Cervical and Breast Cancer: Uncontrolled Epithelial Growth Driven by Xenoestrogen Dominance, Disrupted Paracrine Signaling, and Arrested Apoptosis

Cervical cancer and breast cancer represent two serious challenges in modern gynecological oncology. Despite their anatomical accessibility for screening, significant investments in research, and the development of therapeutic strategies, their global incidence and mortality rates continue to rise. Interstitial spaces, paracrine signaling, hormonal imbalance linked to xenoestrogens (XE) and the consequent inhibition of apoptosis constitute a common, yet unfortunately insufficiently recognized, link in the carcinogenesis of both cervical and breast cancer. The aim of this paper is to supplement the classical paradigm of cervical and breast carcinogenesis by incorporating a broader context currently missing from the understanding of both forms of cancer. XEs are widely distributed chemical substances, found in a wide range of everyday products, food and environment, that mimic the action of endogenous estrogen. In the world of basic science, the connection between estrogen dominance and apoptosis avoidance is unquestionable and can undeniably impact progression of breast and cervical cancer. In the development of breast cancer, the association between XE facilitated estrogen dominance and arrested apoptosis is of great importance. In the pathogenesis of cervical cancer, the activity of viral oncogenes E6/E7 is the main driver of the pathological condition; however, in the context of arrested apoptosis, there is an area of overlap between estrogen dominance and HPV virus action. In this sense, estrogen dominance, triggered by the agonistic action of XEs on the membrane-bound GPER receptor of fibroblasts, is a cofactor in cervical carcinogenesis that remains insufficiently researched.