Alterations of Adenomatous Polyposis Coli (APC) gene in oral squamous cell carcinoma

Abstract

The present study assessed the roles of Adenomatous Polyposis Coli (APC) tumor suppressor gene during oral carcinogenesis. Reduction of APC transcript levels and APC loss of heterozygosity (LOH) were found in 39% (7/18) and 29% (10/34) cases of oral squamous cell carcinoma (OSCC), respectively. The apparent APC heterozygosity (27%) in non-cancerous matched oral tissue (NCMOT) adjacent to OSCC at an exon 11 locus was significantly lower than normally found in the Taiwanese population (49%). These findings suggest that the allelic status of APC could indicate a cancer risk. No polymorphism of 11307 allele of APC was identified in NCMOT or OSCC. Our data indicated that alterations of APC are frequent molecular changes of OSCC. Advances in understanding of the APC alterations that accompany OSCC development might provide a means for early diagnosis and possibly new therapeutic strategies.

Cytoplasmic expression of E‐cadherin and β‐Catenin correlated with LOH and hypermethylation of the APC gene in oral squamous cell carcinomas

“…Two of them were related to cytoplasmic expression of β ‐Catenin, one was related to loss of β ‐Catenin expression, the remaining one was not available for IHC staining. Because of the low frequency of LOH and the limited number of patients it was difficult to show differences in patients from Denmark and Taipei, although LOH at APC gene locus has been demonstrated more frequently in Western than in Asian patients (11–13).…”

Comparative genomic hybridization reveals genetic progression of oral squamous cell carcinoma from dysplasia via two different tumourigenic pathways

“…Tanimoto et al 19 reported that a change in the fragile histidine triad gene ( FHIT ), which maps to 3p14.2, is involved in OSCC as well as in cancers of other organs. Chang et al 20 reported that loss of the adenomatous polyposis coli gene, which maps to 5q21–22, is important in the development of OSCC. In this study, OSCCs were categorized as either OSCC‐L or OSCC‐S according to the number of DSCNAs identified.…”

Frequent hypermethylation of WNT pathway genes in laryngeal squamous cell carcinomas

“…Moreover, the activity of WNT negative feedback regulators that are active antagonists of this pathway is often lost due to genetic or epigenetic changes. The inactivation of APC gene by loss of heterozygosity was observed in over a quarter of HNSCC cases . Importantly, the expression of many WNT antagonists may undergo silencing due to the methylation of their promoter regions.…”