p53 immunoexpression in non-malignant oral mucosa adjacent to oral squamous cell carcinoma: potential consequences for clinical management

Transformation analysis of oral epithelial dysplasia to carcinoma in-situ and squamous cell carcinoma by p53 expression and gene mutations

“…Many study of p53 gene mutation and protein overexpression in oral SED and SCC, 14,17,22 but most of their study used sample from different case/patient. In this present study we use sequential cases included SED, CIS and SCC that were taken from the same case/sample, therefore with this method we can see the molecular behavior concomitantly.…”

“…It caused the mutation was stop codon or frame shifts resulting no protein can be detected by antibody. Cruz, et al 22 reported that p53 protein expression in basal cell layer is an early even of malignant transformation. 24 All of SED and CIS cases showed preservation of basement membrane and without stoma induction, 11 but CIS should get more intention because the basaloid formation intra epithelial more dominant than SED, it is a sign of malignant transformation from precancerous lesion (SED), as Syafriadi and Saku reported basaloid cell is dysplastic cell that can replaced the normal intra epithelium, even though they have been toward keratinization but they are cancerous cells, 27 and potentially transform to SCC which ability to destruct basement membrane and carcinomatous foci perform, that invade to adjacent tissue followed by stromal formation.…”

“…12 Many studies reported that the p53 protein overexpression is frequently found in both malignant and dysplastic lesions which increased due to grades of dysplasia, and may be an early event in multistage carcinogenesis of head and neck cancer. [13][14][15][16][17]18 The abnormal p53 protein expression reported in 10 to 80% of oral SED [19][20][21][22]24 that some cases related to p53 gene mutation, 13,14,24,25 and nearly 60% of human cancers are accompanied by mutation in p53 gene, 13 however, in some cases it is possible to observe protein over expression but they did not show any mutation gene or p53 gene mutation. 25 As reported before, oral CIS have shown p53 gene mutation almost distributed in exon 7 and exon 8, eventhough this lesion is not invasive yet.…”

Non-smoking and non-drinking patients with head and neck squamous cell carcinoma: a distinct population

“…Individuals who smoke more than 20 cigarettes and consume more than 100 grams of alcohol a day were shown to have a 200 times increased risk 21 . Nonetheless, a small population of patients with HNSCC do not possess this traditional risk factor profile [32][33][34][35] . These non-smoking and non-drinking patients with HNSCC will be subject of study in this thesis.…”

“…Hence a predictive value of p53 and Ki67 for multiple HNSCC could not be confirmed by our study. Literature regarding this subject is contradictory [32][33][34] . In our opinion it seems that expression of these markers are not crucial for recurrent HNSCC, but merely epiphenomenal.…”