LAUSR

Adenoid cystic carcinoma (ACC) is a biphasic salivary gland malignancy that is characterized by cellular, morphologic, and clinical heterogeneity [1]. ACCs are the secondmost common salivary gland malignancy, are the most common malignancy of minor salivary glands, and comprise 15–25% of all salivary carcinomas. Despite locally aggressive growth with frequent perineural invasion, ACCs demonstrate slow biologic progression and lymph node metastasis is rare [1]. ACC arises from the intercalated ducts, which are composed of inner ductal epithelial and outer myoepithelial cell [2]. The histogenesis of these tumors is uncertain, and an origin from stem cells with multidirectional differentiation is likely possible. Histologic architecture alone determines the grade of ACC; tubular and cribriform growth patterns are associated with a longer survival time than solid forms are [1–3]. Myoepithelial cells may play a role in restraining the aggressive biological behavior of (solid) ACC. In breast cancer, myoepithelial cells have been labeled Bnatural tumor suppressors^ owing to their negative effects on tumor cell growth, invasion, and angiogenesis achieved via the secretion of protease inhibitors and downregulation of matrix metalloproteinase (MMP) levels [4, 5]. We are starting to understand and get insights into intrinsic molecular subtypes of this cancer directly linked to the dominant myoepithelial (M)ACC or epithelial (E)-ACC cell type [6]. The purpose of this study was to revisit outcomes of a cohort of 54 consecutive ACC patients treated at a single institution and classified according to their dominant cell type as E-ACC and M-ACC.