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Good Guy or Bad Guy? The Duality of Wild-Type p53 in Hormone-Dependent Breast Cancer Origin Treatment and Recurrence

机译:好人还是坏人?野生型p53在激素依赖性乳腺癌的起源治疗和复发中的双重性

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摘要

“Lactation is at one point perilously near becoming a cancerous process if it is at all arrested”, Beatson, 1896. 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 TP53 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.
机译:Beatson,1896年:“一旦完全被阻止,泌乳就会危险地接近癌变过程。”大多数乳腺癌来自产奶细胞,其特征在于细胞,分子和表观遗传学翻译异常。通过了解导致癌症起源的潜在分子破坏,我们可能能够设计出更有效的治疗方法,或者雄心勃勃地转移癌变过程的新策略。已经确定的现实是,年轻女性的充分妊娠可以终生降低乳腺癌的风险,而充分妊娠的延迟则增加了短期乳腺癌的风险和潜在的乳腺癌发展的可能性。已确定在妊娠关键时刻乳腺中p53蛋白的激素激活(由TP53基因编码)是确定乳腺是否发展潜伏性乳腺癌的最重要决定因素之一。这篇评论讨论了女性荷尔蒙在年轻的产后妇女中的保护作用,特别关注野生型p53重编程在乳腺细胞分化中的适当作用。还探讨了p53在激素依赖性乳腺癌,治疗耐药性和复发中作为保护者或作案者的重要性。

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