Lingual Squamous Cell Carcinoma Research Articles

Glutathione S-transferase pi-class as a tumour marker in lingual preneoplastic and neoplastic lesions of rats and humans.

Immunocytochemical expression of the pi class glutathione S-transferase (GST) was investigated in preneoplastic and neoplastic lingual lesions in a 4-nitro-quinoline 1-oxide (4NQO)-induced rat genetic model [Wistar/Furth rats (WF) and Dark-Agouti rats (DA)] and in human surgical material [fibrous polyp, mild to moderate dysplasia, severe dysplasia, carcinoma in situ (CIS), squamous cell carcinoma (SCC)]. Two polyclonal antibodies raised against rat (GST-P) and human (GST-pi) antigens were used. In the rat model, DA and WF rats showed contrasting susceptibility to 4NQO, DA rats having a much higher tumour incidence and a significantly shorter survival time than WF rats. While the established lingual SCC in DA and WF rats all expressed GST-P, the number of GST-P+ foci in the preneoplastic lingual epithelium was significantly higher in DA (14.5 +/- 6.5) than in WF rats (5.5 +/- 2.6; P < 0.0001). In contrast, GST-pi epithelial staining in human specimens was more variable and the results overlapped in different groups. More frequent nuclear and/or basal cell staining was detected in severe dysplasia, CIS and SCC than in benign and mild to moderate dysplastic lesions. Although the pi class GST may be a useful marker for rat lingual carcinogenesis, its value in clinical applications is unclear. GST-pi staining patterns and their distribution may be helpful in identifying high-risk lingual lesions in humans.

Relationship of tobacco/alcohol use to p53 expression in patients with lingual squamous cell carcinomas.

This study examined p53 expression immunocytochemically in 40 lingual squamous cell carcinomas from Dutch patients with known histories of smoking and/or drinking alcohol. 30% of neoplasms showed positive p53 reactivity, suggesting increased levels of p53 protein. No alcohol or tobacco risk factors were evident in 33.3% (4/12) of p53-positive neoplasms whereas only 7.1% (2/28) of p53-negative neoplasms showed an absence of these risk factors. 25% (3/12) of p53-positive neoplasms and 71.4% (20/28) of p53-negative neoplasms were found in patients who had been exposed to both alcohol and tobacco. A similar negative association with p53 reactivity was also found when either tobacco or alcohol were used in isolation. The results contrast with previous observations in head/neck and oral carcinomas and indicate that the association of alcohol/tobacco and p53 expression remains open to question.