Sclerosing microcystic adenocarcinoma of the tongue: a report of 2 further cases and review of the literature.

We present 2 further cases of sclerosing microcystic adenocarcinoma occurring in the tongue in 2 female patients, one age 68 years and the other 49 years. Histopathologically, both tumors were characterized by a diffusely infiltrative lesion consisting of small cuboidal cells arranged in discrete dispersed cords, isolated tubules, and bilayered strands with intervening microcystic lumina set in a sclerotic background. Both lesions showed striking neurotropism with perineural and intraneural infiltration. Extensive invasion of adjacent skeletal muscle was also observed. The tumor cells showed diffuse staining with antibodies to cytokeratin 7 (CK7). A dual population of ductal and myoepithelial cells was identified, with antibodies to CAM5.2 and CK5/6 decorating the inner epithelial layer and antibodies to p63, p40, and S100 staining the outer myoepithelial cell layer. The Ki-67 proliferation index in both cases was less than 5%. An initial diagnosis of adenocarcinoma NOS (not otherwise specified) of salivary gland origin was made on both incisional biopsies and a possible metastatic origin, particularly from the breast, also raised. A local minor salivary gland origin was confirmed after staging investigations and surgical resection. Both patients were t.

Assessment of TP53 mutations in benign and malignant salivary gland neoplasms.

Despite advances in the understanding of the pathogenesis of salivary gland neoplasms (SGN), the molecular pathways associated with enhanced tumor growth and cell survival remain to be established. The aim of the present study was to investigate whether TP53 mutations are relevant to SGN pathogenesis and if they impact on p53 protein expression. The study included 18 benign and 18 malignant SGN samples. Two polymorphic microsatellite markers at the TP53 genetic locus were chosen to assess loss of heterozygosity (LOH) in the samples that had matched normal DNA. The TP53 exons 2-11 were amplified by PCR, and all of the products were sequenced. Reverse transcription-PCR of the TP53 open reading frame (ORF) was carried out in the samples that had fresh tissue available, and immunohistochemistry for the p53 protein was performed in all samples. TP53 LOH was only found in two pleomorphic adenomas. We found two missense mutations in exon 7 (one in a pleomorphic adenoma and the other in a polymorphous low grade adenocarcinoma), another in exon 8 (in a carcinoma ex pleomorphic adenoma) and a fourth missense mutation in exon 10 (in a mucoepidermoid carcinoma). In addition, a nonsense mutation was found in exon 8 of an adenoid cystic carcinoma. Several intronic and exonic SNPs were detected. Although almost all of the malignant samples were immunopositive for p53, approximately 37% of the benign samples were positive, including the sample harboring the missense mutation and one of the samples that showed LOH. The complete TP53 ORF could be amplified in all samples analyzed, including the IHC negative samples, the samples showing LOH and one sample displaying a missense mutation. In summary, our results show that TP53 mutations are not a frequent event in SGN and that p53 immunopositivity might not be associated with sequence mutations in SGN.