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P16INK4a In Oular Surface Squamous Neoplasia | 12183
ISSN: 2155-952X

Journal of Biotechnology & Biomaterials
Open Access

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p16INK4a in Oular Surface Squamous Neoplasia

4th World Congress on Biotechnology

Sheeta Chauhan, Seema Sen, Neeta Singh, Anjana Sharma, Bhavna Chawla, Neelam Pushker, Seema Kashyap and Rajvardhan Azad

ScientificTracks Abstracts: J Biotechnol Biomater

DOI: 10.4172/2155-952X.S1.023

Abstract
Ocular Surface Squamous Neoplasia (OSSN) is the most common tumour of ocular surface and encompasses both conjunctival intraepithelial neoplasia (CIN) and squamous cell carcinoma (SCC). p16INK4a is a tumor suppressor protein, Its inactivation by aberrant methylation of CpG islands is frequent in various cancers. Sixty-four cases of OSSN and 15 normal conjunctival controls were included in this study. Immunohistochemistry and Methylation specific PCR was used to evaluate expression of p16INK4a protein and its methylation status. Follow-up data (16 to 36 months) was available in 48 (75%) cases. Loss of p16INK4a immunoexpression was observed in 72% cases (48) and promoter hypermethylation in 53% (34). P16INK4a promoter hypermethylation showed significant association with immunoexpression(P=<0.0001). Hypermethylation of p16INK4a was not however associated significantly with any clinicopathological features or survival. p16INK4a Overexpression was observed in 18 (28%) OSSN and was absent in all control conjunctival tissues. p16INK4a positive cases belonged to younger age group (P=0.03), had higher T stage (P=0.007), larger tumour size (P=0.04) and invasive SCC (P=0.03). Its expression was seen in all the cases with metastasis (6/6) (P= 0.0002) and death (4/4) (P= 0.004). Although in our study disease free survival was worst in p16INK4a positive cases, the difference was not statistical significant (P=0.09). Loss of p16INK4a expression is frequent in OSSN cases and is caused by aberrant DNA methylation. Overexpression of p16INK4a is a useful indictor of aggressive disease and suggests alteration in pRb pathway in this subset of tumors which may play an important role in the pathogenesis and progression of OSSN.
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