Chapter 084. Head and Neck Cancer (Part 1)

Harrisons Internal Medicine Chapter 84. Head and Neck CancerHead and Neck Cancer: IntroductionEpithelial carcinomas of the head and neck arise from the mucosal surfaces in the head and neck area and typically are squamous cell in origin. This category includes tumors of the paranasal sinuses, the oral cavity, and the nasopharynx, oropharynx, hypopharynx, and larynx. Tumors of the salivary glands differ from the more common carcinomas of the head and neck in etiology, histopathology, clinical presentation, and therapy. Thyroid malignancies are described in Chap. 335.Incidence and Epidemiology The number of new cases of head and neck cancers in...
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Chapter 084. Head and Neck Cancer (Part 1) Chapter 084. Head and Neck Cancer (Part 1) Harrisons Internal Medicine > Chapter 84. Head and Neck Cancer Head and Neck Cancer: Introduction Epithelial carcinomas of the head and neck arise from the mucosal surfacesin the head and neck area and typically are squamous cell in origin. This categoryincludes tumors of the paranasal sinuses, the oral cavity, and the nasopharynx,oropharynx, hypopharynx, and larynx. Tumors of the salivary glands differ fromthe more common carcinomas of the head and neck in etiology, histopathology,clinical presentation, and therapy. Thyroid malignancies are described in Chap.335. Incidence and Epidemiology The number of new cases of head and neck cancers in the United States was40,500 in 2006, accounting for about 3% of adult malignancies. The worldwideincidence exceeds half a million cases annually. In North America and Europe, thetumors usually arise from the oral cavity, oropharynx, or larynx, whereasnasopharyngeal cancer is more common in the Mediterranean countries and in theFar East. Etiology and Genetics Alcohol and tobacco use are the most common risk factors for head andneck cancer in the United States. Smokeless tobacco is an etiologic agent for oralcancers. Other potential carcinogens include marijuana and occupationalexposures such as nickel refining, exposure to textile fibers, and woodworking. Dietary factors may contribute. The incidence of head and neck cancer ishighest in people with the lowest consumption of fruits and vegetables. Certainvitamins, including carotenoids, may be protective if included in a balanced diet.Supplements of retinoids such as cis-retinoic acid have not been shown to preventhead and neck cancers (or lung cancer) and may increase the risk in activesmokers. Some head and neck cancers may have a viral etiology. The DNA of humanpapillomavirus (HPV) has been detected in the tissue of oral and tonsil cancers,and may predispose to oral and tonsillar cancer in the absence of tobacco andalcohol use. These patients can present at a somewhat younger age. The incidenceof HPV-related head and neck cancer may be increasing. Epstein-Barr virus(EBV) infection is associated with nasopharyngeal cancer. Nasopharyngeal canceroccurs endemically in some countries of the Mediterranean and Far East, whereEBV antibody titers can be measured to screen high-risk populations.Nasopharyngeal cancer has also been associated with consumption of salted fish. No specific risk factors or environmental carcinogens have been identifiedfor salivary gland tumors. Histopathology, Carcinogenesis, and Molecular Biology Squamous cell head and neck cancers can be divided into well-differentiated, moderately well-differentiated, and poorly differentiated categories.Poorly differentiated tumors have a worse prognosis than well-differentiatedtumors. For nasopharyngeal cancers, the less common differentiated squamouscell carcinoma is distinguished from nonkeratinizing and undifferentiatedcarcinoma (lymphoepithelioma) that contains infiltrating lymphocytes. Salivary gland tumors can arise from the major (parotid, submandibular,sublingual) or minor salivary glands (located in the submucosa of the upperaerodigestive tract). Most parotid tumors are benign, but half of submandibularand sublingual gland tumors and most minor salivary gland tumors are malignant.Malignant tumors include mucoepidermoid and adenoidcystic carcinomas andadenocarcinomas. The mucosal surface of the entire pharynx is exposed to alcohol- andtobacco-related carcinogens and is at risk for the development of a premalignant ormalignant lesion, such as erythroplakia or leukoplakia (hyperplasia, dysplasia),that can progress to invasive carcinoma. Alternatively, multiple synchronous ormetachronous cancers can develop. In fact, over time patients with early-stagehead and neck cancer are at greater risk of dying from a second malignancy thanfrom a recurrence of the primary disease. Second head and neck malignancies are usually not therapy-induced; theyreflect the exposure of the upper aerodigestive mucosa to the same carcinogensthat caused the first cancer. These second primaries develop in the head and neckarea, the lung, or the esophagus. Rarely, patients can develop a radiationtherapy–induced sarcoma after having undergone prior radiotherapy for a headand neck cancer. Chromosomal deletions and other alterations, most frequently involvingchromosomes 3p, 9p, 17p, and 13q, have been identified in both premalignant andmalignant head and neck lesions, as have mutations in tumor suppressor genes,such as the p53 gene. Amplification of oncogenes is less common, ...