Low-Grade Ovarian Serous Neoplasms (Low-Grade Serous Carcinoma and Serous Borderline Tumor) Associated With High-Grade Serous Carcinoma or Undifferentiated Carcinoma

2012 ◽  
Vol 36 (3) ◽  
pp. 368-375 ◽  
Author(s):  
Clinton Boyd ◽  
W. Glenn McCluggage

F1000Research ◽  
2019 ◽  
Vol 8 ◽  
pp. 1630
Author(s):  
Mariana Rei ◽  
Sofia Raposo ◽  
Paulo Figueiredo ◽  
Rita Sousa ◽  
Luís Sá

Ovarian borderline serous tumors present with peritoneal involvement in 20% of cases, either as non-invasive or invasive implants, the latter also known as extraovarian low-grade serous carcinoma. The coexistence of high-grade serous carcinoma is rare, suggesting a synchronous neoplasia with a distinct and independent tumor biology and behavior. We aim to describe a case of a synchronous ovary-peritoneum neoplasia: serous borderline tumor and primary peritoneal high-grade serous carcinoma. A discussion and literature review concerning the optimal diagnostic and therapeutic approach is provided.



F1000Research ◽  
2019 ◽  
Vol 8 ◽  
pp. 1630
Author(s):  
Mariana Rei ◽  
Sofia Raposo ◽  
Paulo Figueiredo ◽  
Rita Sousa ◽  
Luís Sá

Ovarian borderline serous tumors present with peritoneal involvement in 20% of cases, either as non-invasive or invasive implants, also known as extraovarian low-grade serous carcinoma. The coexistence of high-grade serous carcinoma is rare, suggesting a synchronous neoplasia with a distinct and independent tumor biology and behavior. We aim to describe a case of a synchronous ovary-peritoneum neoplasia: serous borderline tumor and primary peritoneal high-grade serous carcinoma. A discussion and literature review concerning the optimal diagnostic and therapeutic approach is provided.



2011 ◽  
Vol 29 (30) ◽  
pp. e763-e765 ◽  
Author(s):  
Donata Rohsbach ◽  
Fabian Trillsch ◽  
Marc Regier ◽  
Matthias Choschzick ◽  
Friedrich Kommoss ◽  
...  


2020 ◽  
Vol 38 (8) ◽  
pp. 782-789
Author(s):  
Masaya Kawaguchi ◽  
Hiroki Kato ◽  
Yuichiro Hatano ◽  
Hiroyuki Tomita ◽  
Akira Hara ◽  
...  


2014 ◽  
Vol 2014 ◽  
pp. 1-11 ◽  
Author(s):  
Masafumi Koshiyama ◽  
Noriomi Matsumura ◽  
Ikuo Konishi

Type I ovarian tumors, where precursor lesions in the ovary have clearly been described, include endometrioid, clear cell, mucinous, low grade serous, and transitional cell carcinomas, while type II tumors, where such lesions have not been described clearly and tumors may developde novofrom the tubal and/or ovarian surface epithelium, comprise high grade serous carcinomas, undifferentiated carcinomas, and carcinosarcomas. The carcinogenesis of endometrioid and clear cell carcinoma (CCC) arising from endometriotic cysts is significantly influenced by the free iron concentration, which is associated with cancer development through the induction of persistent oxidative stress. A subset of mucinous carcinomas develop in association with ovarian teratomas; however, the majority of these tumors do not harbor any teratomatous component. Other theories of their origin include mucinous metaplasia of surface epithelial inclusions, endometriosis, and Brenner tumors. Low grade serous carcinomas are thought to evolve in a stepwise fashion from benign serous cystadenoma to a serous borderline tumor (SBT). With regard to high grade serous carcinoma, the serous tubal intraepithelial carcinomas (STICs) of the junction of the fallopian tube epithelium with the mesothelium of the tubal serosa, termed the “tubal peritoneal junction” (TPJ), undergo malignant transformation due to their location, and metastasize to the nearby ovary and surrounding pelvic peritoneum. Other theories of their origin include the ovarian hilum cells.



2015 ◽  
Vol 46 (10) ◽  
pp. 1455-1463 ◽  
Author(s):  
Hiroko Imamura ◽  
Yoshihiro Ohishi ◽  
Murasaki Aman ◽  
Kaai Shida ◽  
Tomoko Shinozaki ◽  
...  


Cancers ◽  
2021 ◽  
Vol 13 (20) ◽  
pp. 5240
Author(s):  
Sandra Wessman ◽  
Beatriz Bohorquez Fuentes ◽  
Therese Törngren ◽  
Anders Kvist ◽  
Georgia Kokaraki ◽  
...  

Background: We examined whether molecular characterization of high-grade epithelial ovarian cancer can inform the diagnosis and/or identify potential actionable targets. Methods: All of the consecutively sequenced high-grade ovarian tumours with consent between 2014 until 2019 were included. A total of 274 tumours underwent next generation sequencing using a targeted panel. Results: Patients with high-grade ovarian epithelial cancer were consented to prospective molecular characterization. Clinical information was extracted from their medical record. Tumour DNA was subjected to sequencing, and selected patients received PARP inhibitor therapy. Conclusions: Tumours from 274 women were sequenced, including high-grade serous carcinoma (n = 252), clear cell carcinoma (n = 4), carcinosarcoma (n = 9), endometrioid carcinoma (n = 3), undifferentiated carcinoma (n = 1), and mixed tumours (n = 5). Genomic profiling did not influence histologic diagnosis. Mutations were identified in TP53, BRCA1, BRCA2, as well as additional homologous recombination repair pathway genes BARD1, ATR, CHEK2, PALB2, RAD51D, RAD50, SLX4, FANCA, RAD51C, and RAD54L. In addition, mutations in PTEN and CDKN2A were identified. Several somatic mutations with implications for germline testing were identified, including RMI1, STK11, and CDH1. Germline testing identified 16 previously unknown BRCA1/2 carriers. Finally, 20 patients were treated with the PARP inhibitor olaparib based on the sequencing results.



2008 ◽  
Vol 18 (3) ◽  
pp. 487-491 ◽  
Author(s):  
R. SALANI ◽  
R. J. KURMAN ◽  
R. GIUNTOLI ◽  
G. GARDNER ◽  
R. BRISTOW ◽  
...  

The TP53 mutation frequency in ovarian serous carcinomas has been reported to range between 50% and 80%, but a stringent analysis of TP53 using purified epithelial samples has not yet been performed to accurately assess the mutation frequency and to correlate it with the histologic grade. The purpose of this study was to assess the TP53 mutational profile in a relatively large series of high-grade (53 primary and 18 recurrent) and 13 low-grade ovarian serous tumors using DNA isolated from affinity-purified tumor cells and to correlate it with in vitro drug resistance. All samples were affinity purified, and the tumor DNA was analyzed for TP53 mutations in exons 4–9. In vitro drug resistance assays to carboplatin, cisplatin, paclitaxel, and taxotere were performed on the same tumor samples and correlated with the TP53 mutation status. TP53 mutations were detected in 57 (80.3%) of 71 high-grade carcinomas and in one (7.8%) of 13 low-grade serous tumors (an invasive low-grade serous carcinoma). The mutations were predominantly missense mutations (59.6%). TP53 mutations were associated with high-grade serous carcinomas and recurrent disease (P < 0.0001). There was no statistically significant correlation between TP53 mutation status and drug resistance assays or clinical stage (P > 0.25). The frequency of TP53 mutations using purified tumor DNA from ovarian serous carcinomas was 80.3%, which is much higher than previously reported. Furthermore, we found that TP53 is not directly involved in the development of drug resistance in high-grade ovarian serous carcinomas.



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