Bisphenol A and ovarian cancer: emerging evidence and potential biological mechanisms

Endocrine Disruptors and Gynecological Malignancies

Background/Objectives: Endocrine-disrupting chemicals (EDCs) interfere with hormonal homeostasis and have been implicated in gynecological malignancy pathogenesis. This narrative review synthesizes current evidence regarding EDC exposure and breast, endometrial, ovarian, and cervical cancers, examining molecular mechanisms, epidemiology, and diagnostic and clinical implications. Methods: We conducted a literature review using PubMed/MEDLINE, Embase, Scopus, and Cochrane databases through April 2026, including systematic reviews, meta-analyses, prospective cohorts, case-control studies, and mechanistic investigations examining EDC-cancer associations. Methodological quality was appraised using the Newcastle-Ottawa Scale and AMSTAR-2, with overall certainty of evidence rated using the GRADE framework. Results: Major EDC classes—bisphenol compounds, phthalates, polychlorinated biphenyls, organochlorine pesticides, and per- and polyfluoroalkyl substances—demonstrate carcinogenic potential through estrogen receptor modulation, epigenetic alterations, oxidative stress, and oncogenic signaling disruption. Breast cancer shows the strongest evidence, with prenatal and early-life DDT/DDE exposure associated with up to a 3.7-fold increased risk. Endometrial cancer demonstrates associations with xenoestrogen mixtures exhibiting non-monotonic dose-responses, whereas ovarian and cervical cancers show emerging but limited associations. Common mechanisms include receptor crosstalk, epigenetic dysregulation with transgenerational effects, oxidative genomic instability, metabolic reprogramming, and cancer stem cell enrichment. Conclusions: Evidence supports EDC contributions to gynecological malignancy through convergent pathways, though causal inference remains constrained by observational epidemiology, long latency periods, and challenges in characterizing real-world mixture exposures. Diagnostic and prevention strategies should integrate EDC exposure into risk-prediction models, leverage multi-omics biomarkers for early detection, and emphasize exposure reduction during critical developmental windows alongside regulatory reform.

Pesticide Exposure and Gynecological Cancers: A Review of Epidemiological Evidence and Mechanistic Pathways

Environmental exposure to pesticides is considered a risk factor for gynecological cancers, contributing to their onset and progression through various mechanisms. This narrative review investigates the role of different pesticides in the development and progression of ovarian, endometrial, and cervical cancers, and provides a comprehensive synthesis of epidemiological findings along with molecular mechanisms, highlighting carcinogenic pathways, conflicting findings, and potential therapeutic implications. Relevant epidemiological and experimental studies published between 2000 and 2025 were identified through searches of major scientific databases. Various pesticides, particularly organochlorines, contribute to gynecological cancers through mechanisms such as estrogen mimicry, DNA damage, oxidative stress, increased pro-inflammatory cytokines, and disruption of cellular signaling pathways. However, most studies found no significant association between certain pesticides, such as Triazines and Atrazine, and gynecological cancers. Furthermore, some pesticides, like Carbendazim, exhibit a dual role; while carcinogenic, they can also serve therapeutic purposes in cancer treatment when utilized with nanotechnology. Overall, pesticide exposure is a significant factor in the development and progression of women’s cancers, although the strength of the evidence varies across pesticide classes. Despite numerous studies, contradictory findings necessitate further research to clarify causal relationships.

Bisphenol exposure and gynecological health: A narrative review of current evidence and knowledge gaps.

The widespread use of plastic has led to exposure to chemicals like bisphenols (BPs), particularly bisphenol A (BPA), which are crucial in the production of polycarbonate plastics and epoxy resins. Recent studies have raised concerns about the effect of bisphenols as endocrine disruptors as the risk factor for hormone-dependent gynecological diseases. Taking into attention the mechanism of BPs' action, particularly their ability to bind to estrogen receptors and subsequently activate further estrogen pathways, it seems essential to understand their impact on different diseases. Moreover, it is not only the estrogen pathway, which is activated, but also signaling pathways, contributing to cell proliferation and potentially leading to carcinogenesis, particularly in tissues with hormonal dependencies. This review examines the mechanisms by which BPs interact with hormonal pathways and highlights their potential role in various hormone-related conditions, including benign gynecological diseases: endometriosis and polyendocrine metabolic ovarian syndrome (PMOS)/polycystic ovary syndrome (PCOS) and female gynecological cancers concerning breast, uterus and ovaries. The review also highlights the need to re-evaluate pre-analytical, analytical, and post-analytical standard operating procedures to reduce confounding factors in measuring BPs in clinical samples and to better model their potential roles as risk factors in disease etiology.

Microplastics and Mammary Carcinogenesis: A Review of In Vitro and In Vivo Experimental Evidence.

Microplastics have emerged as environmental contaminants of growing concern due to their potential impacts on human health. The mammary gland represents a biologically relevant target because of its hormonal sensitivity, lipid-rich composition, and dynamic cellular remodeling. This integrative review synthesized experimental evidence on the effects of micro- and nanoplastics on breast tissue and breast cancer biology. A literature search was conducted in PubMed, Scopus, Google Scholar, and CAPES databases following PRISMA guidelines, identifying 14 eligible studies involving detection in breast milk and breast tissue, as well as toxicological investigations in in vitro and in vivo models. Experimental evidence indicates that microplastics can be internalized by mammary epithelial and breast cancer cells, inducing oxidative stress, mitochondrial dysfunction, inflammatory signaling, and genomic instability. Exposure was also associated with altered gene and protein expression, disruption of cell cycle regulation, and modulation of signaling pathways involved in tumor progression. Animal studies further suggest potential effects on tumor growth, inflammatory microenvironments, and histopathological changes in mammary tissue. Overall, current findings provide mechanistic and hypothesis-generating evidence that microplastics may influence biological processes associated with breast carcinogenesis under specific experimental conditions. However, methodological heterogeneity remains a major limitation, highlighting the need for standardized and translational studies.

Vitamin D₃ in cancer prevention and therapy: molecular mechanisms, clinical evidence, and future perspectives

Linking bisphenol a exposure to pancreatic cancer: Evidence from population epidemiology, multi-omics screening, and cellular validation.

These findings provide population-level, computational, biophysical, and functional evidence supporting an association between BPA and pancreatic cancer, with AHR identified as a potential key molecular mediator.