Beta-catenin and E-cadherin expression in salivary gland tumors

This study evaluated the expression of E-cadherin and beta-catenin in salivary gland tumors. Twelve biopsy specimens from cases diagnosed as pleomorphic adenoma, 17 adenoid cystic carcinomas, 10 epithelial-myoepithelial carcinomas, and 4 polymorphous low-grade adenocarcinomas were immunohistochemically labeled for E-cadherin and beta-catenin antibodies. Healthy salivary glands were used as controls. Membrane-associated E-cadherin and beta-catenin expression was present in all the tumor types studied. E-cadherin and beta-catenin showed a similar distribution; however, beta-catenin labeling was weaker than that for E-cadherin. In the epithelial-myoepithelial carcinomas, myoepithelial cells exhibited diffuse nuclear staining, although occasional cells presented only focal labeling. Epithelial-myoepithelial carcinomas present changes in [.beta]-catenin expression but the other salivary tumors studied do not, which may reflect divergence in tumorigenesis of this extensive subset of salivary gland tumors.     

Immunohistochemical localization of WT1 in epithelial salivary tumors

The subcellular localization of WT1 is controversial and has received little attention in the epithelial tumors of salivary glands. Paraffin-embedded, surgical specimens from 80 salivary tumors were investigated by immunohistochemistry using a monoclonal, anti-WT1 antibody (6F-H2, Dako). Immunostaining was seen in 14/14 pleomorphic adenomas (PAs), 6/6 myoepitheliomas, 4/4 basal cell adenomas, 4/4 canalicular adenomas, 0/7 Warthin tumors, 0/1 oncocytoma, 1/6 acinic cell carcinomas (Cas), 0/11 mucoepidemoid Cas, 1/11 adenoid cystic Cas, 11/12 polymorphous low-grade adenocarcinomas (PLGAs), 1/2 Ca ex PA, 0/1 salivary duct Ca and 0/1 clear cell adenocarcinoma. Stained-cell subpopulations up to 90% were not uncommon in the benign tumors. Up to 80% of cells in PLGA could be stained. Staining was weak to intense and confined to the cytoplasm of preferentially non-luminal or adjacent to stroma cells. One adenoid cystic Ca showed nuclear staining. The results suggest that WT1 is often highly expressed in benign non-oncocytic salivary tumors whereas the malignant tumors show decreased expression, the exception being PLGA. The expression is usually cytoplasmic and associated with non-luminal cells. PLGA immunoreactivities could be useful in histological differential diagnosis.     

WHO International Histological Classification of Tumours. Tentative Histological Classification of Salivary Gland Tumours

The principles of the proposed modified WHO Histological Typing of Salivary Gland Tumours are based on the following: 1) The classification of tumours is oriented to the routine work of the practicing surgical pathologists, those who do not see tumours of the salivary glands very often. The inclusion of rare, but clearly defined tumour entities should be helpful to surgical pathologists consulting with clinical specialists. 2) The different types of carcinomas must be distinguished not only by precise histopathological definitions, but also considering differences in prognosis and treatment. For example, the polymorphous low-grade adenocarcinoma and the epithelial-myoepithelial carcinoma are characterized by a relatively good prognosis in contrast to the salivary duct carcinoma. 3) Special points of discussion are: subclassification and grading of carcinomas (e.g. acinic cell carcinoma, mucoepidermoid carcinoma and adenoid cystic carcinoma), the classification of basal cell tumours (basal cell adenoma, basal cell carcinoma, solid type of adenoid cystic carcinoma), malignant tumours in pleomorphic adenomas and the differential diagnosis between primary tumours and metastases.     

Immunoexpression of c-erbB-2 and p53 in benign and malignant salivary neoplasms with myoepithelial differentiation.

AIM: To evaluate whether the immunoexpression of c-erbB-2 and p53 is involved in the pathogenesis and progression of salivary tumours with myoepithelial differentiation. METHODS: 233 tumours from 211 patients were studied. These included 76 primary and 24 recurrent adenocarcinomas (polymorphous low grade adenocarcinoma, 13; epithelial-myoepithelial carcinoma, 19; adenoid cystic carcinoma, 56; and basal cell adenocarcinoma, 12) and 133 pleomorphic adenomas and myoepitheliomas, 96 being primary and the remaining recurrent tumours. All cases were formalin fixed and paraffin wax embedded. A StrepABC peroxidase method and polyclonal c-erbB-2 and p53 specific antisera were used. RESULTS: Cell membrane staining of c-erbB-2 was not found in any benign or malignant tumour. There was p53 protein accumulation in one primary and one recurrent pleomorphic adenoma and in 10 adenocarcinomas (polymorphous low grade adenocarcinoma, one; epithelial-myoepithelial carcinoma, one; adenoid cystic carcinoma, five; and basal cell adenocarcinoma, three), three of them being recurrences. CONCLUSIONS: The c-erbB-2 and p53 proteins are not involved in the pathogenesis of pleomorphic adenoma and myoepithelioma and do not constitute biomarkers in assessing the risk of recurrence. c-erbB-2 is not involved in the genesis of low grade salivary neoplasia with myoepithelial differentiation. The percentage of this type of neoplasia with p53 accumulation is low (10%) and does not appear to be related to tumour recurrence.     

Terminal duct carcinoma of minor salivary glands. A nonpapillary subtype of polymorphous low-grade adenocarcinoma

The clinicopathologic features of five terminal duct carcinomas arising in minor salivary glands are presented. These nonpapillary, low-grade adenocarcinomas are part of the spectrum of polymorphous low-grade adenocarcinoma. The patients ranged in age from 47 to 77 years. Symptoms were nonspecific and related to a mass that usually was present for several years. Histologically, the tumors had a ductal pattern with areas of solid and cribriform architecture. Cytologically, they were composed of uniform, cuboid cells with round to oval nuclei and fine chromatin. One patient developed a recurrence after 13 years, but none of the tumors has metastasized. One lesion in this series was studied ultrastructurally and demonstrated both glandular and pseudoglandular structures analogous to those of adenoid cystic carcinoma. Nonetheless, terminal duct carcinoma is cytologically distinctive from adenoid cystic carcinoma and appears to have a more favorable prognosis.     

Glial fibrillary acid protein immunoreactivity in fine-needle aspiration of salivary gland lesions: a useful adjunct for the differential diagnosis of salivary gland neoplasms

The value of immunocytochemical staining for glial fibrillary acid protein (GFAP) in salivary gland lesions was investigated in 33 fine-needle aspiration smears. The study utilized cytologic material from ten pleomorphic adenomas, six normal salivary glands, three cases of chronic sialadenitis, three Warthin's tumors, two adenoid cystic carcinomas, three adenocarcinomas, two malignant mixed tumors, one acinic cell carcinoma, and three mucoepidermoid carcinomas. All tested pleomorphic adenomas stained positively. The adenoid cystic carcinomas and the cases of chronic sialadenitis, along with the low-grade mucoepidermoid carcinoma, were negative for GFAP immunoreactivity. These results indicate that immunostaining for GFAP may be a valuable aid in the diagnosis of pleomorphic adenoma; GFAP may be especially helpful in distinguishing those cases for which the differential diagnosis includes the aforementioned salivary gland neoplasms.     

Hierarchical cluster analysis of myoepithelial/basal cell markers in adenoid cystic carcinoma and polymorphous low-grade adenocarcinoma.

Distinguishing adenoid cystic carcinoma from polymorphous low-grade adenocarcinoma of the salivary glands is important for their management. We studied the expression of several myoepithelial and basal/stem cell markers (smooth muscle actin, calponin, smooth muscle myosin heavy chain, metallothionein, maspin, and p63) by immunohistochemistry in 23 adenoid cystic carcinoma and 24 polymorphous low-grade adenocarcinoma, to identify the most useful marker or combination of markers that may help their diagnoses. The results were analyzed using hierarchical cluster analysis and chi(2) test for trend. We noted diffuse expression of smooth muscle actin in 20 adenoid cystic carcinoma vs one polymorphous low-grade adenocarcinoma (P<0.0001), calponin in 15 adenoid cystic carcinoma vs one polymorphous low-grade adenocarcinoma (P<0.0001), smooth muscle myosin heavy chain in 15 adenoid cystic carcinoma vs one polymorphous low-grade adenocarcinoma (P=0.001), metallothionein in 22 adenoid cystic carcinoma vs eight polymorphous low-grade adenocarcinoma (P<0.001), maspin in 22 adenoid cystic carcinoma vs 14 polymorphous low-grade adenocarcinoma, and p63 in 21 adenoid cystic carcinoma vs 14 polymorphous low-grade adenocarcinoma. Hierarchical clustering of smooth muscle actin, calponin, smooth muscle myosin heavy chain, and metallothionein was virtually identical (kappa< or =0.0035), suggesting no significant advantage to their use in combination than individually. Diffuse smooth muscle actin expression showed the highest accuracy (91.5%) and positive predictive value (95.2%) for adenoid cystic carcinoma. Thus, diffuse expression of smooth muscle actin, calponin, smooth muscle myosin heavy chain, and metallothionein was highly predictive of adenoid cystic carcinoma, whereas maspin and p63 were frequently expressed in both tumors. In differentiating adenoid cystic carcinoma from polymorphous low-grade adenocarcinoma, smooth muscle actin as a single ancillary test in support of the histological findings, appears to be as efficient as multiple immunohistochemical tests.     

Cell proliferation in salivary gland adenocarcinomas with myoepithelial participation

We used three markers of cell proliferation — mitotic counts, mitotic index and expression of proliferating cell nuclear antigen - to assess the proliferative activity of a series of 78 low-grade salivary adenocarcinomas with myoepithelial participation classified according to: their histological type, the predominant architectural type, and the predominant cytological type. The series included adenoid cystic carcinomas (40), epithelial-myoepithelial carcinomas (19), polymorphous low-grade adenocarcinomas (12) and basal cell adenocarcinomas (7). The proliferation indicators were found to be similar in the first three groups, being significantly lower than in the last. Tumours formed by basal cells had statistically significant higher mitotic indexes than those predominantly composed of clear cells of myoepithelial type and ductal cells. Tubular tumours, irrespective of the histological classification of the neoplasm, had proliferation indexes similar to those found in cribriform neoplasms. Solid tumours, whether formed by ductal or clear myoepithelial-type cells, had higher indexes than the neoplasms with differentiated (cribriform and tubular) patterns. The highest mean values for every proliferation indicator used were found in tumours with solid organization that were predominantly formed by basal cells. These results agree with the hypothesis that cell proliferation is inversely related to neoplastic differentiation. The identification of the prevalent cell phenotype and architecture may extend our knowledge from adenoid cystic carcinoma, whose solid variant carries a worse prognosis, and supports that the usual classification of this group of salivary adenocarcinomas would benefit to be complemented with information on tumour architecture and cellular composition.     

Cytologic diagnosis of adenoid cystic carcinoma of salivary glands.

The cytomorphologic features in fine-needle aspiration (FNA) biopsies from 31 primary and 33 recurrent adenoid cystic carcinomas (ACC) were investigated. The correct FNA diagnosis was established in 24 of 31 primary ACC (77%). The diagnostic clue in aspirates from ACC are large globules of extracellular matrix, partially surrounded by basaloid tumor cells. In FNAs with predominance of basaloid tumor cells, but lacking characteristic globules, all other benign and malignant salivary gland tumors of epithelial-myoepithelial differentiation should be considered in the cytologic diagnosis. Pleomorphic adenoma is most frequently confused with ACC, and therefore, the cytologic findings in FNAs from 50 pleomorphic adenomas were compared with those diagnosed as ACC. Furthermore, rare neoplasms of salivary glands with epithelial-myoepithelial cell differentiation, including basal-cell adenoma and carcinoma, epithelial-myoepithelial carcinoma, and polymorphous low-grade adenocarcinoma, as well as some nonsalivary gland neoplasms presenting an adenoid cystic pattern, must be considered. The cytologic features of these entities are discussed in detail with respect to the cytologic diagnostic criteria of ACC.     

Myoepithelial differentiation markers in salivary gland neoplasia]

Salivary gland tumors frequently present myoepithelial cell differentiation that is not always easily identified on routinely stained sections. Recently novel markers of myoepithelium have been studied, such as calponin (CALP), caldesmon (CALD), and smooth muscle myosin heavy chain. These markers, together with smooth muscle actin may be useful tools for identifying myoepithelial cells. We immunohistochemically studied a series of 23 benign and malignant salivary gland tumors using antibodies to these four markers. The tumors were classified as follows: pleomorphic adenoma (n = 8), basal cell adenoma (n = 3), myoepithelioma with plasmacytoid cells (n = 2), epithelial-myoepithelial cell carcinoma (n = 6) and adenoid cystic carcinoma (n = 4). All tumors were positive for at least one of the four markers. CALP and smooth muscle actin were the markers more frequently expressed. Positivity was mostly located in the myoepithelial cells that constitute the external layer of the glandular or tubular neoplastic structures. In poorly differentiated epithelial myoepithelial carcinomas, composed of solid sheets of neoplastic cells and sometimes of clear cells, immunohistochemical staining for myoepithelial markers evidenced rudimentary glandular structures. CALP and smooth muscle actin were positive in the two cases of myoepithelioma with plasmacytoid cells. In conclusion, the combined staining with four markers helps to disclose myoepithelial cell differentiation and can be a useful tool for the correct histopathological diagnosis of salivary gland tumors. Among the four markers studied, CALP and smooth muscle actin were the most useful to identify myoepithelial cell differentiation.     

Epithelial-myoepithelial cell carcinoma of the parotid gland: A case report and comparison of cytologic features with other stromal,epithelial, and myoepithelial cell containing lesions of the salivary glands

The salivary glands are the site of many neoplasms characterized by a mixture of epithelial and myoepithelial cells and stromal fragments. Cytologic distinction of these neoplasms may be very difficult but careful attention to cellular details and the interaction between the cells and stroma can correctly classify these neoplasms as monomorphic or pleomorphic adenomas, adenoid cystic carcinomas, or epithelial-myoepithelial cell carcinomas. Diagn Cytopathol 1996;14:298–304. © 1996 Wiley-Liss, Inc.     

Immunohistochemical expression of cytokeratins 7 and 20 in malignant salivary gland tumors.

On the basis of the heterogeneity of cytokeratins 7 and 20 expression in malignant epithelial tumors, the cytokeratin 7/20 immunophenotype has served as a useful diagnostic tool for discrimination of primary and/or metastatic carcinomas of unknown origin. However, the expression pattern of these cytokeratins in malignant salivary gland tumors has not been thoroughly studied. Our study material was composed of 84 malignant tumors of primary major or minor salivary gland origin. Nine histologic types of carcinoma were represented, including mucoepidermoid (26 cases), adenoid cystic (25), polymorphous low grade (11), salivary duct (8), acinic cell (4), ex mixed tumor (3), not otherwise specified (3), clear cell (2), and basal cell (2). In all, 13 cases of primary skin or mucosal squamous cell carcinoma with secondary salivary gland involvement were also examined. Immunoreactivity for cytokeratin 7 was evident in all malignant salivary gland tumors; the staining pattern was diffuse and strong in 62 cases, and focal and strong in 22 cases. In contrast, 78 cases were negative for cytokeratin 20, whereas only six cases (two mucoepidermoid, one adenoid cystic, and three salivary duct) displayed focal weak positivity. Overall, 92.9% of malignant salivary gland tumors were characterized by a cytokeratin 7 positive/20 negative immunoprofile, the remaining 7.1% of cases being positive for both cytokeratins. The latter phenotype was more common in salivary duct carcinomas (P< or =0.05). On the other hand, most squamous cell carcinomas (69%) were negative for both cytokeratins, while the remaining cases (31%) were negative for cytokeratin 20 and focally weakly positive for cytokeratin 7. We suggest that assessment of cytokeratin 7/20 immunoprofile may facilitate the differential diagnosis of (a) primary malignant salivary gland tumors from metastatic tumors, (b) metastatic salivary gland tumors, (c) primary salivary gland tumors, especially mucoepidermoid carcinomas, from squamous cell carcinomas, and (d) salivary duct carcinomas from other malignant salivary gland tumors.     

Dendritic interstitial and myofibroblastic cells at the border of salivary gland tumors

OBJECTIVE: CD34-positive dendritic interstitial cells may be associated with the regulation of tumor growth. This association has been studied in various human neoplasms, especially skin tumors. In this study, we evaluated the distribution of dendritic interstitial cells and myofibroblastic cells at the tumor periphery of various benign and malignant salivary gland neoplasms. METHODS: Forty-nine cases of salivary gland tumors were selected: 16 pleomorphic adenomas, 12 Warthin tumors, 8 polymorphous low-grade tumors, 5 adenoid cystic carcinomas, 6 acinic cell carcinomas, and 2 mucoepidermoid carcinomas. Immunohistochemical analysis was performed by using antibodies for CD34 (dendritic cells) and alpha-smooth muscle actin (myofibroblast) on formalin-fixed, paraffin-embedded archival tissue. Staining intensity was graded as marked (3+), moderate (2+), weak (1+), and absent (0). RESULTS: Staining intensity for CD34 was 3+ in 24 (86%) of 28 benign tumors (pleomorphic adenomas and Warthin tumors) and 6 (29%) of 21 malignant tumors (polymorphous low-grade tumors, acinic cell carcinomas, adenoid cystic carcinomas, and mucoepidermoid carcinomas) and 2+ in 4 (19%) of 21 malignant tumors. None of the benign tumors displayed 2+ staining with CD34. Three (11%) of 28 benign and 11 (52%) of 21 of malignant tumors failed to stain with CD34. alpha-Smooth muscle actin staining was 3+ in 10 (36%) of 28 benign tumors and 6 (29%) of 21 malignant tumors, and 2+ in 11 (39%) of 28 benign and 2 (9%) of 21 malignant tumors. Five (18%) of 28 benign and 11 (52%) of 21 malignant tumors failed to stain with alpha-smooth muscle actin. CONCLUSION: We conclude that the dendritic interstitial cells and myofibroblastic cells may be associated with the regulation of tumor growth in salivary gland tumors.     

Low-grade mucoepidermoid carcinoma of salivary glands: characteristic immunohistochemical profile and evidence of striated duct differentiation

The purpose of the present study is to determine the presence and distribution of epithelial and myoepithelial cells in mucoepidermoid carcinoma (MEC) of salivary glands and to compare them with normal salivary gland tissue and other primary carcinomas. This is in order to establish novel diagnostic criteria and to better understand MEC histogenesis. Formalin-fixed paraffin-embedded tissues from ten well-differentiated MECs, three adenoid cystic carcinomas (ACC), four acinic cell carcinomas (AC), and three epithelial-myoepithelial carcinomas (EMCC) of salivary glands were studied with immunohistochemistry using antibodies that recognise antigens indicative of epithelial and myoepithelial cell differentiation. An anti-mitochondrial antibody was also employed. Normal salivary tissue was present for comparative study in non-tumorous areas of the same section from 12 cases. MEC contained numerous keratin-positive cells. Anti mitochondrial antibody was diffusely positive in all ten of these tumours. Smooth muscle actin, h-caldesmon, and smooth muscle heavy chain myosin, which are indicative of myoepithelial cell differentiation, were negative. Rare cells in only one case were stained by calponin. Cytokeratin 14 (CK14) and anti mitochondrial antibody stained cells located mainly at the periphery of neoplastic nests and cystic spaces, while CK7 was mainly present in cells bordering gland lumina (zoning pattern). The immunohistochemical cell profile was similar to that seen in striated normal ducts. All others tumours studied showed a different immunohistochemical pattern, mostly consisting of a lack of mitochondrion-rich cells and the presence of myoepithelial cells in ACC and EMCC. Immunoreactivity in MEC for CK7, CK14 and mitochondrial antibodies appears as a peculiar pattern of staining, different from that of other salivary gland tumors; this seems helpful for diagnostic purposes. In addition, a differentiation of the "striated duct phenotype" is suggested.     

DOG1: a novel marker of salivary acinar and intercalated duct differentiation

Anoctamin-1 (ANO1) (DOG1, TMEM16a) is a calcium-activated chloride channel initially described in gastrointestinal stromal tumors, but now known to be expressed in a variety of normal and tumor tissues including salivary tissue in murine models. We herein perform a comprehensive survey of DOG1 expression in 156 cases containing non-neoplastic human salivary tissues and tumors. ANO1 mRNA levels were significantly higher (8-fold increase, P<0.0001) in normal parotid tissue (n=6) as compared with squamous mucosa (n=15). By immunohistochemistry, DOG1 showed a diffuse moderate (2+) apical membranous staining pattern in normal serous acini, 1+ apical membranous pattern in mucous acini, and variable 1-2+ apical staining of distal intercalated ducts. Myoepithelial cells, striated and excretory ducts were invariably negative. All acinic cell carcinomas (n=28) were DOG1 positive demonstrating a complex mixture of intense (3+) apical membranous, cytoplasmic and complete membranous staining. Most ductal tumor types were negative or only showed a subset of positive cases. Within the biphasic tumor category, adenoid cystic carcinomas (18/24 cases) and epithelial-myoepithelial carcinomas (8/15 cases) were frequently positive, often showing a distinctive combined apical ductal and membranous/cytoplasmic myoepithelial staining profile. Thus, DOG1 staining is a marker of salivary acinar and to a lesser extent intercalated duct differentiation. Strong staining can be used to support the diagnosis of acinic cell carcinoma. DOG1 may also be a marker of a 'transformed' myoepithelial phenotype in a subset of biphasic salivary gland malignancies.     

Myoepithelial cells in salivary gland tumors. An immunohistochemical study

Normal salivary glands and 55 salivary gland tumors were examined by immunostaining (immunoperoxidase [IMP] and immunofluorescence [IMF]) to identify myoepithelial cells (MCs) and speculate on their role in the histogenesis of the tumors. The classic (C) MCs of normal salivary glands stained by IMP with antibodies to cytokeratin and S100 protein and stained by IMF with the same antibodies and with antibodies to vimentin and actin. Modified (M) MCs of pleomorphic adenomas stained positively by IMP and IMF with all of the preceding antibodies. In many mucoepidermoid carcinomas, adenoid cystic carcinomas, and basal cell adenomas, variable numbers of CMCs and MMCs stained positively by IMP with anti-cytokeratin and anti-S100 protein antibodies. No MCs were detected in adenolymphomas or acinic cell carcinomas. We believe that MCs play a major role in the histogenesis of pleomorphic adenomas and may also be important in many mucoepidermoid carcinomas, adenoid cystic carcinomas, and basal cell adenomas.     

Keratin 14 immunoreactive cells in pleomorphic adenomas and adenoid cystic carcinomas of salivary glands

Our recent study of developing myoepithelial cells (MECs) in rat salivary glands demonstrated that developing MECs begin to express α-smooth muscle actin (αSMA) first and, thereafter, keratin 14. Therefore, it is unlikely that duct basal cells expressing keratin 14 alone are immature or undifferentiated MECs. In this study we carried out immunohistochemistry of pleomorphic adenomas and adenoid cystic carcinomas including normal salivary glands using monoclonal antibodies to keratin 14, smooth muscle proteins and keratin 19. The smooth muscle proteins examined included αSMA, h-caldesmon and h1-calponin; h1-calponin was observed in keratinocytes and nerve fibers, indicating that the protein is not specific to smooth muscle, whereas αSMA and h-caldesmon turned out to be highly specific markers for smooth muscle cells in normal tissues. In normal glands, MECs were positive for both keratin 14 and smooth muscle proteins (αSMA and h-caldesmon). Non-MEC cells were essentially devoid of smooth muscle proteins. Non-MEC duct basal cells expressed keratin 14 with or without keratin 19, and luminal cells keratin 19 with or without keratin 14. This suggests that the keratin 14-positive, smooth muscle proteins-negative duct basal cells are luminal cell progenitors. Luminal cells in tubular structures of both tumors were positive for keratin 19 with or without keratin 14. Nonluminal peripheral cells of pleomorphic adenomas were mostly positive for keratin 14, and a small fraction of them expressed smooth muscle proteins. Conversely, peripheral cells of adenoid cystic carcinomas were mostly positive for smooth muscle proteins, and some of them expressed keratin 14. These results strongly suggest (1) that the luminal cell progenitors transform into major constituents of pleomorphic adenoma cells with keratin 14 but not smooth muscle proteins, and (2) that the peripheral cells of adenoid cystic carcinoma are derived from undifferentiated MECs. Solid structures of pleomorphic adenomas were formed by proliferation of the peripheral cells. MECs were observed only occasionally in the periphery. Solid and cribriform structures of adenoid cystic carcinomas were formed by proliferation of the luminal cells. MECs were observed in the periphery and around the pseudocyst. Received: 2 December 1999 / Accepted: 12 January 2000     

Basaloid carcinomas of salivary glands

Three cases of carcinoma of major salivary glands with basaloid morphology are presented. One case was a clear example of a basal cell adenocarcinoma, an uncommon and infrequently recognized, low-grade tumour of major salivary glands. The remaining two cases showed a higher cytological grade of malignancy but shared some features of basal cell adenocarcinoma. Common features included the architectural pattern and myoepithelial cell differentiation, as demonstrated by smooth muscle-specific actin positivity, in cells associated with the deposition of extracellular basal lamina-like material. The relationship between these cases and adenoid cystic carcinoma is discussed.     

Fine-needle aspiration cytological findings in five cases of epithelial-myoepithelial carcinoma of salivary glands

The cytologic features of five cases of epithelial-myoepithelial carcinoma arising in major salivary glands (four parotid and one submandibular gland) are presented. All cases were initially diagnosed as low-grade malignancies. The smears were generally cellular, with no specific architectural pattern. Single cells and naked nuclei were prominent in all cases. A biphasic epithelial (small-cell) and myoepithelial (large/clear-cell) pattern was identified readily in two cases and with difficulty in one case. The biphasic pattern may be subtle or absent since the clear cells have a fragile cytoplasm and often appear as naked nuclei. The differential diagnosis includes adenoid cystic carcinoma, polymorphous low-grade adenocarcinoma, and cellular pleomorphic adenoma.