| http://purl.uniprot.org/citations/20811686 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/20811686 | http://www.w3.org/2000/01/rdf-schema#comment | "Epigenetic DNA methylations plays an important role in oral carcinogenesis. The soluble frizzled receptor protein (SFRP) family together with WIF-1 and DKK-3 encodes antagonists of the WNT pathway. Silencing of these genes leads to constitutive WNT signalling. Because aberrant expression of beta-catenin might be associated with the epigenetic inactivation of WNT inhibitors, we analyzed, in a collection of primary OSCC with matched normal oral mucosa, the methylation status of a complete panel of genes, SFRP-1, SFRP-2, SFRP-4, SFRP-5, WIF-1, DKK-3, that are involved directly and indirectly in WNT pathway, in order to demonstrate WNT-pathway activation in the absence of beta-catenin and/or APC/Axin mutations during oral carcinogenesis. Methylation-specific PCR (MSP) was performed to study inactivation of SFRP-1, SFRP-2, SFRP-4, SFRP-5, WIF-1, DKK-3 genes in 37 cases of paraffin embedded oral cancer. This study showed that the methylation is an important epigenetic alteration in oral cancer. In particular, SFRP-2, SFRP-4, SFRP-5, WIF-1, DKK-3 revealed methylation status of their promoter in OSCC, whereas SFRP-1 showed demethylation in cancer. Fisher's exact test revealed statistically significant results (p<0.05) for all genes. The Wald test confirmed the statistically significant association between SFRP2-4-5 gene methylation and OSCC (p<0.05). SFRP-1 was also characterized by a different statistically significant epigenetic behaviour, because of it was demethylated in cancer (p<0.05). Statistical regression test showed high levels of sensitivity, specificity and accuracy for SFRP genes, while WIF-1 and DKK-3 have reportedly high specificity, moderate accuracy but low sensitivity. This study suggests that a cause of catenin delocalization in oral cancer could be due to WNT pathway activation, by epigenetic alterations of SFRP, WIF-1 and DKK-3 genes."xsd:string |
| http://purl.uniprot.org/citations/20811686 | http://purl.org/dc/terms/identifier | "doi:10.3892/or.2010.1035"xsd:string |
| http://purl.uniprot.org/citations/20811686 | http://purl.uniprot.org/core/author | "Franco R."xsd:string |
| http://purl.uniprot.org/citations/20811686 | http://purl.uniprot.org/core/author | "Santoro A."xsd:string |
| http://purl.uniprot.org/citations/20811686 | http://purl.uniprot.org/core/author | "Botti G."xsd:string |
| http://purl.uniprot.org/citations/20811686 | http://purl.uniprot.org/core/author | "Caraglia M."xsd:string |
| http://purl.uniprot.org/citations/20811686 | http://purl.uniprot.org/core/author | "Abbruzzese A."xsd:string |
| http://purl.uniprot.org/citations/20811686 | http://purl.uniprot.org/core/author | "Papagerakis S."xsd:string |
| http://purl.uniprot.org/citations/20811686 | http://purl.uniprot.org/core/author | "Longo F."xsd:string |
| http://purl.uniprot.org/citations/20811686 | http://purl.uniprot.org/core/author | "Lo Muzio L."xsd:string |
| http://purl.uniprot.org/citations/20811686 | http://purl.uniprot.org/core/author | "Bufo P."xsd:string |
| http://purl.uniprot.org/citations/20811686 | http://purl.uniprot.org/core/author | "Pannone G."xsd:string |
| http://purl.uniprot.org/citations/20811686 | http://purl.uniprot.org/core/author | "Serpico R."xsd:string |
| http://purl.uniprot.org/citations/20811686 | http://purl.uniprot.org/core/author | "Aquino G."xsd:string |
| http://purl.uniprot.org/citations/20811686 | http://purl.uniprot.org/core/author | "Cafarelli B."xsd:string |
| http://purl.uniprot.org/citations/20811686 | http://purl.uniprot.org/core/date | "2010"xsd:gYear |
| http://purl.uniprot.org/citations/20811686 | http://purl.uniprot.org/core/name | "Oncol Rep"xsd:string |
| http://purl.uniprot.org/citations/20811686 | http://purl.uniprot.org/core/pages | "1035-1041"xsd:string |
| http://purl.uniprot.org/citations/20811686 | http://purl.uniprot.org/core/title | "WNT pathway in oral cancer: epigenetic inactivation of WNT-inhibitors."xsd:string |
| http://purl.uniprot.org/citations/20811686 | http://purl.uniprot.org/core/volume | "24"xsd:string |
| http://purl.uniprot.org/citations/20811686 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/20811686 |
| http://purl.uniprot.org/citations/20811686 | http://xmlns.com/foaf/0.1/primaryTopicOf | https://pubmed.ncbi.nlm.nih.gov/20811686 |
| http://purl.uniprot.org/uniprot/#_A0A140VJU3-mappedCitation-20811686 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/20811686 |
| http://purl.uniprot.org/uniprot/#_B3KSM5-mappedCitation-20811686 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/20811686 |