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Head and neck cancers are a diverse group of diseases, each with distinct epidemiologic, anatomic, and pathologic features. The natural history and treatment considerations may vary widely. In this chapter, our focus is on the primary management of squamous cell carcinomas (SCCs) of the head and neck (SCCHN). In recent years, we have observed significant advances in diagnosis and treatment, and recognition of the human papillomavirus (HPV) as a significant causative agent for cancers of the oropharynx. Tumor imaging is increasingly precise. Primary therapy eradicates disease in a majority of patients with early-stage SCCHN, and the long-term management of these patients currently involves an emphasis on general medical care, avoiding known carcinogens such as alcohol and tobacco, and participation in chemoprevention strategies to reduce the risk of second primary tumors (SPTs). Therapy for patients with locally advanced disease has become multimodal, and success has been achieved in improving local tumor control, disease remission, organ preservation, and overall survival. The integration of chemotherapy and novel "targeting" systemic treatment approaches with surgery and/or radiotherapy is under study and is discussed.

In the United States, SCCHN represented approximately 3% (48,000) of new cancer cases and 2% (11,000) of cancer deaths in 2009 (1). However, the disease is more common in many developing countries, with a worldwide annual incidence of more than 500,000 (2).

The risk of developing head and neck cancer increases with age; most patients are above age 50. There has been a clearly demonstrated association with tobacco and alcohol use. Molecular studies provide evidence that carcinogens found in these substances have a causal role. The prevalence and spectrum of p53 mutations are greater in cancers of patients with a history of tobacco and alcohol usage than in those without (3). Cancers of the floor of the oral cavity, larynx, and hypopharynx are uncommon in persons with no smoking history.

HPV infection is now widely accepted as another etiologic factor for SCCHN. In the United States, more than 50% of cancers arising in the oropharynx, particularly in the palatine tonsils and tongue base, contain oncogenic HPV (4). It appears that the HPV-positive oropharyngeal malignancy represents a distinct clinical and pathological subgroup of SCCHN, with poorly differentiated, basaloid histopathology (5), and marked tumor responsiveness to radiation and chemotherapy. Moreover, SCCHNs with transcriptionally active HPV-16 DNA are characterized by occasional chromosomal loss, while those lacking HPV DNA typically have gross deletions, involving chromosomal arms known to be abnormal in SCCHN (6). Thus, HPV-16 infection may be an early carcinogenic event. HPV DNA-positive tumors, particularly those associated with E6 and E7 proteins, have improved survival after chemoradiotherapy when compared to HPV-negative tumors (7). A recent case-control study reported that HPV-16-positive SCCHN were independently associated with several measures of sexual behavior and exposure to marijuana but not with cumulative measures of tobacco smoking, alcohol use, or poor oral hygiene (...

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