癌症风险受遗传和体细胞突变、暴露、年龄、性别和性别的影响。性别和性别单独发挥作用以及与其他癌症危险因素结合发挥作用的机制仍未得到充分探索。一般来说，无论遗传血统、地理位置和年龄如何，与 XX 个体相比，男性和女性中发生的癌症在 XY 个体中更常见。此外，XY 个体的癌症治愈率较低，这凸显了需要更好地了解性别和性别对肿瘤学的影响。这对于最佳的实验室和临床癌症研究是必要的。为此，我们回顾了性分化的表观遗传学及其对一生中癌症标志途径的影响。具体来说，我们将探讨新陈代谢、免疫、多能性和肿瘤抑制功能方面的性别差异如何通过印记、性染色体补体、X失活、逃避X失活的基因、性激素和生活史的表观遗传效应来形成模式。

Cancer risk is modulated by hereditary and somatic mutations, exposures, age, sex, and gender. The mechanisms by which sex and gender work alone and in combination with other cancer risk factors remain underexplored. In general, cancers that occur in both the male and female sexes occur more commonly in XY compared with XX individuals, regardless of genetic ancestry, geographic location, and age. Moreover, XY individuals are less frequently cured of their cancers, highlighting the need for a greater understanding of sex and gender effects in oncology. This will be necessary for optimal laboratory and clinical cancer investigations. To that end, we review the epigenetics of sexual differentiation and its effect on cancer hallmark pathways throughout life. Specifically, we will touch on how sex differences in metabolism, immunity, pluripotency, and tumor suppressor functions are patterned through the epigenetic effects of imprinting, sex chromosome complement, X inactivation, genes escaping X inactivation, sex hormones, and life history.