The correlation between p16 expression and INK4a locus mutation with grades and stages in oral squamous cell carcinoma

Abstract

Loss of p16INK4a expression occurred in initial stages of oral squamous cell carcinoma. Evaluation of TS and CS for p16INK4a might be a useful clinical indicator concerning the tumor. However, gene mutation is believed to have minor rate of genetic alteration in carcinogenesis.

Detection and comparison of microsatellite marker D9S1747 with clinical stages and grades of oral squamous cell carcinoma

“…[ 22 ] Sargolzaei et al found that expression of p16 was 33.3%, 31.6% and 33.3% in WDSCC, MDSCC and PDSCC which were consistent in all grades when compared to our findings. [ 6 ] In contrast to this study, Mahale and Saranath found 83% positivity in PDSCC as compared to 46% of MDSCC to WDSCC. [ 16 ] Tsai et al found an elevation in histological grades showing 54% in WDSCC, 56.5% in MDSCC and 58% in PDSCC.…”

“…Sargolzaei et al found expression of p16 higher in Stage I compared to Stage II–IV. [ 6 ] Our study showed higher positivity in Stage 2 OSCC cases. Hiroshi et al found LOH at chromosome 9p and suggested that LOH at chromosome 9p could be detected in early stage and the frequencies of LOH tend to be higher in later clinical stages.…”

“…[ 25 ] To our knowledge, as far as grade and stage are concerned, only few studies have been conducted to understand the correlation between the alterations and clinicopathologic characteristics of OSCC and have shown different results. [ 6 22 25 ] The difference in the results could be attributed to the diversity in the distribution of different grades and stages in all the studies. In our study, WDSCC showed higher positivity p16 microsatellite marker this suggests that there is an early change seen in the development of OSCC and also it may be involved in tumorigenesis.…”

“…It was observed that these markers that have provided evidence up to 87% of oral cancers show inactivation of p16 and in that homozygous deletion is the most common mechanism of inactivation. [ 5 6 7 8 9 17 ]…”

“…p16 is considered as the first TSG to be inactivated in OSCC, and it is an early event that occurs during initial stages of OSCC. [ 4 5 6 ] More than 80% of head and neck tumors show early inactivation of p16, whereas deregulation of p53 and cyclin D1 occurs later in sequence of molecular progression to frank carcinoma. In head and neck cancers, p16 protein is often inactivated by any one or a combination of homozygous deletions, promoter methylations or point mutations.…”