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2023
Asian Pac J Cancer Prev
A study of 360 participants found that agricultural workers exposed to pesticides who carry genetic variations that impair their body’s ability to detoxify chemicals (null mutations in GSTT1 and GSTM1 genes) had substantially increased cancer risk, with 4-7 times higher odds of developing lymphoma or breast cancer compared to those with normal detoxification genes. The study also found elevated markers of oxidative stress (cellular damage) in farm workers with these genetic variants who developed leukemia, suggesting that pesticide exposure combined with impaired detoxification capacity triggers cancer development. These findings indicate that certain genetic profiles make agricultural workers particularly vulnerable to pesticide-related cancers, highlighting the importance of protective measures for farm workers and potential genetic screening to identify high-risk individuals.
2020
Basic Clin Pharmacol Toxicol
This case-control study of serum-levels of persistent organic pollutants among Greenlandic Inuit included 74 breast cancer cases and 80 matched controls. Researchers measured blood methylation of repetitive elements (LINE-1) and genes such as ATM and ESR2, alongside serum persistent organic pollutant (POP) levels. They found that women in the second tertile of ATM methylation had OR ≈ 2.33 (95% CI: 1.04–5.23) and those in the third tertile of ESR2 methylation had OR = 2.22 (95% CI: 0.97–5.05); women in the highest tertile of LINE-1 methylation had OR = 0.42 (95% CI: 0.18–0.98). These results suggest that altered DNA methylation associated with environmental pollutant burdens may play a role in breast cancer etiology in this population.
2025
Ecotoxicol Env Saf
A Mendelian randomization study using genetic data from European populations found that specific endocrine-disrupting chemicals (EDCs) were causally associated with different breast cancer subtypes: n-butyl paraben (n-BuP) increased Luminal A risk, mono-methyl phthalate decreased Luminal B risk, and mono-iso-butyl phthalate (MiBP) increased triple-negative breast cancer risk. Mediation analysis revealed that blood metabolites—including caffeic acid sulfate and caffeine metabolism ratios—partially explained the n-BuP effect on Luminal A, while methylsuccinate mediated the MiBP effect on triple-negative cancer, and epigenetic analysis identified specific DNA methylation sites associated with EDC exposure and breast cancer risk. These findings provide the first genetic evidence suggesting causal relationships between specific EDC exposures and breast cancer subtypes through distinct metabolic and epigenetic pathways, identifying potential biomarkers for early detection and highlighting the heterogeneous effects of different EDCs on breast cancer biology—underscoring the need for chemical-specific and subtype-specific prevention strategies rather than treating all EDCs or breast cancers as uniform entities.
2023
Front Oncol
A study of 80 Black and White women with breast cancer at Emory University Hospitals (2008-2017) examined associations between contemporary neighborhood redlining—a structural racism measure derived from Home Mortgage Disclosure Act data—and DNA methylation patterns in breast tumor tissue. Contemporary redlining was significantly associated with aberrant methylation at 5 CpG sites (FDR<0.10) in genes implicated in breast carcinogenesis, inflammation, immune function, and stress response (ANGPT1, PRG4), with additional top sites showing interaction by ER status and association with mortality; redlining was also associated with epigenetic age acceleration (β=5.35; 95% CI: 0.30-10.4 by Hannum metric). These novel findings suggest that structural racism—manifested through discriminatory housing policies leading to inequitable social and environmental exposures—may biologically embed in the breast tumor epigenome through altered DNA methylation patterns, potentially contributing to documented racial disparities in breast cancer outcomes and highlighting the need for further research on epigenetic mechanisms linking neighborhood-level structural racism to cancer prognosis.
2023
Sci Total Environ
In a transgenic mouse model (MMTV-Erbb2) that naturally develops mammary tumors, mice given oral cadmium (3.6 mg/L in drinking water for 23 weeks) developed palpable tumors significantly earlier and showed accelerated tumor growth compared with unexposed controls. Cadmium exposure increased the proliferation marker Ki-67, enhanced focal necrosis and new blood vessel formation in mammary tumors, and triggered greater intratumoral glutamine metabolism. Notably, disrupting gut microbiota with antibiotics delayed tumor onset and reduced tumor weight, implicating gut-microbiome–mediated metabolic reprogramming in cadmium-driven mammary tumorigenesis.
2023
Cancer Causes Control
A review examining how low socioeconomic status (SES) contributes to early chronic disease onset and reduced life expectancy found that neighborhood-level factors—including environmental pollutants, deprivation, social isolation, structural racism, and discrimination—create chronic life stress that affects molecular processes like DNA methylation, inflammation, and immune response, contributing to more aggressive tumor biology, particularly in Black Americans. Despite decades of research showing associations between neighborhood factors and cancer outcomes in marginalized communities, the biological mechanisms linking SES to cancer disparities remain poorly understood, though emerging evidence suggests chronic stress pathways may play a central role. The authors summarize current methods for measuring neighborhood-level deprivation, discrimination, and structural racism in cancer disparities research and recommend adopting a multi-faceted intersectional approach to reduce cancer health inequities and develop effective interventions promoting health equity.
2022
Eur J Epidemiol
A comprehensive study combining meta-analysis of observational data with genetic (Mendelian randomization) analysis found that each 10 grams per day increase in alcohol consumption was associated with a 4% increased breast cancer risk, and importantly, genetic predisposition to problematic alcohol use showed a 76% increased risk even after accounting for alcohol quantity consumed. The study identified four specific DNA methylation sites (epigenetic modifications) affected by alcohol—near the CDC7, ZNF318, RIN3, and RP11-867G23.13 genes—where alcohol-induced changes were causally linked to increased breast cancer risk, providing mechanistic insight into how alcohol drives carcinogenesis. These findings confirm that even low-dose alcohol consumption increases breast cancer risk and suggest that the harm stems not just from the amount consumed but from pathological drinking patterns and specific epigenetic changes that could serve as targets for prevention strategies.
2022
Molec Carcinogen
A case-control study of 708 breast cancer patients and 598 controls from Long Island found that paraben exposure—particularly methylparaben—was associated with significantly increased breast cancer risk among women with hypomethylated (undermethylated) DNA, showing a 46% increased risk in the highest versus lowest exposure group and a 32% increased risk per one-quantile increase in combined paraben exposure. Importantly, paraben exposure was specifically associated with breast tumors characterized by hypomethylation of the CCND2 gene promoter, with methylparaben showing a 25% increased risk and combined parabens showing a 55% increased risk for this tumor subtype. These findings suggest that parabens—ubiquitous preservatives in personal care products—may contribute to breast cancer development through epigenetic mechanisms, particularly in women with pre-existing DNA methylation abnormalities, identifying a potentially vulnerable subpopulation and a specific molecular pathway through which these chemicals may promote carcinogenesis.
2022
Biomed Pharmacother
A review of endocrine-disrupting chemicals (EDCs)—ubiquitous substances found in cosmetics, plastic food packaging, and medicines that enter the body through skin, digestive, or respiratory routes—examined their toxic effects even at microgram doses on the female reproductive system and genetic mechanisms. EDCs disrupt endocrine functions by binding to steroid hormone receptors, interfering with hormone synthesis and secretion, and modulating epigenetic processes that can lead to gene expression disturbances, contributing to neoplastic diseases, neurological disorders, circulatory problems, and reproductive dysfunction. Prenatal exposure can affect offspring development, with particular impacts on ovarian function leading to reduced fertility through disturbances in steroid receptor function, steroidogenesis, and gametogenesis. The review emphasizes that despite widespread exposure to these chemicals in everyday products, continued research is needed to fully understand their effects on the female reproductive system and potential transgenerational impacts mediated through epigenetic mechanisms.
2018
Tox Lett
This study investigated how butyl benzyl phthalate (BBP), a common environmental contaminant linked to breast cancer, promotes cancer cell growth and identified the molecular mechanisms involved. The researchers found that BBP increased proliferation in both estrogen receptor-positive (MCF-7) and negative (MDA-MB-231) breast cancer cells by promoting cell cycle progression and upregulating growth-promoting proteins while downregulating tumor suppressor proteins. For the first time, the study revealed that BBP works through modulating microRNA-19a/b, which targets the tumor suppressor gene PTEN, leading to activation of the AKT signaling pathway that promotes cell growth. These findings provide new insights into how BBP contributes to breast cancer development at the molecular level and suggest potential targets for intervention.
2018
Cancer Epidemiol Biomark Prev
A systematic review and meta-analysis of 24 studies found suggestive evidence that physical activity may reduce breast cancer risk through increased global DNA methylation, with higher activity levels showing a trend toward higher methylation (19% standardized mean difference) and higher methylation associated with a 30% reduced breast cancer risk, though neither association reached statistical significance overall. Subgroup analyses revealed that the protective pathway became clearer when examining long-term physical activity patterns and prospective cohort studies specifically, where both associations were statistically significant. This is the first systematic review to examine the complete biological pathway linking physical activity to breast cancer prevention through epigenetic mechanisms, suggesting that exercise may alter DNA methylation patterns in ways that protect against cancer development—a finding that could help explain how physical activity exerts its well-established cancer-preventive effects at the molecular level.
2018
Oncol Rep
This study investigated whether exposure to bisphenol A (BPA) and phthalate metabolites affects breast cancer risk through epigenetic changes in the ADAM33 gene, which plays a role in cancer progression. The researchers conducted a case-control study with 44 breast cancer patients and 22 controls, analyzing ADAM33 gene methylation patterns in blood samples and measuring urinary concentrations of endocrine-disrupting chemicals. They found that certain phthalate metabolites (MEHHP, MECPP, MEOHP) were positively associated with increased methylation of the ADAM33 gene, which was linked to higher gene expression levels. Surprisingly, the study suggests these phthalate metabolites may have a protective effect against breast cancer by increasing ADAM33 methylation and expression, contrary to the typical expectation that endocrine disruptors increase cancer risk.
2015
Carcinogenesis
This study explores the relationship between chemical carcinogens, cellular senescence, and the process of cellular immortalization, which is a sign of cancer development. The article discusses how certain chemicals can disrupt normal cellular processes, leading to cellular senescence, the process where cells stop dividing but remain metabolically active. This thereby enables the progression of cancer. These chemicals interfere with key regulatory pathways, such as those involving the p53 and pRb proteins, which are crucial for maintaining the balance between cell division and arrest. The authors emphasize that exposure to certain chemicals can lead to disruptions to cellular senescence pathways.
2015
Environ Health Perspect
This study investigates how low concentrations of Bisphenol A (BPA) affect DNA integrity and cell proliferation in breast cells, focusing on the involvement of the oncogene c-Myc. They found that exposure to low doses of BPA resulted in significant DNA damage in estrogen receptor-alpha (ERα)-negative mammary cells, meaning that BPA can promote cancer in ways independent of standard estrogen receptor pathways. Additionally, BPA exposure led to the upregulation of c-Myc, which is a gene known to regulate cell proliferation and death., and the study did observe enhanced proliferation of ERα-negative mammary cells upon BPA exposure. This suggests that BPA may promote cancer pathways through c-Myc activation. This was then confirmed when the researchers silenced c-Myc gene expression and found that oncogenic effects in the presence of BPA were decreased. Overall, these findings raise concerns about BPA’s potential role in breast cancer formation, even at low exposure levels.
2014
Aging Dis
The following review article described how exposure to EDCs during early development can lead to adverse health outcomes later in life through epigenetic mechanisms based on existing studies. The article emphasizes that exposure to EDCs during critical developmental periods such as in utero and early childhood, can have lasting effects on health since, during these periods, the body’s systems are particularly vulnerable to exposures. Additionally, the article finds a link between early-life exposure to EDCs and increased risk of various health issues later on in life, including metabolic disorders and cancers. The suspected mechanism by which these chemicals do this is thought to be mediated by epigenetic changes, which are changes to gene expression without altering the DNA. Therefore, the article emphasizes understanding how exposure during such sensitive periods in development can pose such drastic problems later on in life.