ArticleMolecular cancer2004
CpG methylation of the FHIT, FANCF, cyclin-D2, BRCA2 and RUNX3 genes in Granulosa cell tumors (GCTs) of ovarian origin.
Article in Molecular cancer, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 89 citations in OpenAlex.
- The Effects ofCells · 2026Article
- BRCA1 promoter methylation predicts PARPi response in ovarian cancer: insights from the KOMET study.Clinical epigenetics · 2025Article
- Oncogenic properties of wild-type DNA repair gene FANCA in breast cancer.Cell reports · 2025Article
- Significance and implications of FHIT gene expression and promoter hypermethylation in acute lymphoblastic leukemia (ALL).Discover oncology · 2024Article
- Measurement of Cyclin D2 (CCND2) Gene Promoter Methylation in Plasma and Peripheral Blood Mononuclear Cells and Alpha-Fetoprotein Levels in Patients with Hepatitis B Virus-Associated Hepatocellular Carcinoma.Medical science monitor : international medical journal of experimental and clinical research · 2020Article
- RUNX3 Promotes the Tumorigenic Phenotype in KGN, a Human Granulosa Cell Tumor-Derived Cell Line.International journal of molecular sciences · 2019Article
- FHIT, a Novel Modifier Gene in Pulmonary Arterial Hypertension.American journal of respiratory and critical care medicine · 2019Article
- Folate deficiency and aberrant DNA methylation and expression of FHIT gene were associated with cervical pathogenesis.Oncology letters · 2018Article
- Integration and bioinformatics analysis of DNA-methylated genes associated with drug resistance in ovarian cancer.Oncology letters · 2016Article
- An unsupervised learning approach to find ovarian cancer genes through integration of biological data.BMC genomics · 2015Article
- Article
- Fanconi anemia repair pathway dysfunction, a potential therapeutic target in lung cancer.Frontiers in oncology · 2014Article
- Article
- Fanconi anaemia: from a monogenic disease to sporadic cancer.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2011Review
- Epigenetic changes of DNA repair genes in cancer.Journal of molecular cell biology · 2011Review
- Promoter de-methylation of cyclin D2 by sulforaphane in prostate cancer cells.Clinical epigenetics · 2011Article
- Susceptibility pathways in Fanconi's anemia and breast cancer.The New England journal of medicine · 2010Review
- MicroRNA let-7a inhibits proliferation of human prostate cancer cells in vitro and in vivo by targeting E2F2 and CCND2.PloS one · 2010Article
- Messenger RNA expression and methylation of candidate tumor-suppressor genes and risk of ovarian cancer-a case-control analysis.International journal of molecular epidemiology and genetics · 2010Article
- Epigenetic targeting in breast cancer: therapeutic impact and future direction.Drug news & perspectives · 2009Review
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundGranulosa cell tumors (GCTs) are relatively rare and are subtypes of the sex-cord stromal neoplasms. Methylation induced silencing in the promoters of genes such as tumor suppressor genes, DNA repair genes and pro-apoptotic genes is recognised as a critical factor in cancer development.
methodsWe examined the role of promoter hypermethylation, an epigenetic alteration that is associated with the silencing tumor suppressor genes in human cancer, by studying 5 gene promoters in 25 GCTs cases by methylation specific PCR and RT-PCR. In addition, the compatible tissues (normal tissues distant from lesion) from three non-astrocytoma patients were also included as the control.
resultsFrequencies of methylation in GCTs were 7/25 (28 % for FHIT), 6/25 (24% for FNACF), 3/25 (12% for Cyclin D2), 1/25 (4% for BRCA2) and 14/25 (56%) in RUNX3 genes. Correlation of promoter methylation with clinical characteristics and other genetic changes revealed that overall promoter methylation was higher in more advanced stage of the disease. Promoter methylation was associated with gene silencing in GCT cell lines. Treatment with methylation or histone deacetylation-inhibiting agents resulted in profound reactivation of gene expression.
conclusionsThese results may have implications in better understanding the underlying epigenetic mechanisms in GCT development, provide prognostic indicators, and identify important gene targets for treatment.
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