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

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

Overall, evidence linking BPA exposure to ovarian-cancer-related outcomes remains limited, and current findings do not establish that BPA causes OC or worsens patient prognosis in humans.

Current Evidence Linking Microplastic Exposure and Reproductive Cancers

Microplastics (MPs) and nanoplastics (NPs) have emerged as pervasive environmental contaminants with increasing evidence of human exposure and biological accumulation. Recent studies have confirmed their presence in multiple human reproductive tissues and fluids, including semen, testicular tissue, ovarian follicular fluid, cervicovaginal secretions, placenta, and breast milk, raising concerns regarding their potential implications for reproductive health. Beyond their widespread distribution, MPs have been shown in experimental studies to interact with cellular and molecular processes, including oxidative stress, inflammatory responses, mitochondrial dysfunction, and DNA damage, which are pathways commonly implicated in carcinogenesis. This review provides a comprehensive and critical synthesis of current evidence linking microplastic exposure to reproductive cancers, including prostate, testicular, ovarian, endometrial, cervical, and vaginal malignancies. Available mechanistic studies suggest that MPs may influence cancer-related biological processes through dysregulation of programmed cell death, genotoxicity, endocrine disruption, and modulation of signaling pathways such as PI3K/AKT and MAPK. Experimental findings also indicate that MPs may alter the tumor microenvironment and affect cellular behaviors associated with proliferation, migration, and invasion. However, the majority of current evidence is derived from in vitro studies, animal models, and indirect mechanistic observations, while direct epidemiological evidence in humans remain limited. Furthermore, methodological heterogeneity in microplastic detection and characterization complicates comparisons across studies and hinders causal inference. Overall, current evidence supports the biological plausibility of an association between microplastic exposure and reproductive cancer-related processes, while highlighting the need for standardized methodologies and well-designed longitudinal human studies to clarify potential health risks.

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

Occupational Medicine In The Prevention And Management Of Workplace Related Cancer: Mechanisms, Strategies And Emerging Challenges

The role of occupational medicine in identifying, managing, and preventing cancers linked to workplace exposures, while addressing diagnostic advances, regulatory frameworks, and preventive strategies is examined.

Environmental Genotoxins and Human Health Risks: Exposure Pathways, Mechanisms, Biomarkers and Challenges for Causal Risk Assessment

This critical narrative review integrates evidence on major environmental genotoxin classes, exposure routes, molecular mechanisms, human biomonitoring, disease associations and risk-assessment practice for well-established and less mature evidence domains.

Medical Cannabis and the Hallmarks of Cancer: A Critical Narrative Review

Cancer remains a highly complex and heterogeneous disease, causing major morbidity and mortality worldwide despite advances in diagnosis and treatment. The hallmarks of cancer enlighten the biological mechanisms supporting tumourigenesis and malignant evolution, while helping to identify potential therapeutic targets. Medical cannabis has mostly been used in oncology for supportive care, but increasing preclinical evidence suggests interference with cancer-related signalling pathways. This narrative review summarizes the current evidence on cannabinoids, in particular the phytocannabinoids cannabidiol (CBD) and Δ9-tetrahydrocannabinol (THC), framing their prospective anticancer effects in the hallmarks of cancer. Preclinical studies imply that CBD exerts antiproliferative effects by modulating oncogenic signalling pathways, including EGFR, PI3K/AKT, RAS/RAF/ERK, mTOR and Wnt/β-catenin, while also influencing tumour suppressor pathways involving p53, p21 and p27, causing cell cycle arrest. CBD has additionally been shown to promote programmed cell death via mitochondrial dysfunction and autophagy, altering cancer metabolism as well. Furthermore, CBD has shown anti-invasive and antiangiogenic properties and also appears to modulate immune responses and interactions with the tumour microenvironment, including emerging links with the microbiome. Overall, cannabinoids exhibit biologically plausible antitumour activity across multiple cancer hallmarks and may present promising candidates for combination therapeutic strategies. Nonetheless, the current evidence remains predominantly preclinical, and robust translational studies and clinical trials are needed to clarify their pharmacokinetic and pharmacodynamic profiles, determine their clinical efficacy and safety while assessing their potential integration into multimodal cancer treatment.