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Oral administration of tartrazine (E102) accelerates the incidence and the development of 7,12-dimethylbenz(a) anthracene (DMBA)-induced breast cancer in rats.

Zingue et al,

2021

BMC Complement Med Ther

This study focused on the effect that tartrazine (E102), a common yellow food dye, had on the progression of breast cancer in rats that were exposed to 7,12-Dimethylbenz(a)anthracene (DMBA), a polycyclic aromatic hydrocarbons (PAH) that is widely known for its carcinogenicity. The researchers discovered that tartrazine accelerated the development and growth of tumors in the rats with 100% of rats having early incidents of breast cancer when exposed to both DMBA and tartrazin, and only 80% having early incidence when exposed to DMBA alone. The authors also hypothesized that tartrazine could cause oxidative stress, leading to DNA damage by producing Reactive Oxygen Species. These results may apply to humans as well, and raise concerns about the safety of prolonged or high-dose exposure to synthetic food dyes like tartrazine, especially in individuals who may already have other risk factors for cancer.

Signs of carcinogenicity induced by parathion, malathion, and estrogen in human breast epithelial cells (Review).

Calaf et al,

2021

Oncol Rep

A review of organophosphorus pesticides (OPs)—among the most commonly used insecticides—and their association with hormone-mediated cancer found that OPs combined with estrogen induce transformation events in human breast epithelial cells, with in vitro studies showing these substances cause genomic instability through inactivation of tumor-suppressor genes and activation of oncogenes. Studies using immortalized non-tumorigenic human breast epithelial cell lines (MCF-10F) demonstrated that OPs like malathion and parathion, particularly in the presence of estrogen, affect cell cycle regulation, epidermal growth factor signaling pathways, drug metabolism, and genomic stability, leading to cellular transformation and signs of carcinogenesis. The findings suggest hormone-mediated carcinogenic effects of these widely used insecticides on breast cancer risk in women, with experimental models revealing the multistep process by which normal breast cells transform into malignant ones through combined exposure to environmental pesticides and estrogen, providing mechanistic insights into how occupational and environmental OP exposure may contribute to breast cancer development.

Deep frying cooking oils promote the high risk of metastases in the breast-A critical review.

Ganesan et al,

2020

Food Chem Tox

This article discusses the harmful impacts of polycyclic aromatic hydrocarbons (PAHs) found in deep-fried foods. It highlights their endocrine-disrupting, genotoxic, and carcinogenic abilities when oils used for deep frying are heated repeatedly or at high temperatures. PAHs disrupt steroidogenic pathways which can lead to hormonal imbalances of estrogen and testosterone causing lower sperm quality, estrogenic effects, and endocrine related disorders. Furthermore, PAHs are linked to increased cancer risks through genotoxicity which can cause mutations in the cell. Organ sites that can be affected by this cancer risk are the breast, prostate, colorectal, renal, and pancreas.

Disruptive chemicals, senescence and immortality.

Carnero et al,

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.

Effects of Low-Dose Bisphenol A on DNA Damage and Proliferation of Breast Cells: The Role of c-Myc.

Pfeifer et al,

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.

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