Saudi Journal of Gastroenterology
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ORIGINAL ARTICLE
Year : 2016  |  Volume : 22  |  Issue : 6  |  Page : 435-440

p16 protein is upregulated in a stepwise fashion in colorectal adenoma and colorectal carcinoma


1 Department of Medicine, Faculty of Medicine, King Abdulaziz University; Scientific Chair for Colorectal Cancer, King Abdulaziz University, Jeddah, Saudi Arabia
2 Department of Pathology, Faculty of Medicine, King Abdulaziz University, Jeddah, Saudi Arabia; Department of Pathology, Faculty of Medicine, Minia University, Al-Minia, Egypt
3 Department of Pathology, Faculty of Medicine, King Abdulaziz University, Jeddah, Saudi Arabia; Department of Pathology, Faculty of Medicine, Alexandria University, Alexandria, Egypt
4 Department of Pathology, Faculty of Medicine, King Abdulaziz University, Jeddah, Saudi Arabia
5 Centre of Excellence in Genomic Medicine Research, King Abdulaziz University, Jeddah, Saudi Arabia
6 Faculty of Medicine, King Abdulaziz University, Jeddah, Saudi Arabia
7 Department of Pathology, Faculty of Medicine, King Abdulaziz University; Scientific Chair for Colorectal Cancer, King Abdulaziz University, Jeddah, Saudi Arabia

Correspondence Address:
Jaudah Al-Maghrabi
Department of Pathology, Faculty of Medicine, King Abdulaziz University, Jeddah - 21589
Saudi Arabia
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/1319-3767.195560

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Background/Aims: p16 is tumor suppressor gene acting as a cell cycle regulator. The present study was conducted to compare p16 expression in normal, dysplastic, and malignant colonic mucosae, and to explore its relation to clinicopathological variables and follow-up data in colorectal carcinoma (CRC). Patients and Methods: Tissue microarrays were performed from 25 normal colonic mucosae, 41 colonic adenomas, and 191 CRC, with corresponding 50 nodal metastases. Immunohistochemistry was performed using anti-p16 antibody, sections were scored, and statistical analysis was performed. K-ras mutation detection was also performed. Results: Immunoexpression of p16 was significantly higher in CRC than in adenomas (P = 0.033) and normal colonic mucosa (P = 0.005). There was no statistically significant difference between p16 expression in CRC and nodal metastasis. There was no significant association between p16 immunoexpression in CRC and all clinicopathological data and survival probability. K-ras mutations were detected in 34% of CRC. However, there was no correlation between K-ras status and p16 expression (P = 0.325). Conclusion: Absence of p16 expression is correlated to a benign course of CRC adenomas. p16 has a key role in CRC progression and can be used as a marker for colorectal adenoma. On the other hand, it has no role as a predictive and/or prognostic factor in CRC. Further extended studies are required to explore the role of p16 as indicator of premalignant lesions in the colon and to test its relation with CRC histological grade, as well as to test its value as a new therapeutic target.


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