Cancer development is a multistep process that may be induced by a variety of compounds. Environmental substances, such as pesticides, have been associated with different human diseases. Organophosphorus pesticides (OPs) are among the most commonly used
insecticides. Despite the fact that organophosphorus has been associated with an increased risk of
cancer, particularly hormone‑mediated
cancer, few prospective studies have examined the use of individual
insecticides. Reported results have demonstrated that OPs and
estrogen induce a cascade of events indicative of the transformation of human breast epithelial cells. In vitro studies analyzing an immortalized non‑tumorigenic human breast epithelial cell line may provide us with an approach to analyzing cell transformation under the effects of OPs in the presence of
estrogen. The results suggested hormone‑mediated effects of these
insecticides on the risk of
cancer among women. It can be concluded that, through experimental models, the initiation of
cancer can be studied by analyzing the steps that transform normal breast cells to malignant ones through certain substances, such as pesticides and
estrogen. Such substances cause
genomic instability, and therefore
tumor formation in the animal, and signs of
carcinogenesis in vitro.
Cancer initiation has been associated with an increase in
genomic instability, indicated by the inactivation of tumor‑suppressor genes and activation of oncogenes in the presence of
malathion,
parathion, and
estrogen. In the present study, a comprehensive summary of the impact of OPs in human and rat
breast cancer, specifically their effects on the cell cycle, signaling pathways linked to
epidermal growth factor,
drug metabolism, and
genomic instability in an MCF‑10F
estrogen receptor‑negative breast cell line is provided.