RGD Reference Report - CpG methylation of the FHIT, FANCF, cyclin-D2, BRCA2 and RUNX3 genes in Granulosa cell tumors (GCTs) of ovarian origin. - Rat Genome Database

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CpG methylation of the FHIT, FANCF, cyclin-D2, BRCA2 and RUNX3 genes in Granulosa cell tumors (GCTs) of ovarian origin.

Authors: Dhillon, VS  Shahid, M  Husain, SA 
Citation: Dhillon VS, etal., Mol Cancer. 2004 Dec 1;3:33.
RGD ID: 2298508
Pubmed: PMID:15574200   (View Abstract at PubMed)
PMCID: PMC538268   (View Article at PubMed Central)
DOI: DOI:10.1186/1476-4598-3-33   (Journal Full-text)

BACKGROUND: Granulosa 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. METHODS: We 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. RESULTS: Frequencies 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. CONCLUSIONS: These results may have implications in better understanding the underlying epigenetic mechanisms in GCT development, provide prognostic indicators, and identify important gene targets for treatment.

RGD Manual Disease Annotations    Click to see Annotation Detail View
TermQualifierEvidenceWithReferenceNotesSourceOriginal Reference(s)
granulosa cell tumor disease_progressionIDA 2298508DNA:hypermethylation:promoterRGD 
granulosa cell tumor  IDA 2298508DNA:hypermethylation:promoter and ovaryRGD 
granulosa cell tumor disease_progressionISOFANCF (Homo sapiens)2298508; 2298508DNA:hypermethylation:promoterRGD 
granulosa cell tumor  ISOFHIT (Homo sapiens)2298508; 2298508DNA:hypermethylation:promoter and ovaryRGD 

Objects Annotated

Genes (Rattus norvegicus)
Fancf  (FA complementation group F)
Fhit  (fragile histidine triad diadenosine triphosphatase)

Genes (Mus musculus)
Fancf  (Fanconi anemia, complementation group F)
Fhit  (fragile histidine triad gene)

Genes (Homo sapiens)
FANCF  (FA complementation group F)
FHIT  (fragile histidine triad diadenosine triphosphatase)


Additional Information