scholarly journals Rare ovarian tumours. Other treatments for ovarian cancer

2020 ◽  
Vol 15 ◽  
pp. 96-103
Author(s):  
Marta Gil-Martin ◽  
Beatriz Pardo ◽  
Maria-Pilar Barretina-Ginesta
2021 ◽  
Author(s):  
Yingfeng Zhang ◽  
Yanhong Gao ◽  
Congcong Sun ◽  
Yanhua Mao ◽  
Benyuan Wu ◽  
...  

Abstract Background: KIAA1456 is effective in the inhibition of tumorigenesis. We previously confirmed that KIAA1456 inhibits cell proliferation and metastasis in epithelial ovarian tumours. In the current study, the specific molecular mechanisms and clinical significance of KIAA1456 underlying the repression of epithelial ovarian cancer were investigated.Methods: Immunohistochemistry was used to evaluate the protein expression of KIAA1456 and SSX1 in epithelial ovarian tumours and normal ovarian tissues. The relationship of KIAA1456 and SSX1 with overall survival of patients with epithelial ovarian cancer was analysed with Kaplan–Meier survival curve and log-rank tests. KIAA1456 was overexpressed and silenced in HO8910PM cells with a lentivirus. The anticancer activity of KIAA1456 was tested by CCK8, plate clone formation assay, flow cytometry, wound healing assay and Transwell invasion assay. Xenograft tumour models were used to investigate the effects of KIAA1456 on tumour growth in vivo. Bioinformatics analyses of microarray profiling indicated that SSX1 and the PI3K/AKT signalling pathway were differentially expressed in KIAA1456-overexpressing and control cells. Therefore, the biological function of HO8910PM cotransfected with KIAA1456- and SSX1-overexpressing cells was detected to validate the rescue effect of SSX1. The downstream factors of PI3K/AKT that are related to cell growth and apoptosis, including p-AKT, PCNA, MMP9, CyclinD1 and Bcl-2, were detected by Western blot analysis.Results: KIAA1456 expression was lower in epithelial ovarian tumours than in normal ovarian tissues. Its expression level negatively correlated with pathological grade. Pearson’s correlation analysis showed that KIAA1456 negatively correlated with SSX1 expression. The overexpression of KIAA1456 in HO8910PM cells inhibited proliferation, migration and invasion and promoted apoptosis. By contrast, the silencing of KIAA1456 resulted in the opposite behaviour. A xenograft tumour experiment showed that KIAA1456 overexpression inhibited tumour growth in vivo. Mechanistically, the overexpression of KIAA1456 inhibited SSX1 expression and AKT phosphorylation in HO8910PM cells, causing the inactivation of the AKT signalling pathway and eventually reducing the expression of PCNA, CyclinD1, MMP9 and Bcl2. Similarly, the silencing of KIAA1456 resulted in the opposite behaviour. Finally, SSX1 overexpression could partially reverse the KIAA1456-induced biological effect.Conclusion: KIAA1456 may serve as a tumour suppressor via the inactivation of SSX1 and the AKT pathway, providing a promising therapeutic target for epithelial ovarian cancers.


2013 ◽  
Vol 28 (12) ◽  
pp. 3358-3369 ◽  
Author(s):  
C. C. M. Buis ◽  
F. E. van Leeuwen ◽  
T. M. Mooij ◽  
C. W. Burger ◽  

2009 ◽  
Vol 137 (1-2) ◽  
pp. 47-51 ◽  
Author(s):  
Tibor Pastor ◽  
Branka Popovic ◽  
Ana Gvozdenovic ◽  
Aleksandar Boro ◽  
Bojana Petrovic ◽  
...  

Introduction. According to clinical and epidemiological studies, ovarian cancer ranks fifth in cancer deaths among women. The causes of ovarian cancer remain largely unknown but various factors may increase the risk of developing it, such as age, family history of cancer, childbearing status etc. This cancer results from a succession of genetic alterations involving oncogenes and tumour suppressor genes, which have a critical role in normal cell growth regulation. Mutations and/or overexpression of three oncogenes, c-erbB-2, c-Myc and K-ras, and of the tumour suppressor gene p53, have been frequently observed in a sporadic ovarian cancer. Objective. The aim of the present study was to analyze c-Myc and c-erbB-2 oncogene alterations, specifically amplification, as one of main mechanisms of their activation in ovarian cancers and to establish a possible association with the pathogenic process. Methods. DNA was isolated from 15 samples of malignant and 5 benign ovarian tumours, using proteinase K digestion, followed by phenol-chloroform isoamyl extraction and ethanol precipitation. C-Myc and c-erbB-2 amplification were detected by differential PCR. The level of gene copy increase was measured using the Scion image software. Results. The amplification of both c-Myc and c-erbB-2 was detected in 26.7% of ovarian epithelial carcinoma specimens. Only one tumour specimen concomitantly showed increased gene copy number for both studied genes. Interestingly, besides amplification, gene deletion was also detected (26.7% for c-erbB-2). Most of the ovarian carcinomas with alterations in c-Myc and c-erbB-2 belonged to advanced FIGO stages. Conclusion. The amplification of c-Myc and c-erbB-2 oncogenes in ovarian epithelial carcinomas is most probably a late event in the pathogenesis conferring these tumours a more aggressive biological behaviour. Similarly, gene deletions point to genomic instability in epithelial carcinomas in higher clinical stages as the result of clonal evolution and selection.


2007 ◽  
Vol 25 (18_suppl) ◽  
pp. 5512-5512
Author(s):  
C. R. James ◽  
J. E. Quinn ◽  
P. B. Mullan ◽  
P. G. Johnston ◽  
D. P. Harkin

5512 Background: First line treatment of ovarian cancer (OC) involves both Platinum and Taxane based chemotherapy and reduced BRCA1 mRNA and protein expression levels are observed in up to 70% of sporadic ovarian tumours. We, therefore, investigated whether BRCA1 may represent a biomarker of response to chemotherapy in sporadic ovarian cancer. Methods: As in vitro models of sporadic ovarian cancer, we used both antisense and siRNA to abrogate BRCA1 expression in BG-1 and OVCAR5 ovarian cancer cells, respectively. Apoptotic responses to DNA damaging agents and antimicrotubule agents were measured using dose inhibition assays and Annexin V flow cytometry. Quantitiative real time PCR analysis (qRTPCR) was employed to measure BRCA1 mRNA expression in 54 surgically resected ovarian tumours. Univariate analysis provided an evaluation of the effect of BRCA1 mRNA expression and response to platinum or platinum/Taxane containing chemotherapy. Results: We provide in vitro evidence that BRCA1 differentially modulates chemosensitivity in sporadic ovarian cancer. Specifically, we demonstrate that antisense and siRNA inhibition of BRCA1 expression in both BG1 and OVCAR5 ovarian cancer cells, respectively, results in increased sensitivity to both cisplatin and carboplatin and decreased apoptotic response to both paclitaxel and docetaxel. Subsequently, by retrospective clinical analysis of 54 fresh frozen sporadic ovarian tumours we demonstrate that patients with low levels of BRCA1 have a significantly improved overall survival when treated with a platinum based chemotherapy regimen in comparison to patients with high levels of BRCA1 (30.4 months vs 21 months, p=0.047, HR 0.5). In addition, overall median survival for high BRCA1 expressing patients was found to double upon the addition of a taxane containing regimen (46.82 months vs 21 months, p=0.068, HR 0.44). Conclusions: We demonstrate both in vitro and in vivo evidence to support a role for BRCA1 as a predictive marker of response to chemotherapy in sporadic ovarian cancer. We believe that this study is significant given the high incidence of reduced BRCA1 mRNA and protein levels observed in sporadic ovarian cancer and may therefore have implications for the future management of this disease. No significant financial relationships to disclose.


1999 ◽  
Vol 14 (Suppl_3) ◽  
pp. 129-129
Author(s):  
E. Siebzehnrübl ◽  
T. Klein ◽  
P. Licht ◽  
S. Kissler

2019 ◽  
Vol 8 (11) ◽  
pp. 1784 ◽  
Author(s):  
Vincent Dochez ◽  
Mélanie Randet ◽  
Céline Renaudeau ◽  
Jérôme Dimet ◽  
Aurélie Le Thuaut ◽  
...  

Background: Presumed benign ovarian tumours (PBOT) are defined by the International Ovarian Tumour Analysis (IOTA) group, without suspected sonographic criteria of cancer, without ascites or metastasis. The aim is to evaluate the efficacy of human epididymis protein 4 (HE4), cancer antigen 125 (CA125), the risk of malignancy index (RMI) and the risk of ovarian malignancy index (ROMA) to predict ovarian cancer in women with PBOT. Methods: It is a prospective, observational, multicentre, laboratory-based study including women with PBOT in four hospitals from 11 May 2015 through 12 May 2016. Preoperative CA125 and HE4 plasma levels were measured for all women. The primary endpoint was the specificity of CA125 and HE4 for diagnosing ovarian cancer. The main secondary endpoints were specificity and likelihood ratio of RMI, ROMA and tumours markers. Results: Two hundred and fifty patients were initially enrolled and 221 patients were finally analysed, including 209 benign ovarian tumours (94.6%) and 12 malignant ovarian tumours (5.4%). The malignant group had significantly higher mean values of HE4, CA125, RMI and ROMA compared to the benign group (p < 0.001). Specificity was significantly higher using a combination of HE4 and CA125 (99.5%) compared to either HE4 or CA125 alone (90.4% and 91.4%, respectively, p < 0.001). Moreover, the positive likelihood ratio for combination HE4 and CA125 was significantly higher (104.5; 95% CI 13.6–800.0) compared to HE4 alone (5.81; 95% CI 2.83–11.90) or CA125 alone (6.97; 95% CI 3.91–12.41). Conclusions: The combination of HE4 and CA125 represents the best tool to predict the risk of ovarian cancer in patients with a PBOT.


Author(s):  
W G Haije

Cancer of the ovary is the commonest cause of death from gynaecological neoplasms. As ovarian tumours are relatively inaccessible, there is a great need for methods to improve early diagnosis and to assist with the management of patients with this disease. In this presentation the state of the art is discussed with regard to the usefulness of the presently recognised ‘tumour antigens’ and other biochemical markers in ovarian cancer. Of the oncodevelopmental antigens, only alpha fetoprotein and chorionic gonadotropin are well established as good markers in tumours with, respectively, yolk sac and trophoblastic elements. Carcinoembryonic antigen seems from our own experience to be an unreliable marker in cancer of the ovary. In epithelial tumours, which constitute the majority of ovarian malignancies, mostly serous and mucinous cystadenocarcinomas, some tumour products have been described, which may have potential as a marker, for example, ovarian cancer associated antigens, some glycoprotein glycosyltransferases, and also carcinoplacental alkaline phosphatases (CPAP). Recently, in patients with epithelial ovarian tumours attending our institute, multiple biochemical markers have been studied, including CPAP, phosphohexose isomerase, and some acute phase reactant proteins. The preliminary results, which will be discussed, show that longitudinal studies of some of these markers could have clinical application in follow-up. It must be concluded that, in spite of all efforts so far, and although some markers may become useful, early detection of ovarian cancer is a goal still to be reached by clinical chemistry in the field of oncology.


2020 ◽  
Author(s):  
Marek Nowak ◽  
Marcin Misiek ◽  
Łukasz Janas ◽  
Iwona Piwowarczyk ◽  
Malwina Soja ◽  
...  

Sign in / Sign up

Export Citation Format

Share Document