Description

• Adult neoplasms:
  • Benign: Pleomorphic adenoma, Warthin tumor (adenolymphoma), oncocytoma, and monomorphic adenoma
  • Malignant: Mucoepidermoid carcinoma, adenoid cystic carcinoma, acinic cell carcinoma, carcinoma ex-pleomorphic adenoma, squamous cell carcinoma (SCC), adenocarcinoma
• Total distribution of salivary gland neoplasms by type:
  • Pleomorphic adenoma (most common): 45% overall
  • Monomorphic adenoma: 12% overall
  • Mucoepidermoid carcinoma: 12% overall
  • Adenoid cystic carcinoma: 6% overall
  • Remaining neoplasms: 25% overall
• Distribution: Parotid (80%); submandibular (10–15%); sublingual and minor (5–10%):
  • Parotid (80% benign; 20% malignant):
    • Pleomorphic adenoma: 60%
    • Monomorphic adenoma: 8%
    • Warthin tumor: 8%
    • Mucoepidermoid carcinoma: 12%
    • Adenoid cystic carcinoma: 5%
    • Adenocarcinoma and SCC: 5%
  • Submandibular (60% benign; 40% malignant):
    • Pleomorphic adenoma: 40%
    • Mucoepidermoid carcinoma: 10%
    • Adenoid cystic carcinoma: 20%
  • Lingual and minor salivary glands (40% benign; 60% malignant):
    • Pleomorphic adenoma: 40%
    • Mucoepidermoid carcinoma: 25%
    • Adenoid cystic carcinoma: 25%; generally, as the size of the neoplasm decreases, the incidence of malignancy increases.
• Pediatric neoplasms:
  • These tumors are most frequently benign, but may be malignant.
  • Benign: 65% of overall cases; the most common types are hemangiomas and pleomorphic adenomas.
  • Malignant: 35% of overall cases; most common type is mucoepidermoid carcinoma.

Epidemiology

• 1.5 cases per 100,000 individuals in the US
• ~700 deaths annually
• Median age:
  • Benign: 45 years
  • Malignant: 60 years
• Gender predilection:
  • Benign: Female > Male
  • Malignant: Male = Female

Prevalence
Make up 6–8% of all head and neck neoplasms (1)

Risk Factors

• Tobacco and alcohol abuse associated with Warthin tumor, but not with SCC
• Alcohol increases likelihood ratio by 2:1 (2).
• Radiation has shown a 4-fold increased dose-related response in salivary gland cancer 15–20 years after treatment. Increased risk has also been reported in atomic bomb survivors (2).
• EBV has been associated with lymphoepithelial carcinoma in Asians, but there is no evidence of causal association in other tumors (2).
• Silica dust has been associated with a 2.5-fold increase in salivary gland neoplasia (2).
• Kerosene cooking fuel exposure (2)
• Nitrosamine exposure in rubber workers (2)
• Early menarche and nulliparity (2)

Genetics
Increased incidence of adenocarcinoma of parotid in Eskimos; otherwise, no known genetic pattern

General Prevention

Cessation of tobacco and alcohol use

Pathophysiology

Pathophysiology not fully understood; certain pathways and oncogenes have been implicated: p53, Bcl-2, PI3K/Akt, MDM2, VEGF, HGF, and ras.

Etiology

• Etiology is not fully understood.
• Predominant theory: Tumors arise from either the secretory duct reserve cell or the intercalated duct reserve cell.