Farina Sara, Sabatelli Alessandra, Boccia Stefania, Scambia Giovanni
Section of Hygiene, University Department of Life Sciences and Public Health, Università Cattolica del Sacro Cuore, Rome, Italy.
Department of Woman and Child Health and Public Health-Public Health Area, Fondazione Policlinico Universitario A. Gemelli IRCCS, Rome, Italy.
Int J Gynaecol Obstet. 2025 Apr 25. doi: 10.1002/ijgo.70156.
Environmental and lifestyle factors significantly contribute to gynecological cancers. The risk of ovarian cancer, one the most lethal gynecological cancer, is associated with obesity, poor dietary habits, and environmental pollutants, exacerbating hormonal imbalances, inflammation, and oxidative stress. Protective factors, such as the Mediterranean diet and oral contraceptives, modulate risk by reducing ovulatory cycles, particularly in genetically predisposed women. Uterine cancer is associated with metabolic factors, with obesity driving hormonal disruptions and systemic inflammation. Physical inactivity and diets rich in animal fats increase the risk of endometrial cancer, along with air pollution and microbiome imbalances contribute to endometrial carcinogenesis. Cervical cancer is primarily driven by persistent high-risk HPV infection, with smoking enhancing viral persistence and oncogenesis. Nutritional deficiencies in antioxidants and folate weaken immune defenses, while vaginal and gut microbiome dysbiosis fosters neoplastic progression. Vulvar and vaginal cancers, though less common, share risk factors such as obesity, smoking, and occupational exposures, disrupting immune responses and epithelial integrity. Microbial imbalances exacerbate these malignancies, creating a pro-inflammatory microenvironment. The interplay between modifiable factors and genetic predisposition, including high-penetrance mutations and polygenic risk scores, highlights the complexity complexity of prevention of gynecological cancers. Epigenetic mechanisms, such as DNA methylation and histone modifications, further modulate susceptibility and tumor progression, influenced by environmental and lifestyle exposures. In addition, promoting and supporting healthy lifestyle changes, including smoking cessation, increased physical activity, and a balanced diet, are crucial for improving long-term outcomes and quality of life in gynecological cancer survivors. Addressing these factors through personalized prevention, leveraging predictive models incorporating genetics and modifiable risks, enables tailored lifestyle interventions and avoidance of environmental exposures. Combined with equitable public health initiatives, these strategies have the potential to reduce the burden of gynecological cancers and improve women's health globally.
环境和生活方式因素在很大程度上导致了妇科癌症。卵巢癌是最致命的妇科癌症之一,其风险与肥胖、不良饮食习惯和环境污染物有关,会加剧激素失衡、炎症和氧化应激。一些保护因素,如地中海饮食和口服避孕药,通过减少排卵周期来调节风险,尤其是在有遗传易感性的女性中。子宫癌与代谢因素有关,肥胖会导致激素紊乱和全身炎症。缺乏体育锻炼和富含动物脂肪的饮食会增加子宫内膜癌的风险,空气污染和微生物群失衡也会导致子宫内膜癌的发生。宫颈癌主要由持续的高危人乳头瘤病毒(HPV)感染引起,吸烟会增强病毒的持续性和致癌作用。抗氧化剂和叶酸的营养缺乏会削弱免疫防御,而阴道和肠道微生物群失调会促进肿瘤进展。外阴癌和阴道癌虽然不太常见,但有共同的风险因素,如肥胖、吸烟和职业暴露,这些会破坏免疫反应和上皮完整性。微生物失衡会加剧这些恶性肿瘤,营造促炎微环境。可改变因素与遗传易感性之间的相互作用,包括高外显率突变和多基因风险评分,凸显了预防妇科癌症的复杂性。表观遗传机制,如DNA甲基化和组蛋白修饰,会进一步调节易感性和肿瘤进展,其受环境和生活方式暴露的影响。此外,促进和支持健康的生活方式改变,包括戒烟、增加体育锻炼和均衡饮食,对于改善妇科癌症幸存者的长期预后和生活质量至关重要。通过个性化预防来解决这些因素,利用纳入遗传学和可改变风险的预测模型,能够进行量身定制的生活方式干预并避免环境暴露。结合公平的公共卫生举措,这些策略有可能减轻全球妇科癌症负担并改善女性健康。