abstract Major metabolic pathway in cancer initiation by estrogens.

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“…Over the last few years, several mechanisms have been postulated regarding the etiology and progression of breast cancer. 3 It has been shown that chronic inflammatory responses play essential roles in development of all kinds of cancers. Inflammatory cells can regulate the tumor microenvironment and are clearly implicated in tumor development by facilitating proliferation, migration, and survival.…”

Section: Introductionmentioning

confidence: 99%

Association of interleukin 10 rs1800896 polymorphism with susceptibility to breast cancer: a meta-analysis

Zhu

Liu

et al. 2020

J Int Med Res

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Objective To evaluate the correlation between interleukin 10 (IL-10) −1082A/G polymorphism (rs1800896) and breast cancers by performing a meta-analysis. Methods The Embase and Medline databases were searched through 1 September 2018 to identify qualified articles. Odds ratios (OR) and corresponding 95% confidence intervals (CIs) were applied to evaluate associations. Results In total, 14 case-control studies, including 5320 cases and 5727 controls, were analyzed. We detected significant associations between the IL10 −1082 G/G genotype and risk of breast cancer (AA + AG vs. GG: OR = 0.88, 95% CI = 0.80–0.97). Subgroup analyses confirmed a significant association in Caucasian populations (OR = 0.89, 95% CI = 0.80–0.99), in population-based case-control studies (OR = 0.87, 95% CI = 0.78–0.96), and in studies with ≥500 subjects (OR = 0.88, 95% CI = 0.79–0.99) under the recessive model (AA + AG vs. GG). No associations were found in Asian populations. Conclusions The IL10 −1082A/G polymorphism is associated with an increased risk of breast cancer. The association between IL10 −1082 G/G genotype and increased risk of breast cancer is more significant in Caucasians, in population-based studies, and in larger studies.

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The etiology and prevention of breast cancer

Cited by 13 publications

References 107 publications

The Effect of Exercise Training on Mediators of Inflammation in Breast Cancer Survivors: A Systematic Review with Meta-analysis

The Effect of Exercise Training on Mediators of Inflammation in Breast Cancer Survivors: A Systematic Review with Meta-analysis

Depurinating estrogen‐DNA adducts, generators of cancer initiation: their minimization leads to cancer prevention

Association of interleukin 10 rs1800896 polymorphism with susceptibility to breast cancer: a meta-analysis

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