Mucoepidermoid carcinoma of the bronchus: a review

• Published in: Archives of pathology & laboratory medicine (1976) Vol. 131; no. 9; pp. 1400 - 1404
• Main Authors: Liu, Xiuli, Adams, Amy L
• Format: Journal Article
• Language: English
• Published: United States College of American Pathologists 01.09.2007
• Subjects: Airway management; Biopsy; Bronchi - metabolism; Bronchi - pathology; Bronchial Neoplasms - genetics; Bronchial Neoplasms - metabolism; Bronchial Neoplasms - pathology; Cancer; Carcinoma, Mucoepidermoid - genetics; Carcinoma, Mucoepidermoid - metabolism; Carcinoma, Mucoepidermoid - pathology; Care and treatment; Causes of; Cellular signal transduction; Cyclin D1 - genetics; Cyclin D1 - metabolism; Cysts; Diagnosis; Diagnosis, Differential; Exocrine glands; Gene Expression Regulation, Neoplastic; Health aspects; Humans; Lung cancer; Pediatrics; Pneumonia; Prognosis; Respiratory Mucosa - metabolism; Respiratory Mucosa - pathology; Tomography; Translocation, Genetic - genetics; Tumors; United States
• ISSN: 0003-9985; 1543-2165; 1543-2165
• DOI: 10.5858/2007-131-1400-MCOTBA

Although mucoepidermoid carcinoma of the salivary gland is relatively common, mucoepidermoid carcinoma arising from the mucous glands of the bronchus is rare. Bronchial mucoepidermoid carcinoma usually presents as an intraluminal mass producing luminal occlusion. Symptoms are airway obstruction and recurrent pneumonia. Macroscopically, mucoepidermoid carcinoma appears as an exophytic intrabronchial mass with intact or ulcerated bronchial mucosa. Microscopically, the tumors are located in the submucosa of the large bronchi. The tumors are usually well differentiated and contain a combination of mucus-secreting, squamous, and intermediate cells. The increased frequency of this tumor in the pediatric population suggests a genetic abnormality. Recent genetic studies have demonstrated reciprocal chromosomal translocations including t(1;11)(p22;q13), t(11;19)(q14-21;p12), and t(11; 19)(q21;p13). Chromosome 11 in the first translocation appears to have been altered resulting in up-regulation of the cyclin D1 gene and overexpression of cyclin D1. The t(11;19)(q21;p13) encodes a novel fusion product capable of disrupting the Notch signaling pathway.