After adjusting for possible confounding factors, COX-2 -765C allele vs. -765G/G genotype (OR=0.22, 95%CI=0.12-0.39) was a protective factor against OSCC development, but was a risk factor for malignant potential of OSF (OR=3.20, 95%CI=1.32-8.94) and OL (OR=6.73, 95%CI=2.84-19.87).
Although COX-2 is commonly overexpressed in a variety of premalignant and malignant conditions including oral leukoplakia and squamous cell carcinoma, relatively little research has compared the effects of various COX-2 inhibitors (celecoxib, NS-398, nimesulide and meloxicam).
Although COX-2 is commonly overexpressed in a variety of premalignant and malignant conditions including oral leukoplakia and squamous cell carcinoma, relatively little research has compared the effects of various COX-2 inhibitors (celecoxib, NS-398, nimesulide and meloxicam).
KRT6A mutations were associated with oral leukokeratosis, hoarseness, youngest age or highest number of fingernails/toenails involvement and walking aids.
We observed a higher likelihood of oral leukokeratosis in individuals harboring KRT6A mutations, and a strong association of natal teeth and cysts in carriers of a KRT17 mutation.
Pachyonychia congenita type 1 (PC-1) is an autosomal dominant ectodermal dysplasia characterized by hypertrophic nail dystrophy, focal non-epidermolytic palmoplantar keratoderma and variable features of oral leukokeratosis and follicular keratosis.
P<sub>A</sub> (P-value of the association test) and ORs (odd ratios) with their corresponding 95% CIs (confidence intervals) were calculated to quantitatively evaluate the influence of TP53rs1042522 on the susceptibility of patients to OSCC or OL.
However, LOH at 9p, but also mutated TP53 in biopsies of oral leukoplakia have a significant association with malignant transformation and are promising candidate biomarkers to predict the risk for malignant progression.
TP53 gene losses and MYC, ERBB2, CCND1 and EGFR copy number gains and amplifications were detected in a higher proportion in OSCC and lymph node samples than in OLK and OLP samples (P < 0·005).
A positive association exists between the isolated or combined null genotype of GSTM1 and GSTT1 and oral leukoplakia development and the null GSTT1 genotype shows increased risk of p53 overexpression, in oral leukoplakia.
The peak of the mitotic and Ki-67 indices and p53 expression shifted basally, possibly as a result of malignant transformation, whilst the peak of apoptosis and the expression of apoptotic-related proteins in oral leukoplakia showed no transformation.
These studies suggest that p53 protein stabilization, or indeed the spectrum of mutations of p53, has no major relationship to the biological characteristics and outcome of oral leukoplakia.
Molecular analysis of the same specimen showed mutations of the p53 gene in 13.3% of OLs and 9, 6% of OSCCs. p53 protein expression was not detected by IHC in 3 out of 7 OSCC with p53 mutations.
The immunohistochemical detection of epithelial p53 protein expression in oral lichen planus (OLP) biopsies was supplemented with molecular analysis for mutations of the p53 gene using the polymerase chain reaction - single stranded conformational polymorphism (PCR-SSCP) technique. p53 protein expression, in the basal epithelial cell layer, as detected by the DO7 and 1801 antibodies, was significantly more frequent in OLP compared with other oral keratoses and normal mucosa, as was the growth fraction.
In the second part of the study, accumulation of p53 protein was determined in 42 archival paraffin-embedded specimens from oral leukoplakia and correlated with the degree of epithelial dysplasia.