HRAS Mutations in Epithelial–Myoepithelial Carcinoma

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Abstract
The molecular profile of epithelial–myoepithelial carcinomas (EMCa) has not been well studied, though a recent association with Harvey rat sarcoma viral oncogene homolog (HRAS) mutations has been noted. To confirm and validate this, we surveyed fifteen EMCa for HRAS codon 61 mutations and correlated HRAS status with clinicopathologic parameters. There were 11 females and 4 males and mean patient age was 64 (range 49–90). Parotid gland was most commonly involved (n = 10) and the most common histologic appearance was that of a ‘classic’ EMCa (7/15). Four of fifteen (26.7 %) cases demonstrated local recurrence, while 2/15 (13.3 %) demonstrated distant metastases. Other variant morphologies included EMCa arising from pleomorphic adenoma (3/15), and high grade EMCa (2/15). HRAS exon 3, codon 61 mutations, p.Q61R (n = 3) and p.Q61 K (n = 1) were identified in 4 of 15 successfully tested EMCAs (14 patients). Two cases were classic type, while the other cases consisted of one oncocytic variant, and one tumor with myoepithelial overgrowth, the latter of which showed the same mutation in both the primary and recurrence. Of note, the high grade EMCa and EMCa ex pleomorphic adenoma were negative for mutations. Given the small number of cases, there were no significant differences between mutation positive and mutation negative cases in terms of age, gender and outcome.

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