Ls of fallopian tubes, ovarian fimbria, ovarian surface epithelium, inclusion cysts
Ls of fallopian tubes, ovarian fimbria, ovarian surface epithelium, inclusion cysts, peritoneal mesothelium, or endometriosis, is the most lethal gynecologic malignancy* Correspondence: [email protected] 1 Department of Obstetrics and Gynecology, The Jikei University School of Medicine, 3-25-8, Nishi-Shinbashi, Minato-ku, Tokyo 105-8461, Japan Full list of author information is available at the end of the articlein western countries and in Japan [1]. EOC can be classified into four major histological types: serous, mucinous, endometrioid adenocarcinoma, and clear cell carcinoma (CCC). PubMed ID:https://www.ncbi.nlm.nih.gov/pubmed/28380356 CCC has unique clinical characteristics that differ from other histological types of EOC. CCC accounts for 5?5 of all EOC, depending on the population. The prevalence of CCC among EOCs in North America and Europe is 1?2 , while that in Japan is approximately 20 [2]. CCC is frequently associated with coexistent endometriosis and thrombosis, with 20 of patients?2014 Hirata et al.; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.Hirata et al. BMC Cancer 2014, 14:799 http://www.biomedcentral.com/1471-2407/14/Page 2 ofdeveloping deep venous thrombosis. Endometriosis has been identified in more than 30 of tumors and is reported to be a precursor of CCC as well as endometrioid adenocarcinoma [3]. The incidence of venous thromboembolic events was found to be significantly higher in CCC than in other epithelial ovarian cancers [4,5]. A greater proportion of CCC presents in the early stage as a large pelvic mass, which may account for their earlier diagnosis. However, CCC is generally refractory to standard platinum agent-based chemotherapy with a response rate of only 11?5 ; therefore, this type of tumor typically has a poor prognosis, particularly in late stages. The survival rates of patients with CCC are significantly lower than those of patients with serous EOC [6]. Identifying novel therapeutic targets and establishing new treatment strategies for CCC is thus important. The common molecular genetic alterations identified so far in CCC include mutations in ARID1A and PI3K as well as HNF1B overexpression. However, the molecular landscape of CCC oncogenesis remains poorly understood [7,8]. Since chromosomal aberrations are a cardinal feature of carcinogenesis, the identification of amplified or deleted chromosomal regions associated with CCC would elucidate its underlying pathogenetic mechanisms. Amplification at chromosome17q23-25 has been reported to occur with a frequency of approximately 40 in CCC [9]. The PPM1D gene (also known as WIP1) maps to the 17q23.2 amplicon and is amplified and/or RDX5791 cost overexpressed in various types of cancers, including CCC [10]. However, the frequency of PPM1D overexpression in CCC is reported to be only about 10 . In addition, the peak region of 17q23-25 amplification in CCC as assessed by GISTIC analysis maps adjacent to the PPM1D locus. Taken together, these findings suggest the involvement of undiscovered driver genes on 17q23-25 in CCC [11]. Recent evidence has shown that microRNAs (miRNAs) can.