McGowan Eileen M, Lin Yiguang, Hatoum Diana
Central Laboratory, The First Affiliated Hospital of Guangdong Pharmaceutical University, Guangzhou 510080, China.
School of Life Sciences, University of Technology Sydney, Sydney 2007, Australia.
Cancers (Basel). 2018 May 31;10(6):172. doi: 10.3390/cancers10060172.
"", , Most breast cancers arise from the milk-producing cells that are characterized by aberrant cellular, molecular, and epigenetic translation. By understanding the underlying molecular disruptions leading to the origin of cancer, we might be able to design novel strategies for more efficacious treatments or, ambitiously, divert the cancerous process. It is an established reality that full-term pregnancy in a young woman provides a lifetime reduction in breast cancer risk, whereas delay in full-term pregnancy increases short-term breast cancer risk and the probability of latent breast cancer development. Hormonal activation of the p53 protein (encode by the gene) in the mammary gland at a critical time in pregnancy has been identified as one of the most important determinants of whether the mammary gland develops latent breast cancer. This review discusses what is known about the protective influence of female hormones in young parous women, with a specific focus on the opportune role of wild-type p53 reprogramming in mammary cell differentiation. The importance of p53 as a protector or perpetrator in hormone-dependent breast cancer, resistance to treatment, and recurrence is also explored.
大多数乳腺癌起源于产奶细胞，这些细胞具有异常的细胞、分子和表观遗传翻译特征。通过了解导致癌症起源的潜在分子破坏，我们或许能够设计出更有效的治疗新策略，或者更有雄心地扭转癌变过程。年轻女性足月妊娠可使患乳腺癌风险终身降低，而足月妊娠延迟会增加短期患乳腺癌风险以及潜在乳腺癌发展的可能性，这是既定事实。在孕期关键时期乳腺中p53蛋白（由该基因编码）的激素激活已被确定为乳腺是否发展为潜在乳腺癌的最重要决定因素之一。本综述讨论了关于年轻经产妇中女性激素的保护作用的已知情况，特别关注野生型p53重编程在乳腺细胞分化中的适时作用。还探讨了p53作为激素依赖性乳腺癌、治疗抗性和复发中的保护者或肇事者的重要性。
