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Exploring the Role of Fallopian Ciliated Cells in the Pathogenesis of High-Grade Serous Ovarian Cancer

1
Division of Molecular Oncology, Department of Translational Research, IRCCS CRO Aviano-National Cancer Institute, Via Franco Gallini, 2 33081 Aviano PN, Italy
2
Azienda Ospedaliera Universitaria Integrata, University of Verona, 37129 Verona, Italy
3
Scientific Direction, CRO Aviano Italy, Via Franco Gallini, 2 33081 Aviano, Italy
4
Centre for Integrative Biology, University of Trento, 38122 Trento, Italy
5
Department of clinical and molecular medicine, university of Rome “Sapienza”, c/o sant andrea hospital, Via di Grottarossa 1035, 00189 Rome, Italy
*
Author to whom correspondence should be addressed.
Int. J. Mol. Sci. 2018, 19(9), 2512; https://doi.org/10.3390/ijms19092512
Received: 6 August 2018 / Revised: 20 August 2018 / Accepted: 20 August 2018 / Published: 24 August 2018
(This article belongs to the Special Issue Ovarian Cancer: Pathogenesis, Diagnosis, and Treatment)
High-grade serous epithelial ovarian cancer (HGSOC) is the fifth leading cause of cancer death in women and the first among gynecological malignancies. Despite an initial response to standard chemotherapy, most HGSOC patients relapse. To improve treatment options, we must continue investigating tumor biology. Tumor characteristics (e.g., risk factors and epidemiology) are valuable clues to accomplish this task. The two most frequent risk factors for HGSOC are the lifetime number of ovulations, which is associated with increased oxidative stress in the pelvic area caused by ovulation fluid, and a positive family history due to genetic factors. In the attempt to identify novel genetic factors (i.e., genes) associated with HGSOC, we observed that several genes in linkage with HGSOC are expressed in the ciliated cells of the fallopian tube. This finding made us hypothesize that ciliated cells, despite not being the cell of origin for HGSOC, may take part in HGSOC tumor initiation. Specifically, malfunction of the ciliary beat impairs the laminar fluid flow above the fallopian tube epithelia, thus likely reducing the clearance of oxidative stress caused by follicular fluid. Herein, we review the up-to-date findings dealing with HGSOC predisposition with the hypothesis that fallopian ciliated cells take part in HGSOC onset. Finally, we review the up-to-date literature concerning genes that are located in genomic loci associated with epithelial ovarian cancer (EOC) predisposition that are expressed by the fallopian ciliated cells. View Full-Text
Keywords: epithelial ovarian cancer; predisposition; ciliated cells; CCDC170; DNAAF1; LRRC46; MARCH10; C20orf85; LRP2BP; SPAG6; TPPP; RSPH10B2; STK33 epithelial ovarian cancer; predisposition; ciliated cells; CCDC170; DNAAF1; LRRC46; MARCH10; C20orf85; LRP2BP; SPAG6; TPPP; RSPH10B2; STK33
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Coan, M.; Rampioni Vinciguerra, G.L.; Cesaratto, L.; Gardenal, E.; Bianchet, R.; Dassi, E.; Vecchione, A.; Baldassarre, G.; Spizzo, R.; Nicoloso, M.S. Exploring the Role of Fallopian Ciliated Cells in the Pathogenesis of High-Grade Serous Ovarian Cancer. Int. J. Mol. Sci. 2018, 19, 2512.

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