Tongue cancer primary prevention
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Simrat Sarai, M.D. [2]
Overview
Effective measures for the primary prevention of tongue cancer include avoiding the use of tobacco and excessive use of alcohol.
Primary Prevention
- As some of the risk factors of the tongue cancer include age, gender and family history, which cannot be controlled, not all cases of tongue cancer can be prevented. However, avoiding known risk factors such as the use of tobacco and excessive use of alcohol is the best method of tongue cancer prevention.
- The best way to prevent tongue cancer recurrence is to quit tobacco and/or drinking of alcohol. While quitting alcohol and tobacco does not guarantee that you will never develop tongue cancer, it greatly reduces the risk.
- Patients suitable for a chemoprevention trial may have a documented precancerous lesion or have a known risk factor for developing malignancy without having a premalignant lesion. A third group of patients are those with previously treated malignancy who are at a significant risk for developing a second primary tumor [45]. [46,47]. Most of the completed chemoprevention trials for premalignant lesions of the oral cavity and oropharynx have studied either naturally occurring compounds (vitamin A, vitamin E, beta-carotene) or synthetically derived retinoids [48-50]. Vitamin A, vitamin E, and beta-carotene The interest in the antioxidants vitamin A, vitamin E, and beta-carotene as chemopreventive agents is due to their apparent efficacy in inducing regression of oral leukoplakia. Although these agents have been studied relatively extensively, both for primary and secondary chemoprevention, none has an established role.
- the protective effect of diets rich in fresh fruits and vegetables, but with a substantial minority without these established risk factors. The protective effect of diets rich in trace elements and antioxidant vitamins is well demonstrated in many countries.
- Reports on the utility of vitamin A to treat oral leukoplakia date back to 1957, when a 90 percent response rate was described in 20 patients [51]. Subsequent trials supported the activity of vitamin A in oral leukoplakia in populations likely to be deficient in vitamin A and at risk based upon tobacco or betel nut chewing [52,53]. The applicability of these results to disease in relatively developed nations where vitamin deficiency is rare is unclear. High response rates have also been described with the administration of beta-carotene, a precursor of vitamin A, to patients with oral leukoplakia [54-56]. In one series of 24 patients, for example, there were 15 partial and 2 complete responses with no significant toxicity [54]. However, toxicity was particularly severe in patients dosed at the higher dose of isotretinoin (2 mg/kg per day), with 47 percent of patients requiring dose reduction. Patients treated at the lower dose level (1 mg/kg per day) had less toxicity and did not require dose reduction, although most noted xeroderma and 29 percent developed conjunctivitis. Furthermore, over 50 percent of responders relapsed within three months of treatment cessation.