scholarly journals Alterations of c-Myc and c-erbB-2 genes in ovarian tumours

2009 ◽  
Vol 137 (1-2) ◽  
pp. 47-51 ◽  
Author(s):  
Tibor Pastor ◽  
Branka Popovic ◽  
Ana Gvozdenovic ◽  
Aleksandar Boro ◽  
Bojana Petrovic ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Critical Role ◽  
Genetic Alterations ◽  
Tumour Suppressor ◽  
Proteinase K ◽  
Gene Copy ◽  
Tumour Suppressor Genes ◽  
Ovarian Carcinomas ◽  
Benign Ovarian Tumours ◽  
Ovarian Tumours

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.

scholarly journals Tumour suppressor genes in ovarian cancer.

BMJ ◽  
1993 ◽  
Vol 307 (6910) ◽  
pp. 1009-1009 ◽  
Author(s):  
W Foulkes
Keyword(s):  
Ovarian Cancer ◽  
Tumour Suppressor ◽  
Tumour Suppressor Genes ◽  
Suppressor Genes

scholarly journals Tumour suppressor genes and risk of metastasis in ovarian cancer.

BMJ ◽  
1993 ◽  
Vol 307 (6903) ◽  
pp. 542-542 ◽  
Author(s):  
W S Lowry ◽  
R J Atkinson
Keyword(s):  
Ovarian Cancer ◽  
Tumour Suppressor ◽  
Tumour Suppressor Genes ◽  
Suppressor Genes

scholarly journals Metadherin, p50, and p65 Expression in Epithelial Ovarian Neoplasms: An Immunohistochemical Study

2014 ◽  
Vol 2014 ◽  
pp. 1-8 ◽  
Author(s):  
Ioanna Giopanou ◽  
Vasiliki Bravou ◽  
Panagiotis Papanastasopoulos ◽  
Ioannis Lilis ◽  
Panagiotis Aroukatos ◽  
...  
Keyword(s):  
Cancer Progression ◽  
Ovarian Neoplasms ◽  
Immunohistochemical Study ◽  
Gradual Increase ◽  
Immunohistochemical Expression ◽  
Ovarian Carcinomas ◽  
Benign Ovarian Tumours ◽  
Ovarian Carcinogenesis ◽  
Significant Difference ◽  
Ovarian Tumours

NF-κB signaling promotes cancer progression in a large number of malignancies. Metadherin, a coactivator of the NF-κB transcription complex, was recently identified to regulate different signaling pathways that are closely related to cancer. We assessed the immunohistochemical expression of p50, p65, and metadherin in 30 ovarian carcinomas, 15 borderline ovarian tumours, and 31 benign ovarian cystadenomas. Ovarian carcinomas exhibited significantly higher expression of all 3 markers compared to benign ovarian tumours. Borderline ovarian tumours demonstrated significantly higher expression for all 3 markers compared to benign cystadenomas. Ovarian carcinomas demonstrated significantly higher expression of p50 and metadherin compared to borderline ovarian tumours, whereas no significant difference was noted in p65 expression between ovarian carcinomas and borderline ovarian tumours. There was a strong correlation with the expression levels of p50, p65, and metadherin, whereas no correlation was observed with either grade or stage. Strong p50, p65, and metadherin expression was associated with a high probability to distinguish ovarian carcinomas over borderline and benign ovarian tumours, as well as borderline ovarian tumours over benign ovarian neoplasms. A gradual increase in the expression of these molecules is noted when moving across the spectrum of ovarian carcinogenesis, from borderline ovarian tumours to epithelial carcinomas.

The role of the Wnt signalling pathway in colorectal tumorigenesis

2005 ◽  
Vol 33 (4) ◽  
pp. 672-675 ◽  
Author(s):  
J. Behrens
Keyword(s):  
Wnt Pathway ◽  
Genetic Alterations ◽  
Wnt Signalling ◽  
Tumour Suppressor ◽  
Tumour Suppressor Genes ◽  
Adenomatous Polyposis ◽  
Polyposis Coli ◽  
Colorectal Tumorigenesis ◽  
Constitutive Activation

Colorectal cancer (CRC) is the second largest cause of cancer-related deaths in Western countries. CRC arises from the colorectal epithelium as a result of the accumulation of genetic alterations in defined oncogenes and tumour suppressor genes. Mutations in the tumour suppressor APC (adenomatous polyposis coli) genes occur early in the development of CRC and lead to the stabilization of the Wnt pathway component β-catenin and to the constitutive activation of Wnt signalling. Stabilizing mutations of β-catenin can also lead to its accumulation, qualifying β-catenin as a proto-oncogene. Here I will summarize the biochemical interactions occurring in Wnt signalling and describe how alterations in Wnt pathway components lead to CRC.

scholarly journals Paclitaxel-Induced Src Activation Is Inhibited by Dasatinib Treatment, Independently of Cancer Stem Cell Properties, in a Mouse Model of Ovarian Cancer

Cancers ◽  
2019 ◽  
Vol 11 (2) ◽  
pp. 243 ◽  
Author(s):  
Elif Kadife ◽  
Emily Chan ◽  
Rodney Luwor ◽  
George Kannourakis ◽  
Jock Findlay ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Cancer Progression ◽  
Mononuclear Cells ◽  
Ovarian Cancer Cells ◽  
Small Subset ◽  
Ovarian Carcinomas ◽  
Ovarian Cancer Cell Lines ◽  
Benign Ovarian Tumours ◽  
Src Activation

Approximately seventy percent of ovarian cancer patients succumb to the disease within the first 5 years of diagnosis, even after successful surgery and effective chemotherapy treatment. A small subset of chemotherapy resistant cancer stem cells (CSCs) cause relapse of ovarian cancers. This study investigated the association between paclitaxel-mediated Src activation (p-Src) and CSC populations in driving ovarian cancer progression. We demonstrate that patients with high-stage serous ovarian carcinomas have significantly elevated levels of p-Src, compared to patient with low-stage and benign ovarian tumours. Additionally, p-Src was significantly enhanced in ascites-derived tumour cells obtained from recurrent patients, compared to chemonaïve patients. Paclitaxel treatment increased Src activation in ovarian cancer cells, causing enrichment of CSC marker expression in the surviving cells in vitro and in xenografts of nude mice. Dasatinib in combination with paclitaxel significantly suppressed p-Src in ovarian cancer cell lines and xenografts but had no effect on the expression of CSC markers. However, combination of paclitaxel and Dasatinib showed lower trend in invasion in liver and pancreas, compared to paclitaxel-only treatment. The tumours treated with combination therapy also had significantly lower infiltration of mononuclear cells. Robust recurrent tumour growth was observed in all mice groups after termination of treatments. The above results suggest that Dasatinib-mediated inhibition of p-Src may not be crucial for paclitaxel-induced CSC-mediated recurrence in ovarian cancer.

scholarly journals Tumour suppressor genes in sporadic epithelial ovarian cancer

Reproduction ◽  
2002 ◽  
pp. 341-353 ◽  
Author(s):  
Y Liu ◽  
TS Ganesan
Keyword(s):  
Ovarian Cancer ◽  
Epithelial Ovarian Cancer ◽  
Positional Cloning ◽  
Tumour Progression ◽  
Tumour Suppressor ◽  
Western World ◽  
Tumour Suppressor Genes ◽  
Genetic Studies ◽  
Suppressor Genes ◽  
The Past

Ovarian cancer is the most frequent cause of death from gynaecological malignancies in the western world, and sporadic epithelial ovarian cancer is its most predominant form. The aetiology of sporadic ovarian cancer remains unknown. Genetic studies have enabled a better understanding of the evolution of tumour progression. A major focus of research has been to identify tumour suppressor genes implicated in sporadic ovarian cancer over the past decade. Several tumour suppressor genes have been identified by strategies such as positional cloning and differential expression display. Further research is warranted to understand fully their contribution to the pathogenesis of sporadic ovarian cancer.

scholarly journals Efficacy of HE4, CA125, Risk of Malignancy Index and Risk of Ovarian Malignancy Index to Detect Ovarian Cancer in Women with Presumed Benign Ovarian Tumours: A Prospective, Multicentre Trial

2019 ◽  
Vol 8 (11) ◽  
pp. 1784 ◽  
Author(s):  
Vincent Dochez ◽  
Mélanie Randet ◽  
Céline Renaudeau ◽  
Jérôme Dimet ◽  
Aurélie Le Thuaut ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Likelihood Ratio ◽  
Positive Likelihood Ratio ◽  
Ovarian Malignancy ◽  
Cancer Antigen 125 ◽  
Mean Values ◽  
Benign Ovarian Tumours ◽  
Ovarian Tumours ◽  
Risk Of Malignancy ◽  
Risk Of Malignancy Index

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.

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

2020 ◽  
Author(s):  
Marek Nowak ◽  
Marcin Misiek ◽  
Łukasz Janas ◽  
Iwona Piwowarczyk ◽  
Malwina Soja ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Serum Markers ◽  
Benign Ovarian Tumours ◽  
Ovarian Tumours

Gynaecological pathology

2012 ◽  
Author(s):  
James Carton
Keyword(s):  
Endometrial Carcinoma ◽  
Polycystic Ovarian Syndrome ◽  
Skin Diseases ◽  
Cervical Screening ◽  
Ovarian Cysts ◽  
Ovarian Carcinomas ◽  
Vaginal Infections ◽  
Benign Ovarian Tumours ◽  
Ovarian Tumours ◽  
Ovarian Syndrome

Vulval skin diseases 186Benign vulval tumours 187Vulval carcinoma 188Vaginal infections 190Vaginal tumours 191Cervical carcinoma 192Cervical screening 194Endometriosis 195Endometrial carcinoma 196Uterine leiomyomas 198Functional ovarian cysts 200Polycystic ovarian syndrome 202Benign ovarian tumours 204Ovarian carcinomas ...

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