Harim Tavares dos Santos

Mammary analogue secretory carcinoma of salivary glands is a lipid-rich tumour, and adipophilin can be valuable in its identification.

Mammary analogue secretory carcinoma (MASC) of salivary glands shows morphological similarities to milk‐secreting mammary epithelial cells. The aim of this study was to analyse the immunohistochemical expression of adipophilin (a component of milk lipid globule membranes) and of proteins related to secretory mechanisms (STAT5a and mammaglobin) in MASC and other salivary tumours.

Carcinoma ex pleomorphic adenoma of minor salivary glands with major epithelial-myoepithelial component: clinicopathologic and immunohistochemical study of 3 cases

In the present study, 3 cases of very rare intraoral carcinomas ex pleomorphic adenomas showing a striking differentiation of the malignant component towards epithelial-myoepithelial carcinoma were described. The tumors occurred in 2 men and 1 woman with median age of 56 years. Involved sites included palate and buccal mucosa. Two patients experienced local recurrences, of which one died of disease complications. In all cases, residual pleomorphic adenoma was present. The malignant component in all cases shared morphological aspects with epithelial-myoepithelial carcinoma. Those areas were characterized by eosinophilic duct-forming cells surrounded by layers of clear cells. The studied immunohistochemical markers highlighted a biphasic cell population. Duct-forming cells expressed pan-cytokeratin, cytokeratin 7, and focally cytokeratin 14, whereas the clear cell component strongly stained to cytokeratin 14, vimentin, and p63 but weakly stained to pan-cytokeratin and focally to α-smooth muscle actin, an immunophenotype compatible with both epithelial and myoepithelial differentiation. The Ki-67 proliferation index was up to 40% in malignant areas. Carcinoma ex pleomorphic adenomas of minor salivary glands with major epithelial-myoepithelial component are rare, locally aggressive, and potentially lethal tumors. The peculiar morphological and immunohistochemical aspects described may raise problems in diagnosis and classification of such cases, particularly in incisional biopsies.

Doing more with less: the challenging diagnosis of polymorphous low-grade adenocarcinoma in incisional biopsy samples.

The diagnosis of polymorphous low‐grade adenocarcinoma (PLGA) remains difficult for general pathologists, particularly in cases of small biopsy samples. We aimed to characterize the histopathological spectrum and immunohistochemical aspects by using an accessible immunohistochemical panel of cytoskeletal proteins in limited samples of PLGA.

Epstein-Barr Virus in Nasopharyngeal Carcinoma of Guatemalan and Brazilian Patients

Background. Nasopharyngeal carcinoma (NPC) is highly associated with Epstein-Barr virus (EBV), particularly the undifferentiated nonkeratinizing subtype. Prevalence of EBV in NPC in countries such as Guatemala and Brazil has not been studied. Methods. We analyzed 19 cases of NPC, 11 from Guatemala and 8 from Brazil, for the presence of EBV by in situ hybridization and immunohistochemistry. Additionally, 19 hyperplastic adenoids from children were analyzed for EBV by in situ hybridization, 12 from Guatemala and 7 from Brazil. Results. All the NPC cases from Guatemala and 5 from Brazil were of the undifferentiated nonkeratinizing type. EBV-negative cases comprised 2 keratinizing NPC and 1 differentiated nonkeratinizing NPC. All undifferentiated nonkeratinizing NPC from both samples showed intense positivity for EBER, while LMP-1 only focally and scarcely expressed. EBER was positive in 75% and 43% of the adenoids from Guatemala and Brazil, respectively. Conclusions. All undifferentiated nonkeratinizing NPC irrespective of origin from Guatemala or Brazil were highly associated with EBV.

Plasmacytoid-Type Cellular Differentiation in Polymorphous Low-Grade Adenocarcinoma

Introduction. Polymorphous low-grade adenocarcinoma (PLGA) occurs more frequently in minor salivary glands. The diagnosis of PLGA, in general, is not difficult but in occasional tumors showing limited invasion or in small biopsy specimens, PLGA may be confused with cellular pleomorphic adenoma (PA). Plasmacytoid cells, a usual component of PAs, have been considered helpful for correct tumor identification. Objective. The aim of this study was to verify the frequency (if any) of plasmacytoid-type cellular differentiation (PD) in PLGA. Materials and Methods. Thirty-two cases of PLGA were reviewed. PD was recognized in 2 cases (6.25%), in which immunohistochemical expression of AE1/AE3, CK7, CK14, vimentin, α-SMA, p63, S-100, calponin, GFAP, and Ki-67 was evaluated. Results. The 2 cases presented conventional areas of PLGA and variable quantities of cells with PD forming aggregates in the stroma and lining ductal structures. Cells with PD showed positivity for AE1/AE3, CK7, S-100, and vimentin and were negative for CK14, calponin, and GFAP in both cases. In case 1, cells with PD did not present α-SMA and p63 positivity whereas in case 2 they were positive, but for α-SMA such reactivity was restricted to cells forming solid aggregates. Conclusion. Although PD in PLGA is rare, it is necessary to be aware of this possibility, particularly in small incisional biopsies and in PLGA with limited invasion, to avoid confusion with cellular PA.

Lipid droplets are involved in the process of high-grade transformation of adenoid cystic carcinoma

these cases, strong expression of PD-L1 by macrophages was a striking feature (Figure 1); three spMSIH tumours among these also showed membranous PD-L1 immunostaining of the tumour cells. By contrast, considerably less macrophage infiltration was seen in the five MSS tumours with moderate or highdegree tumour budding and, notably, in each case membranous PD-L1 immunostaining was observed in at least some tumour buds (Figure 2), although with low frequencies (<1% of the tumour buds). Applying the classification of cancers outlined by Teng et al., our observations suggest ‘adaptive immune resistance’ in microsatellite-unstable and some macrophage-rich microsatellite-stable colorectal carcinomas. This contrasts with ‘immunological ignorance’ in the microsatellite-stable and macrophage-poor colorectal carcinomas that, however, are apparently capable of mounting an ‘intrinsic induction’ of PD-L1 in some tumour buds.