Department of Histology, "Gr. T. Popa" University of Medicine and Pharmacy, Iasi, Romania.
Histol Histopathol. 2012 Jun;27(6):707-19. doi: 10.14670/HH-27.707.
Starting from the information on ovarian cancer provided by the mainstream publications, we construct a review focusing on the following issues: (i) the genetic profile, (ii) the role of the epithelial-mesenchymal transition in the acquirement of malignant features, (iii) the controversial hypothesis regarding the origin, and (iv) the involvement of the immune system in the tumoral microenvironment. Advances in the decipherment at the genetic level in the pathogenic mechanisms progressively lead to the idea of a genetic signature for the ovarian cancer. Moreover, the complementary approaches oriented towards the decryption of the intrinsic structure of the expressed molecules and, implicitly, the development of proteomics open new perspectives for an early diagnosis and an appropriate treatment. The research on the epithelial-mesenchymal transition (mainly those exploring the signaling pathways responsible for the switch between the loss of the epithelial characteristics and the gain of a mesenchymal cell phenotype, with results in the amplification of differentiation, motility and tumoral invasion) allow a deeper understanding of the complex pathogenic mechanism which governs ovarian carcinogenesis. The classic conception of ovarian cancer pathogeny, based on the role of the ovarian surface epithelium, is currently reconsidered, and a novel hypothesis is formulated, which supports direct involvement of the Fallopian tubes for the serous type. Although recent research suggests the implication of immune/inflammatory cells by specific mechanisms in ovarian cancer pathogenesis, there is yet reliable evidence concerning their modality of direct action and/or modulation of tumoral growth. Thus, ovarian carcinogenesis remains a research challenge, due to still numerous unknown factors involved in the malignant transformation sequences, originating from the genetic-molecular alterations and reflected by cellular and tissue expression patterns.
从主流出版物提供的卵巢癌信息入手，我们构建了一个综述，重点关注以下问题：（i）遗传特征，（ii）上皮-间充质转化在获得恶性特征中的作用，（iii）关于起源的有争议假说，以及（iv）免疫系统在肿瘤微环境中的参与。在致病机制的遗传水平上的进展逐渐导致了卵巢癌的遗传特征的想法。此外，针对表达分子内在结构的解密的互补方法，以及蛋白质组学的发展，为早期诊断和适当治疗开辟了新的前景。对上皮-间充质转化的研究（主要是那些探索负责上皮特征丧失和间充质细胞表型获得之间转换的信号通路的研究，其结果是分化、运动和肿瘤侵袭的扩增）使人们能够更深入地了解控制卵巢癌发生的复杂致病机制。基于卵巢表面上皮作用的经典卵巢癌发病机制概念目前正在重新考虑，并提出了一个新的假说，该假说支持浆液性肿瘤的输卵管直接参与。尽管最近的研究表明免疫/炎症细胞通过特定机制参与卵巢癌的发病机制，但关于它们的直接作用方式和/或肿瘤生长的调节方式仍缺乏可靠证据。因此，由于涉及恶性转化序列的许多未知因素，卵巢癌仍然是一个研究挑战，这些因素源于遗传-分子改变，并反映在细胞和组织表达模式中。
