The Molecular Fingerprint of High Grade Serous Ovarian Cancer Reflects Its Fallopian Tube Origin

International Journal of Molecular Sciences

Mirjana Kessler¹  Christina Fotopoulou² 

[1] Max Planck Institute for Infection Biology, Department of Molecular Biology, Charitéplatz 1, 11017 Berlin, Germany; E-Mail:;Department of Gynecology, Charité, Campus Virchow Clinic, University Hospital Augustenburger Platz 1, 13353 Berlin, Germany; E-Mail:

关键词: serous ovarian cancer;    fallopian tube;    p53 signature;    STIC;    cellular transformation;    cancer stem cells (CSC);    tumor microenvironment;   

DOI  :  10.3390/ijms14046571

来源: mdpi

【 摘 要 】

High grade serous ovarian cancer (HGSC), the most lethal and frequent type of epithelial ovarian cancer (EOC), has poor long term prognosis due to a combination of factors: late detection, great metastatic potential and the capacity to develop resistance to available therapeutic drugs. Furthermore, there has been considerable controversy concerning the etiology of this malignancy. New studies, both clinical and molecular, strongly suggest that HGSC originates not from the surface of the ovary, but from the epithelial layer of the neighboring fallopian tube fimbriae. In this paper we summarize data supporting the central role of fallopian tube epithelium in the development of HGSC. Specifically, we address cellular pathways and regulatory mechanisms which are modulated in the process of transformation, but also genetic changes which accumulate during disease progression. Similarities between fallopian tube mucosa and the malignant tissue of HGSC warrant a closer analysis of homeostatic mechanisms in healthy epithelium in order to elucidate key steps in disease development. Finally, we highlight the importance of the cancer stem cell (CSC) identification and understanding of its niche regulation for improvement of therapeutic strategies.

【 授权许可】

CC BY   
© 2013 by the authors; licensee MDPI, Basel, Switzerland