Clinical and Histopathological Correlation of p16 and p53 Expression in Oral Cancer
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ORIGINAL ARTICLE
Clinical and Histopathological Correlation of p16 and p53 Expression in Oral Cancer Varun Kumar Agarwal 1
&
Rohit Sharma 1
&
GPS Gahlot 2
&
Amiy Arnav 1
Received: 5 March 2020 / Accepted: 17 June 2020 # Indian Association of Surgical Oncology 2020
Abstract p16 is overexpressed in oral squamous cell carcinoma patients who are positive for human papilloma virus. The p53 tumor suppressor gene is commonly mutated in human cancer. The aim is to correlate clinical and pathological features with p16 and p53 expression. This is a prospective, observational study of 50 consecutive cases (43 males and 7 females) who underwent surgery for oral cancer. p16 and p53 were determined by immunohistological staining. The results were obtained and analyzed using chi-square test (Statistical Software SPSS 21.0 version); p value ≤ 0.05 was considered significant. Of the 50 cases, p16 and p53 were overexpressed in 30% and 54% of patients, respectively. Overexpression of p16 was not significantly associated with age, subsites of oral cavity, or degree of differentiation. However, smokeless tobacco was significantly associated with p16 expression (p = 0.012). Similarly, overexpression of p53 was not correlated with age, subsites of oral cavity, or degree of differentiation. Seventy-five percent of poorly differentiated cancers had overexpression of p53 though this did not reach statistical significance (p = 0.279). p53 was overexpressed in smokers (80.95%) and those consuming alcohol (60%). Keywords Oral cancers . p53 . p16 . Human papilloma virus
Introduction Oral squamous cell carcinoma (OSCC) is characterized by mortality and morbidity rates that have changed little despite advances in the field of oncology. Human papilloma virus (HPV) is now identified as a risk factor for oral cancer and is associated with overexpression of p16. These tumors have better survival following surgery and radiotherapy. Globally, the incidence of HPV varies across head and neck cancers, fluctuating from 3% in oral cavity to 12% in oropharyngeal cancers [1]. This site-based variance is attributable to sexual practices and addictions. In India, the incidence of HPV ranges from 0 to 74% in oral cancers and 26 to 70% in oropharyngeal cancers [2]. The p16 marker may mediate its effects by contributing to reduced proliferative
* Rohit Sharma [email protected] 1
Department of Surgical Oncology, Army Hospital (Research & Referral), Delhi, India
2
Department of Pathology, Army Hospital (Research & Referral), Delhi, India
capacity, leading to smaller tumor size and lower invasive potential [3]. TP53 is a tumor suppressor gene located on chromosome 17p. One of the most common events in human carcinogenesis is mutation in p53. The defective, mutated protein accumulates inside cancer cells and can be detected by immunohistochemical methods. Overexpression of p53 in oral cancer portends poor prognosis and resistance to chemotherapy. p53 overexpression in oral cancer varies in different parts of the world, owing to divergent risk factors and
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