Increased PRL-3 in Human Oral Squamous Cell Carcinoma and Dysplasia

Head and neck cancer is the 6th most common cancer and there has been little improvement in patient morbidity in the past 50 years (Hunter et al., 2005). Squamous cell carcinomas (SCCs) are the most common form of head and neck cancer. Oral SCCs (OSCCs) often develop in a normal–dysplasia–carcinoma sequence. Long-term follow-up studies showed that 11–36% of oral epithelial dysplasias transformed into SCC and that dysplasias were generally associated with a risk for malignant transformation (Sudbo et al., 2001; Silverman et al., 1984). Therefore, more reliable biological markers than those presently known are required for earlier diagnosis, prognosis and follow-up. The p53 gene is the most frequent target of genetic alterations, being mutated in half of human cancers (Sigal and Rotter, 2000; Iwakuma et al., 2005). We previously reported that the p53 gene mutations occurred at high frequency (in almost 80% of OSCCs)(Kashiwazaki et al., 1997). In the functional interactions of mutated p53 with the remaining wild-type (WT) p53 allele, the p53 mutations are classified into two types, recessive (R) and dominant-negative (DN) mutations. DN p53 mutants