Department of Obstetrics and Gynecology; College of Medicine; Pennsylvania State University; Hershey, PA USA.
Cancer Biol Ther. 2012 Jan 15;13(2):101-13. doi: 10.4161/cbt.13.2.18873.
Current knowledge of changes in the mammary epithelium relevant to breast carcinogenesis is limited to when histological changes are already present because of a lack of biomarkers needed to identify where such molecular changes might be ongoing at earlier during the of decades-long latent stages of breast carcinogenesis. Breast reduction tissues from young women and teenagers, representative of USA's high breast cancer incidence population, were studies using immunocytochemistry and targeted PCR arrays in order to learn whether a marker of chronic oxidative-stress [protein adducts of 4-hydroxy-2-nonenal (4HNE)] can identify where molecular changes relevant to carcinogenesis might be taking place prior to any histological changes. 4HNE-immunopositive (4HNE+) mammary epithelial cell-clusters were identified in breast tissue sections from most women and from many teenagers (ages 14-30 y) and, in tissues from women ages 17-27 y with many vs. few 4HNE+ cells, the expression of 30 of 84 oxidative-stress associated genes was decreased and only one was increased > 2-fold. This is in contrast to increased expression of many of these genes known to be elicited by acute oxidative-stress. The findings validate using 4HNE-adducts to identify where molecular changes of potential relevance to carcinogenesis are taking place in histologically normal mammary epithelium and highlight differences between responses to acute vs. chronic oxidative-stress. We posit that the altered gene expression in 4HNE+ tissues reflect adaptive responses to chronic oxidative-stress that enable some cells to evade mechanisms that have evolved to prevent propagation of cells with oxidatively-damaged DNA and to accrue heritable changes needed to establish a cancer.
目前,与乳腺癌发生相关的乳腺上皮变化的知识仅限于组织学变化已经存在的情况,因为缺乏识别分子变化可能发生的生物标志物,而这些分子变化可能在乳腺癌发生的数十年潜伏期的早期就已经发生了。本研究使用免疫细胞化学和靶向 PCR 阵列,研究了来自年轻女性和青少年的乳房缩小组织,这些组织代表了美国高乳腺癌发病率人群,目的是了解慢性氧化应激标志物[4-羟基-2-壬烯醛(4HNE)的蛋白加合物]是否可以识别在发生任何组织学变化之前,与致癌相关的分子变化可能发生的部位。在大多数女性和许多青少年(14-30 岁)的乳房组织切片中鉴定出 4HNE 免疫阳性(4HNE+)的乳腺上皮细胞簇,在年龄为 17-27 岁的女性组织中,与 4HNE+细胞少的女性相比,有 30 个 84 个氧化应激相关基因的表达减少,只有一个基因的表达增加了 2 倍以上。这与许多已知由急性氧化应激引发的基因表达增加形成对比。这些发现验证了使用 4HNE 加合物来识别在组织学正常的乳腺上皮中与潜在致癌相关的分子变化发生的部位,并强调了急性与慢性氧化应激反应之间的差异。我们假设,在 4HNE+组织中改变的基因表达反映了对慢性氧化应激的适应性反应,使一些细胞逃避了已进化的机制,这些机制旨在阻止具有氧化损伤 DNA 的细胞的增殖,并积累建立癌症所需的可遗传变化。