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Pleomorphic adenoma (or benign mixed tumor) is a common benign salivary gland neoplasm characterised by neoplastic proliferation of epithelial (ductal) cells along with myoepithelial components, having a malignant potentiality.
Benign tumour of the submandibular gland, also known as pleomorphic adenoma, presented as a painless neck mass in a 40-year-old man. At the left of the image is the white tumour with its characteristic cartilaginous cut surface. To the right is the normally lobated submandibular salivary gland. Warthin's tumor; Myoepithelioma; Basal cell ...
In approximately 75% of cases ca ex PAs arise in a pleomorphic adenoma that is apparent when the tumour is excised. [2] In the other approximately 25% of cases the individual had a pleomorphic adenoma excised previously and the diagnosis is made based on (1) the presence of a carcinoma, and (2) the history of a pleomorphic adenoma at that location.
Benign tumors of bone can be similar macroscopically and require a combination of a clinical history with cytogenetic, molecular, and radiologic tests for diagnosis. [23] Three common forms of benign bone tumors with are giant cell tumor of bone, osteochondroma , and enchondroma ; other forms of benign bone tumors exist but may be less prevalent.
Warthin's tumor primarily affects older individuals (age 60–70 years). There is a slight male predilection according to recent studies. The tumor is slow growing, painless, and usually appears in the tail of the parotid gland near the angle of the mandible.
Most tumors are small, up to 2 cm (given the confines of the tongue, a larger mass would cause significant clinical problems). A very low power hematoxylin and eosin stained slide of an ectomesenchymal chondromyxoid tumor. Note the well demarcated tumor, separate from the overlying, intact squamous mucosa. [1] [5] [6]
Other high grade carcinomas can mimic SDC. About 40-60% of SDC arise in pleomorphic adenomas. [3] Most, if not all, SDCs express androgen receptor by immunohistochemistry. [4] Therapeutically relevant genetic alterations include ERBB2/Her2 amplification, PIK3CA and/or HRAS mutations. [5] [6]
Mucoepidermoid carcinomas of the salivary and bronchial glands are characterized by a recurrent t(11;19)(q21;p13) chromosomal translocation resulting in a MECT1-MAML2 fusion gene. [5]