PDF(Pubmed)
Abstract：
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.
摘要：
癌症风险由遗传和体细胞突变调节，暴露,年龄,性别,和性别。性别和性别单独作用以及与其他癌症风险因素相结合的机制仍未得到充分探索。总的来说,与XX个体相比，男性和女性中发生的癌症在XY中更常见，不管遗传血统如何，地理位置,和年龄。此外，XY个体治愈癌症的频率较低，强调需要更好地了解肿瘤学中的性别和性别影响。这对于最佳的实验室和临床癌症研究是必要的。为此,我们回顾了性别分化的表观遗传学及其对整个生命过程中癌症标志通路的影响。具体来说,我们将探讨新陈代谢中的性别差异，豁免权,多能性,肿瘤抑制功能是通过印记的表观遗传效应形成的，性染色体补体，X失活,逃避X失活的基因，性激素,和生活史。
