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 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 Aberrant Methylation Status of Tumour Suppressor Genes in Ovarian Cancer Tissue and Paired Plasma Samples

2019 ◽  
Vol 20 (17) ◽  
pp. 4119 ◽  
Author(s):  
Dana Dvorská ◽  
Dušan Braný ◽  
Bálint Nagy ◽  
Marián Grendár ◽  
Robert Poka ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Tumour Suppressor ◽  
Tumour Suppressor Genes ◽  
Aberrant Methylation ◽  
Potential Candidate ◽  
Plasma Samples ◽  
Cdh1 Gene ◽  
Suppressor Genes ◽  
Non Invasive ◽  
Malignant Lesions

Ovarian cancer is a highly heterogeneous disease and its formation is affected by many epidemiological factors. It has typical lack of early signs and symptoms, and almost 70% of ovarian cancers are diagnosed in advanced stages. Robust, early and non-invasive ovarian cancer diagnosis will certainly be beneficial. Herein we analysed the regulatory sequence methylation profiles of the RASSF1, PTEN, CDH1 and PAX1 tumour suppressor genes by pyrosequencing in healthy, benign and malignant ovarian tissues, and corresponding plasma samples. We recorded statistically significant higher methylation levels (p < 0.05) in the CDH1 and PAX1 genes in malignant tissues than in controls (39.06 ± 18.78 versus 24.22 ± 6.93; 13.55 ± 10.65 versus 5.73 ± 2.19). Higher values in the CDH1 gene were also found in plasma samples (22.25 ± 14.13 versus 46.42 ± 20.91). A similar methylation pattern with positive correlation between plasma and benign lesions was noted in the CDH1 gene (r = 0.886, p = 0.019) and malignant lesions in the PAX1 gene (r = 0.771, p < 0.001). The random forest algorithm combining methylation indices of all four genes and age determined 0.932 AUC (area under the receiver operating characteristic (ROC) curve) prediction power in the model classifying malignant lesions and controls. Our study results indicate the effects of methylation changes in ovarian cancer development and suggest that the CDH1 gene is a potential candidate for non-invasive diagnosis of ovarian cancer.

scholarly journals The Frizzled-ligand Norrin acts as a tumour suppressor linking oncogenic RAS signalling to p53

2019 ◽  
Author(s):  
Gabriele Sulli ◽  
Errico D’Elia ◽  
M. Cristina Moroni
Keyword(s):  
Human Cancer ◽  
Tumour Progression ◽  
P53 Protein ◽  
Normal Function ◽  
Tumour Suppressor ◽  
Tumour Suppressor Genes ◽  
Suppressor Genes ◽  
P53 Pathway ◽  
Genetic Event

AbstractTumour suppressor genes are frequently affected by somatic alterations in cancer, and the impairment of their normal function provides a strong contribution to tumourigenesis. Short-hairpin (sh) RNA library screens have been employed as powerful genetic tools to uncover important new players in human cancer 1–5. To identify potential novel tumour suppressor genes acting in the p53 pathway, we performed an shRNA screen using a cell-based model in which only a single additional genetic event disrupting the p53 pathway is required to obtain in vitro transformation. By using this approach, we report here on the identification of the Frizzled-ligand Norrin (Norrie disease protein) as a candidate tumour suppressor. Inhibition of Norrin expression promotes anchorage-independent growth, confers a strong growth advantage to cells and causes a reduction in p53 protein levels. Conversely, recombinant human Norrin increases p53 levels in a β-catenin dependent fashion. Interestingly, Norrin expression is stimulated by oncogenic H-RAS and BRAF, suggesting that Norrin is part of an early fail-safe mechanism to suppress transformation, and that mutation or down regulation of Norrin could contribute to tumour progression. Indeed, we found that Norrin expression is significantly decreased in melanoma, breast, prostate and ovarian cancer. These findings support the existence of a novel autocrine/paracrine feedback loop that constrains tumourigenesis, in which the crosstalk between the RAS and β–catenin pathways play an unanticipated role.

scholarly journals Exclusion of BBC1 and CMAR as candidate breast tumour-suppressor genes

1997 ◽  
Vol 76 (12) ◽  
pp. 1550-1553 ◽  
Author(s):  
E Moerland ◽  
MH Breuning ◽  
CJ Cornelisse ◽  
AM Cleton-Jansen
Keyword(s):  
Breast Tumour ◽  
Tumour Suppressor ◽  
Tumour Suppressor Genes ◽  
Suppressor Genes
Sign in / Sign up

Export Citation Format

Share Document