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Oropharyngeal Cancer Treatment (PDQ®): Treatment - Health Professional Information [NCI] - General Information About Oropharyngeal Cancer

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The 3-year rates of overall survival (OS) were 93.0% (95% confidence interval [CI], 88.3–97.7) in the low-risk group, 70.8% (95% CI, 60.7–80.8) in the intermediate-risk group, and 46.2% (95% CI, 34.7–57.7) in the high-risk group.[12]

The risk of developing a second primary tumor in patients with tumors of the upper aerodigestive tract has been estimated to be 3% to 7% per year.[13,14] Because of this risk, patients require lifelong surveillance. Patients need counseling about continued smoking and alcohol consumption after treatment, which has been associated with the development of second primary tumors of the aerodigestive tract.[15,16,17] (Refer to the PDQ Smoking Cessation and Continued Risk in Cancer Patients summary for more information.)

An analysis studied 2,230 patients with index SCC of the oropharynx to determine the likelihood of developing second primary malignancies compared with index SCC of nonoropharyngeal sites (i.e., oral cavity, larynx, and hypopharynx). The second primary malignancy rate was lower for patients with index oropharyngeal SCC than for patients with index nonoropharyngeal cancer (P < .001). Among patients with oropharyngeal SCC, former smokers had a 50% greater risk of second primary malignancy and current smokers had a 100% greater risk than never-smokers (P trend = .008). These data suggest that patients who fit the typical HPV phenotype have a very low, second-primary malignancy risk.[18]

To date, SCC of the oropharynx has not been associated with any specific chromosomal or genetic abnormalities. Genetic and chromosomal aberrations in these cancers are complex.[19,20] Despite the lack of specific genetic abnormalities, testing for genetic alterations or ploidy in early oropharyngeal lesions may identify patients who are at the greatest risk for progression and may lead to more definitive therapy.[21]

Other risk factors may include the following:[4]

  • A diet poor in fruits and vegetables.[22]
  • The consumption of maté, a stimulant beverage commonly consumed in South America.[23]
  • The chewing of betel quid, a stimulant preparation commonly used in parts of Asia.[24]
  • Defective elimination of acetaldehyde, a carcinogen generated by alcohol metabolism. In individuals, primarily East Asians, who carry an inactive mutant allele of alcohol dehydrogenase-2, alcohol consumption is associated with a susceptibility to multiple metachronous oropharyngeal cancers that are caused by the decreased elimination of acetaldehyde.[25]
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