scholarly journals 264 Serum markers and cytokines in patients with ovarian cancer, endometriosis or other benign ovarian tumours

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


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.


2018 ◽  
Vol 164 ◽  
pp. S215 ◽  
Author(s):  
H. Strøm Kahr ◽  
A. Knudsen ◽  
O.B. Christiansen ◽  
A. Grove ◽  
V. Iyer ◽  
...  

2006 ◽  
Vol 24 (18_suppl) ◽  
pp. 15063-15063 ◽  
Author(s):  
E. V. Bakhidze

15063 Background: Ovarian cancer occurs in 1.5–5.6% of all combination of malignant tumours and pregnancy. The purpose of this study was to review patients with ovarian tumours in pregnancy, the efficiency of the available methods of treatment and their prognosis. Methods: A retrospective research of the data about 52 patients with ovarian tumours associated with pregnancy who were operated in The N.N.Petrov Research Institute of Oncology from 1960 to 2002. Results: From 52 patients with ovarian tumours associated with pregnancy there were 40 patients (76.9%) with benign tumours and 12 patients (23.1%) with malignant tumours. Middle age of patients was 24.9 ± 5.2 years. Among malignant tumours there were 4 epithelial tumours, 7 herm cell tumours (6 were dysgerminoma and 1 choriocarcinoma) and 1 sex cord-stromal tumour. 9 patients had I stage, 2 had II stage and 1 patient had III stage by FIGO. 14 patients with benign and 7 patients with malignant tumours was operated during the pregnancy: 13 patients (9 with benign, 4 with malignant tumours) were operated during I trimester, 4 patients (3 with benign, 1 with malignant tumours) were operated during II trimester and 4 patients (2 with benign, 2 with malignant tumours) were operated during III trimester of pregnancy. 26 patients with benign tumours and 7 patients with malignant tumours were operated after delivery or abortion. All patients with benign tumours were treated by unilateral salpingoophorectomy. 6 patients with malignant tumours were treated by organ-preserving operations. The 5-year free reccurance survival rate was 83.3% in patients operated during I trimester both for radical and organ preserving operations. The 5-year free reccurance survival rate was 50% in patients operated during II, and 33.3% in patients operated during III trimester. In 6 patients with Ia stage dysgerminoma associated with pregnancy the 5-year free reccurance survival rate was 100%. Conclusions: Benign ovarian tumours associated with pregnancy occur in much more cases (76.9%). Among malignant ovarian tumours the non-surface epithelial tumours occur more often (66.6%). The majority of patients with malignant ovarian tumours who were operated during pregnancy had I stage by FIGO (75%). Prognosis depended not on but on stage and hystotype of tumour and trimester of pregnancy in which patients were operated. No significant financial relationships to disclose.


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.


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