Research Results
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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
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
PLOS One
This study investigated how phthalates affect the growth of normal breast cells (MCF-10A) when grown alongside breast fibroblasts derived from tissue near estrogen receptor (ER) positive and negative breast cancers. The researchers found that only fibroblasts from ER-positive breast cancer tissue significantly stimulated breast cell proliferation, and when these co-cultures were exposed to estrogen or three phthalates (BBP, DBP, DEHP), cell growth increased significantly along with markers of cell division and estrogen receptor expression. The effects of phthalates on normal breast cells were similar to those of estrogen and depended on estrogen receptor activity, suggesting that phthalates act through hormone-mediated pathways. The study concludes that phthalates should be considered potential endocrine disruptors with breast cancer risk implications, even at low concentrations, particularly in the presence of estrogen-responsive tissue.
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
A review examining the intersection of environmental toxicants, immune function, and cancer development argues that common chemicals like bisphenol A, atrazine, and phthalates can disrupt the delicate balance between pro- and anti-inflammatory immune responses, potentially contributing to tumor development through immune system dysfunction. The authors highlight that while the role of immunity in cancer is well-established, research on how environmental chemicals affect immune cells as co-factors in cancer causation remains underdeveloped compared to studies on autoimmunity and allergies. The review calls for increased research using systems biology approaches to better understand how chemical exposures disturb inflammatory pathways and immune molecules involved in tumor-associated inflammation, arguing that chemically induced immune perturbations represent an important but understudied mechanism of environmental carcinogenesis.
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.
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
Carcinogenesis
This study explores the linkage between environmental chemical exposures and cellular resistance to cell death, a carcinogenic trait. The researchers in this study specifically investigate BPA, chlorothalonil, dibutyl phthalate, and more because of their disruptive effects that may be involved in these carcinogenic pathways. The researchers found that arsenic interferes with cellular signaling pathways and induces oxidative stress, leading to impaired apoptosis; dioxins bind to aryl hydrocarbon receptors (AHRs), which alters gene expression and disrupts normal cell death processes; BPA mimics the estrogen hormone, affecting hormonal balance and promoting cell survival pathways that inhibit cell death. By allowing cells to evade cell death, these environmental chemicals can promote the survival of cells with genetic mutations and therefore increase the risk of cancer development.
2011
J Steroid Biochem Mol Biol
Bisphenol A (BPA) is a widely produced chemical used in plastics and food container linings, with frequent human exposure due to its leaching into food and beverages. BPA, a known endocrine disruptor, was initially deemed a weak estrogen but has shown potency comparable to estradiol, a form of estrogen, shown to affect multiple hormonal pathways. Studies on rodents reveal adverse effects at levels below and at the current acceptable daily intake, raising concerns about human health impacts about concentration. BPA’s estrogenic effects highlight the importance of investigating BPA’s complex, widespread impacts on health.