p53 and ki67 as biomarkers in determining response to chemoprevention for oral leukoplakia

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Excerpt

Chemoprevention has been proposed and evaluated for the management of oral potentially malignant disorders to prevent or delay the development of cancer 1. We performed a randomized controlled trial for the chemoprevention of oral leukoplakia by administrating low dose of beta‐carotene (10 mg/day) and vitamin C (500 mg/day) supplements (experimental arm) or vitamin C (50 mg/day) alone (placebo arm) given orally for 1 year 2. Our results did not support the use of these agents to achieve either clinical remission (17.4% vs. 4.3%; P = 0.346) or for cancer prevention (RR: 0.77, 95%CI, 0.28–1.89). However, it is unclear whether the original clinical presentation of leukoplakia (phenotype) accurately reflects who may respond well to chemoprevention. The term ‘oral leukoplakia’ is used here as per WHO classification and nomenclature 3 to recognize white plaques of questionable risk of malignancy having excluded (other) known diseases or disorders that carry no increased risk for cancer. The term is not used to include any other white lesion.
Several intermediate biomarkers in chemoprevention trials, p53, ki67, retinoic acid receptor‐beta (RAR‐β), cyclin D1, activator protein 1 (AP‐1) proliferating cellular nuclear antigen (PCNA), and cytochrome p450 enzyme 1A1 (CYP1A1), have been used as the indicators of responsiveness to the chemopreventive agents in head and neck squamous cell carcinoma 4. The target chemopreventive agents for these trials were retinoic acid and its natural and synthetic derivatives (retinoids).
The objective was to characterize the baseline expression of p53 and ki67 of participants recruited to our clinical trial and to determine whether these two markers will identify any potential response to chemoprevention for oral leukoplakia and could be better predictors of the trial outcome.
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