These findings reinforce the use of the hamster cheek pouch as an experimental model for the study of oral cancer development, at least in reference to the possible participation of TGF-alpha in the malignant transformation process.
Thus, our data showing loss of H-ras-1 alleles and VTR rearrangement, with relatively high incidence (9/23; 39%) in the oral cancer patients at various stages of the disease, implies H-ras-1 involvement as an early event in the process of oral carcinogenesis.
The authors investigated LOH of the p53 gene in DNA from 27 primary oral cancers using a polymerase chain reaction (PCR)-based restriction fragment length polymorphism assay.
We have investigated the association of RFLP at the H-ras-1 locus and susceptibility to oral cancer by Southern hybridization analysis in 77 primary oral tumors and 99 healthy donors.
These data indicate that "high risk" HPV infections and mutations of p53, Rb, and DCC genes are frequently found in oral cancer cells and may be associated with oral cancer.
While it has been shown that p53 gene mutations in the conserved midregion (exons 5-9) are a common feature of oral cancers in the developed world, there is no information on this type of genetic lesion in betel quid-associatedoral cancers.
The HER-2/neu (also named c-erbB-2) oncogene is known to be overexpressed in many human cancers, including breast, ovarian, lung, gastric and oral cancers.
The unexpected finding of p53 protein in clinically healthy mucosa was confined to subjects aged over 40 years who smoked tobacco, a known risk factor for oral cancer.
To investigate the mechanism of decrease of serum DPP IV activity in oral cancer patients, we analyzed the expression of DPP IV in peripheral blood T lymphocytes of oral cancer patients and healthy subjects.
The present data indicate that p53 mutations are extremely frequent in oral cancers in the Japanese, and suggest that the timing and significance of p53 mutation in oral tumor progression vary in different ethnic populations and areas.
These observations are consistent with other findings of significantly increased p53 protein expression in the oral mucosa and other tissues of smokers and suggests that p53 mutations may be an early event in smoking-induced oral cancers.
The ADH3(1-1) genotype appears to substantially increase the risk of ethanol-related oral cancer, thus providing further evidence for the carcinogenicity of acetaldehyde.
Thus, gene therapy of human oral cancer by increasing the expression of MnSOD activity in target cells might be used to prevent or reduce human oral tumor malignancy.
This case-control study focused on the interactions between oral cancer risk factors and genetic polymorphisms of cytochrome P-450 (CYP) 2E1 and glutathione S-transferase (GST) M1 and GSTT1.