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Co-carcinogenesis and field cancerization oral lesions offer first signs

Tobacco and alcohol use are the major risk factors in the development of oral cancer. Although smokingtobacco offers a more pronounced risk of oral cancer, combining tobacco and alcohol results in an increased cancer incidence many times greater than the additive effects. It is estimated that three-quarters of all oraland pharyngeal cancers are caused by excessive smoking and heavy consumption of alcoholic beverages. Field cancerization is defined as the increased risk of cancer development in the entire upper aerodigestive tract after prolonged exposure to carcinogens. People using the co-carcinogens of tobacco and alcohol increase their risk of developing simultaneous or subsequent second primary epithelialcancers of the upper aerodigestive tract and lungs. CASE I A 65-year-old Caucasian man had gout, arthritis, occasional cluster headaches and an asymptomatic heart murmur. His medications included allopurinol (Zyloprim, BurroughsWellcome), 450 milligrams orally once a day; Sulindac (Clinoril, Merck & Co., Inc.), 200 mg orally twice a day; and 30 mg of Phenobarbital with one tablet of ergotamine(Cafergot, Sandoz Pharmaceuticals), taken orally as needed for cluster headaches. The patient reported no known allergies. His social history included a 100 pack-year (two packs a day X 50 years) history of smoking cigarettes. He stated that he had stopped smoking cigarettes in the last year and currently smoked a pipe and seven to eight cigars each day. He also had a significant history of alcoholconsumption; he said he had drunk several beers a day for years. The patient reported to the University of Texas-Houston Dental Branch in early May 1992. Routine oral examination showed a suspected denture sore in the left maxillary vestibule (Figure 1). No other oral lesions were evident, and there were no palpable nodes. The patient said he'd not been aware of this lesion before this discovery. Thepatient's denture was adjusted and the next visit scheduled a week later. Because of the patient's social history, we needed to exclude erythroplasia. At the second visit, the ulcerative and inflamed velvety tissue was still present. The patient was premedicated according to the American Heart Association's recommended standard prophylactic regimen for patients who are at risk for subacutebacterial endocarditis. An incisional biopsy was performed on the maxillary vestibule and the tissue submitted for routine histopathologic examination. The histopathologic diagnosis was a welldifferentiated squamous cell carcinoma that was superficially invasive. Neoplastic changes extended to the lateral margins of the specimen. The patient was referred the following day to the Department of Head andNeck Surgery, University of Texas M.D. Anderson Cancer Center. At M.D. Anderson, the mouth and oropharynx examination UAl w revealed a small (5-mm) ulcerated area in the left posterior maxillary vestibule. The lesion was not tender. The patient was edentulous and had no other oral lesions. The nasopharynx was clear as shown on indirect mirror examination. A nasopharyngoscopic examination showed whatappeared to be a second lesion-a raised, whitish, nonulcerated area in the posterior inferior pharyngeal wall. The hypopharynx and larynx had no lesions and the cords moved normally. Examination of the neck revealed no masses. The pharyngeal lesion was biopsied, and invasive squamous cell carcinoma was revealed. Chest radiographs disclosed a suspicious lesion at the apex of the

right lung.The patient underwent bronchoscopy. The right apical lesion could not be biopsied by bronchoscopy, but a fungating mass was identified at the origin of the left upper lobe bronchus. Brushings of that lesion were consistent with squamous cell carcinoma. A fluoroscopically guided fine needle aspiration of the right apical lesion later revealed a poorly differentiated carcinoma. The patient was...