The Role of Heavy Metals in the Biology of Female Cancers Original paper

What was studied?

The article reviewed the effects of heavy metals such as lead, cadmium, mercury, and arsenic on the development and progression of female cancers, particularly those related to the reproductive system, including breast, ovarian, and endometrial cancers. The review explores the mechanisms through which these metals disrupt cellular processes, including their potential to act as metalloestrogens, induce oxidative stress, impair DNA repair, and alter gene expression through epigenetic modifications. The paper emphasizes the role of these metals in carcinogenesis, especially in hormone-sensitive tissues.

Who was studied?

This review does not focus on specific individuals. Still, it compiles evidence from various studies involving both in vitro and in vivo models, as well as epidemiological research on the association between heavy metal exposure and cancer risk in women. The studies reviewed involve human tissues, cancer cell lines, and animal models, with a focus on how heavy metals influence estrogen receptors and cellular pathways that regulate growth, proliferation, and apoptosis in cancers such as breast, ovarian, and endometrial cancers.

Most important findings

The review discusses several significant findings, including how heavy metals such as cadmium, lead, and mercury can mimic estrogen by activating estrogen receptors, particularly estrogen receptor-alpha (ERα), and promoting cell proliferation. These metals are categorized as metalloestrogens, which have estrogen-like effects that contribute to the development of hormone-dependent cancers, such as breast and ovarian cancers. Additionally, heavy metals induce oxidative stress by generating reactive oxygen species (ROS), which damage cellular components such as DNA, proteins, and lipids. This oxidative damage leads to genetic mutations and contributes to cancer initiation and progression. Furthermore, heavy metals can cause epigenetic changes, which alter gene expression without changing the DNA sequence, and impair DNA repair mechanisms, which are essential for maintaining genomic integrity. The review also highlights the importance of understanding the molecular mechanisms by which these metals influence cancer biology, particularly in hormone-sensitive cancers.

Key implications

The review underscores the growing concern about environmental exposure to heavy metals and their potential role in the development of female cancers. Despite the known risks, many gaps remain in our understanding of the specific molecular mechanisms by which these metals contribute to cancer progression. The review suggests that heavy metals should be considered an important environmental factor in cancer prevention and treatment strategies. Given the potential for heavy metals to disrupt hormonal balance, further research is needed to develop better regulatory measures to limit exposure, especially in industrial and agricultural settings. Understanding the role of heavy metals in cancer biology also opens new avenues for therapeutic strategies aimed at targeting these metals and their molecular pathways.