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Tongue cancer primary prevention

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Simrat Sarai, M.D. [2] Mohammed Abdelwahed M.D[3]

Overview

Effective measures for the primary prevention of tongue cancer include avoiding the use of tobacco and excessive use of alcohol. Main methods for prevention are natural components such as: vitamin A, vitamin E, and beta-carotene because they are rich in trace elements and antioxidants. There is a protective effect of diets rich in fresh fruits and vegetables to reduce the incidence of leukoplakia. There is no effective oral cancer screening program either a general or a selected high-risk population for oral cancer in the United States. Screening high-risk individuals in developing countries could be an effective prevention strategy that lowered the stage of oral cancer at diagnosis and improved 5-year survival.

Screening

  • Tongue cancer screening is not standard procedure for a health assessment.[1]
  • There is no effective oral cancer screening program either a general or a selected high-risk population for oral cancer in the United States.
  • Screening high-risk individuals in developing countries could be an effective prevention strategy that lowered the stage of oral cancer at diagnosis and improved 5-year survival.[2]
  • Screening subjects in the subgroup who used tobacco or alcohol reduced the mortality rate from oral cancer.[3]

Prevention

  • Avoiding known risk factors such as the use of tobacco and excessive use of alcohol is the best method of tongue cancer prevention.[4]
  • Main methods for prevention are natural components such as: vitamin A, vitamin E, and beta-carotene beacuse they are rich in trace elements and antioxidants.[5]
  • There is a protective effect of diets rich in fresh fruits and vegetables to reduce incidence of leukoplakia.[6]
  • Toxicity of isotretinoin is the main side effect, particularly in patients treated with doses higher than 2 mg/kg per day.
  • Patients treated at the lower dose level (1 mg/kg per day) had less toxicity and did not require dose reduction.[7]

References

  1. ↑ Sankaranarayanan R, Ramadas K, Thomas G, Muwonge R, Thara S, Mathew B; et al. (2005). “Effect of screening on oral cancer mortality in Kerala, India: a cluster-randomised controlled trial”. Lancet. 365 (9475): 1927–33. doi:10.1016/S0140-6736(05)66658-5. PMID 15936419.
  2. ↑ Santana JC, Delgado L, Miranda J, Sánchez M (1997). “Oral Cancer Case Finding Program (OCCFP)”. Oral Oncol. 33 (1): 10–2. PMID 9192546.
  3. ↑ Sankaranarayanan R (1997). “Health care auxiliaries in the detection and prevention of oral cancer”. Oral Oncol. 33 (3): 149–54. PMID 9307722.
  4. ↑ Shin DM, Zhang H, Saba NF, Chen AY, Nannapaneni S, Amin AR; et al. (2013). “Chemoprevention of head and neck cancer by simultaneous blocking of epidermal growth factor receptor and cyclooxygenase-2 signaling pathways: preclinical and clinical studies”. Clin Cancer Res. 19 (5): 1244–56. doi:10.1158/1078-0432.CCR-12-3149. PMC 3693760. PMID 23422093.
  5. ↑ Kreimer AR, Chaturvedi AK (2011). “HPV-associated Oropharyngeal Cancers–Are They Preventable?”. Cancer Prev Res (Phila). 4 (9): 1346–9. doi:10.1158/1940-6207.CAPR-11-0379. PMC 3326607. PMID 21893495.
  6. ↑ Stich HF, Hornby AP, Mathew B, Sankaranarayanan R, Nair MK (1988). “Response of oral leukoplakias to the administration of vitamin A.” Cancer Lett. 40 (1): 93–101. PMID 3370632.
  7. ↑ Wirth LJ, Haddad RI, Lindeman NI, Zhao X, Lee JC, Joshi VA; et al. (2005). “Phase I study of gefitinib plus celecoxib in recurrent or metastatic squamous cell carcinoma of the head and neck”. J Clin Oncol. 23 (28): 6976–81. doi:10.1200/JCO.2005.02.4182. PMID 16172459.

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