Oral squamous cell carcinoma (OSCC) is a public health problem. The hamster buccal pouch model is ideal for analyzing the development of OSCC. This research analysed the effects of sunitinib (tyrosine kinase inhibitor) in precancerous lesions induced by 7,12-dimethylbenz(a)anthracene (DMBA) in this model. Thirty-four male hamsters, divided into six groups: control—C , acetone—A , carbamide peroxide—CP , acetone and CP—A+CP , 1% DMBA in acetone and CP—DA+CP , and 1% DMBA in acetone and CP and 4-week treatment with sunitinib—DA+CP+S . The aspects evaluated were anatomopathological features (peribuccal area, paws, nose, and fur), histological sections of the hamster buccal pouches (qualitatively analyzed), epithelium thickness, and the rete ridge density (estimated). Sunitinib was unable to attenuate the decrease in weight gain induced by DMBA; no increase in volume was detected in the pouch and/or ulceration, observed in 43% of the animals in the DA+CP group. DA+CP groups presented a significant increase in rete ridge density compared to the control groups ( ) which was reverted by sunitinib in the DA+CP+S group. Sunitinib seems to have important benefits in early stage carcinogenesis and may be useful in chemoprevention. 1. Introduction Oral squamous cell carcinoma is a global public health problem with about 300,000 new cases diagnosed per year representing 5% of all cancers for men and 2% for women [1], two-thirds of which are from developing countries [2]. Squamous cell carcinoma of the upper aerodigestive tract has a high risk of primary-treatment failure and death. If cured, patients are often disfigured or cannot speak and/or swallow [2]. Some patients will be at risk for malnutrition, infection [3], severe depression, or suicide. Globally, with few exceptions, survival rates have not improved for decades [1, 4–7]. Oral squamous cell carcinoma (OSCC) is caused by DNA mutation, often spontaneous but increased by the exposure to a range of mutagens [8]—one of them being chemical. The changes in the DNA can progress from a normal keratinocyte to a premalignant or a potentially malignant keratinocyte that is characterized by the ability to proliferate in a less-controlled way than normal. The cells become autonomous and cancer results (characterized by invasion through the epithelial basement membrane) [9]. In the initial phase of OSCC, cells may proliferate in a process known as hyperplasia. From hyperplasia, cells can progress to mild dysplasia; then to moderate dysplasia, and later to severe dysplasia; the last phase would be OSCC [1]. Animal tumor
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