Differential Expression of Myoepithelial Markers in Salivary, Sweat and Mammary Glands

Myoepithelial cells (MECs) are contractile elements showing a combined epithelial and smooth muscle phenotype. Among the numerous immunohistochemical markers employed to detect MECs, smooth muscle actin (SMA) is the most widely used. Recently, other markers of smooth muscle differentiation have been demonstrated in MECs, such as calponin, heavy caldesmon (h-caldesmon), and smooth muscle myosin heavy chain (SMM-HC). In the present study normal salivary, mammary, and sweat glands have been studied with four markers of smooth muscle differentiation (SMA, calponin, h-caldesmon, and SMM-HC). The four markers were differentially expressed in the various types of glands. In parotid glands MECs mainly expressed calponin and caldesmon; in submandibular and in cutaneous apocrine and eccrine glands, MECs strongly expressed SMA, calponin, and caldesmon; in minor salivary glands all four markers were equally strongly expressed; and in mammary glands SMA, calponin, and SMM-HC were present both in periductal and periacinar MECs while caldesmon was present in periductal MECs only. In addition to MECs, SMA stained stromal myofibroblasts, sometimes hampering the identification of MECs. Among the other markers, calponin stained only rare stromal myofibroblasts, while caldesmon and SMM-HC were confined to MECs. In conclusion, these latter markers are very useful for identifying MECs. It is suggested that the differential expression of smooth muscle contractile proteins might reflect different functions of MECs in the various sites. Int J Surg Pathol 8(1):29-37, 2000     

Immunohistochemical staining of papillary breast lesions.

The separation of ductal papilloma from intraductal papillary carcinoma of the breast on hematoxylin and eosin stained sections often presents diagnostic difficulty. Immunohistochemical staining is often employed in diagnosis, historically with smooth muscle actin (SMA). In this study, the staining characteristics of a panel of myoepithelial markers (calponin, p63, P-cadherin), were compared with SMA, and the epithelial expression of CD44s was assessed in 99 papillary lesions. SMA, calponin, and p63 demonstrated myoepithelial cells in 61%, 63%, and 65% of papillary lesions, respectively. However, specificity was quite variable. Calponin-stained stromal myofibroblasts (35% of cases), vessel pericytes (92%), and endothelial cells (69%), though each to a lesser degree than SMA. Calponin also showed cross reactivity with epithelium in 18% of cases. p63 was almost completely restricted to myoepithelial cell nuclei, and did not stain vascular smooth muscle or myofibroblasts. However, p63 stained the epithelial component in one papillary carcinoma, a basal layer of cells in 1 biphasic invasive carcinoma, and the cytoplasm in 1 case. P-cadherin stained both epithelial and myoepithelial cells. The epithelial expression of CD44s and did not distinguish papillomas from papillary carcinomas. Thus, P-cadherin and CD44s are not useful in the characterization of papillary lesions. Given increased specificity as compared with SMA, the combination of p63 and calponin is recommended for analysis of breast papillary lesions.     

Ectopic hamartomatous thymoma in an immunocompromised male

Ectopic hamartomatous thymoma (EHT) is a rare benign neoplasm classically occurring in the lower neck of adult males. Here we present a case of EHT occurring in a 43-year-old immunocompromised male and a brief review of existing literature. The patient presented with a palpable mass overlying the left clavicle which, on imaging, showed a solitary nodule possibly eroding the cortical bone. A biopsy predominantly showed spindle cells that were immunopositive for keratin AE1/AE3 as well as weakly positive for CD99, SMA, and CD34. A diagnosis of synovial sarcoma was favored; at which point surgical resection was performed. The resected mass was well-demarcated with a tan-yellow cut surface. Microscopically, the lesion was composed of a mixture of spindle cells, glands, and mature adipose tissue. The spindle cells were plump with bland nuclei, and the epithelial component showed morphology similar to glands of salivary or breast tissue with a bilayered appearance (luminal and basal). No pleomorphism, mitotic figures, or necrosis was present. Immunohistochemical stains were performed and showed the spindle cells to express a myoepithelial phenotype (cytokeratin AE1/AE3, p63, calponin positive). The glands showed SMA and p63 positivity in the basal cells (similar to salivary gland and breast). Overall, given the clinical context, histomorphologic, and immunohistochemical profile, a diagnosis of EHT was made. At 12 months of follow-up there was no evidence of recurrence.     

Ductal adenomas of salivary gland showing features of striated duct differentiation ('striated duct adenoma'): a report of six cases

Weinreb I, Simpson R H, Skálová A, Perez‐Ordoñez B, Dardick I, Chetty R & Hunt J L
(2010) Histopathology 57 , 707–715
Ductal adenomas of salivary gland showing features of striated duct differentiation (‘striated duct adenoma’): a report of six cases Aims: To describe a salivary adenoma composed largely of unilayered ducts resembling striated ducts, and to differentiate it from similar adenomas, including canalicular and intercalated duct adenoma. Methods and results: Six unilayered ductal adenomas were identified in parotid (four) and palate (two). They were encapsulated, ranged from 0.5 to 3.0 cm and composed of closely apposed ducts with virtually no stroma. The ducts varied in size and showed cysts up to 0.1 cm. The cells were eosinophilic and bland. Prominent cell membranes, reminiscent of ‘striations’ of normal striated ducts, were seen. The typical epithelial ‘beading’ pattern with abundant stroma of canalicular adenoma was absent. The tumours expressed keratins (six of six) and S100 (five of six). Smooth muscle actin (SMA) revealed no myoepithelial cells. Two tumours showed focal bilayered ducts with calponin or smooth muscle myosin heavy chain, but the tumours were largely unilayered. Only isolated cells in three tumours were positive with p63; a pattern identical to striated ducts. In contrast, the normal excretory and intercalated ducts all contained diffuse bilayering with basal or myoepithelial markers. Conclusions: Striated duct adenomas are unilayered ductal tumours that recapitulate normal striated ducts.     

Clear cell adenomyoepithelioma of the ceruminous gland

Ceruminous gland tumours are rare neoplasms. We describe a case of a ceruminous tumour with complex morphology characterised by fibrous hyaline stroma bilayered epithelial ductal structures and nodules of tightly arranged clear cells with abundant Pas-positive cytoplasm. Within nodules among clear cells delicate apocrine ducts were found. Stromal tongues infiltrated with lymphocytes invaginated into nodules producing a lymphadenomatous pattern. Among clear cells, there are also numerous eosinophilic, Pas-positive refractile crystalline inclusions that appeared as floral petals (gerbera) or as a firework-like pattern. By immunohistochemistry, ductal structures were reactive for CK pan, CK7, CK18, CK19, EMA and GCDFP-15. Epithelial ductal basal cells were reactive for CK5, p63, calponin and SMA. Clear cells were weakly positive for CK18 and strongly positive for vimentin; they also displayed S100 protein and focal GFAP immunoreactivity. Interestingly clear cells lacked immunostaining for calponin, p63, caldesmone, SMA and MSA. This result supports the myoepithelial nature of clear cells, which have lost some antigenic specificities, and the diagnosis of adenomyoepithelioma of the ceruminous gland. The lesion appears morphologically benign. The patient is a 47-year-old woman with no evidence of disease after 3 years of follow-up.     

Developing human minor salivary glands: morphological parallel relation between the expression of TGF-beta isoforms and cytoskeletal markers of glandular maturation

Morphogenesis of salivary glands involves complex coordinated events. Synchronisation between cell proliferation, polarisation and differentiation, which are dependent on epithelial–mesenchymal interactions and on the microenvironment, is a requirement. Growth factors mediate many of these orchestrated biological processes and transforming growth factor-beta (TGF-beta) appear to be relevant. Using immunohistochemistry and immunofluorescence, we have mapped the distribution of TGF-beta 1, 2 and 3 and compared it with the expression of maturation markers in human salivary glands obtained from foetuses ranging from weeks 4 to 24 of gestation. TGF-beta 1 first appeared during canalisation stage in the surrounding mesenchyme and, in the more differentiated stages, was expressed in the cytoplasm of acinar cells throughout the adult gland. TGF-beta 2 was detected since the bud stage of the salivary gland. Its expression was observed in ductal cells and increased along gland differentiation, TGF-beta 3 was detected from the canalisation stage of the salivary gland, being weakly expressed on ductal cells, and it was the only factor detected on myoepithelial cells. The data suggest that TGF-beta have a role to play in salivary gland development and differentiation.     

Immunohistochemistry of myoepithelial cells during development of the rat salivary glands

 Using a battery of monoclonal antibodies specific for rat proteins, immunohistochemistry was carried out on the developing myoepithelial cells (MECs) of the rat major salivary glands. The proteins examined were α-smooth muscle actin (αSMA), h1-calponin (calponin), keratin 14 (K14), β subunit of S-100 protein (S-100β), vimentin and glial fibrillary acidic protein (GFAP). The MECs exhibited immunoreactivity for αSMA, calponin and K14, but not that for S-100β, vimentin and GFAP. Immunoreactivity for αSMA appeared in the MECs from the time when the microfilaments were initially deposited in these cells, i.e., at 20 days in utero in the sublingual and submandibular glands and at birth in the parotid gland. Calponin immunoreactivity was seen 1 day earlier than αSMA. The appearance was almost at the same time as the onset of the MEC differentiation in each gland. A small number of the MECs expressed weak K14 immunoreactivity from the time when the acinus-intercalated duct structure was established, i.e., at 21 days in utero in the sublingual gland, at 5 days after birth in the perotid gland and after 5 weeks post-natally in the submandibular gland. In addition, K14 immunoreactivity was observed in the basal cells of the striated and excretory ducts. The first appearance of K14 in these cells again coincided with the emergence of the duct system in each gland, i.e., at 20 days in utero in the sublingual gland, at 21 days in utero in the submandibular gland and at 3 days after birth in the parotid gland. Finally, the MECs in all the glands were found to redistribute as the acini matured. As the acini grew rapidly during the weaning period in the parotid and the sublingual glands, the MECs ceased to surround the acini. Thereafter, they disappeared from the acini in the parotid gland, whereas they reappeared in the sublingual gland. In the submandibular gland, the MECs were confined to the terminal tubules until 4 weeks after birth. Thereafter, the acini were established and invested by the MECs. In conclusion, immunohistochemistry of calponin and αSMA is a useful tool for identification of the MEC during its earliest differentiation, which has hitherto been possible only electron microscopically. In addition, it is suggested that the MEC is heterogeneous and the functionally differentiated MEC appears after weaning around acini of the mucous and seromucous glands. Accepted: 11 January 1999     

Characteristics of aquaporin 1, 3, and 5 expression during early murine salivary gland development

Aquaporins (AQPs) are essential to coordinate the transit of water and ions through the cell membrane. In salivary glands (SGs), AQPs have been associated with saliva formation, facilitating water absorption through the epithelium during the formation of hypotonic saliva, which is then secreted into the oral cavity. Different members of the AQP family have been suggested to play distinct roles during embryonic development, highlighted by their specific expression patterns. Here, we have investigated the expression patterns of AQP-1, AQP-3 and AQP-5 by immunofluorescence at key stages of salivary gland development, utilising cultured mouse embryonic submandibular (SMG) and sublingual (SLG) glands. The expression of AQPs was compared to a mitotic marker, phospho-histone 3 (PH3), a myoepithelial marker, smooth muscle actin (SMA), and a vascular marker, CD31. Qualitative analysis revealed that AQP-1 and AQP-3 were primarily expressed during the earlier phases of SG morphogenesis and were associated with cells undergoing mitotic processes (PH3-positive). AQP-5, in contrast, was not associated to mitotic figures, but was predominantly expressed during late stages of SG morphogenesis. Our results highlight that AQPs are expressed from early stages of SG morphogenesis and exhibit complimentary expression patterns that may contribute to the morphogenesis of salivary glands.     

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.     

p63 and CD10: reliable markers in discriminating benign sclerosing lesions from tubular carcinoma of the breast?

The immunohistochemical detection of myoepithelial cells in benign sclerosing lesions of the breast is useful in distinguishing them from tubular carcinoma. So far, this detection has been carried out using antibodies against cytoskeletal proteins, such as alpha-smooth muscle actin (1A4) and calponin. However, the specificity of these markers has been questioned since they may be expressed in stromal myofibroblasts and vascular smooth muscle. Recently, two novel myoepithelial markers have been described: the nuclear protein p63, a member of the p53 family, and the surface antigen CD10, also known as common acute lymphoblastic leukemia antigen (CALLA). The authors assessed the use of p63 and CD10 in the differential diagnosis between benign sclerosing lesions, such as sclerosing adenosis and radial scar, and tubular carcinoma, in comparison to the traditional myoepithelial markers 1A4 and calponin. p63, CD10, 1A4, and calponin were expressed in myoepithelial cells of all benign lesions and were consistently negative in all cases of tubular carcinoma. In contrast to cytoskeletal proteins, p63 and CD10 were mostly confined to myoepithelial cells and thus were more specific than the traditional counterparts. However, 1A4 was more intensely expressed and more reproducible than the novel markers. In conclusion, p63 and CD10 may be used as a complement to 1A4 in distinguishing benign sclerosing lesions from tubular carcinoma of the breast.     

Necrotizing sialometaplasia versus invasive carcinoma of the head and neck: the use of myoepithelial markers and keratin subtypes as an adjunct to diagnosis

AIMS: To investigate the use of immunohistochemistry in distinguishing necrotizing sialometaplasia (NSM) from squamous cell (SCC) and mucoepidermoid carcinoma (MEC) by (i) the identification of myoepithelial cells and (ii) cytokeratin (CK) expression. METHODS AND RESULTS: Thirteen cases with the histological changes of NSM, eight SCCs and eight MECs were examined with the following immunohistochemical markers: calponin, S100, smooth muscle actin (SMA), p63, CK7, CK5, CK6 and CAM5.2. The distribution and intensity of staining were recorded. Residual myoepithelial cells (best demonstrated by calponin and SMA) were identified at the periphery of the epithelial islands in all cases of NSM (although not in all islands), in contrast to MEC and SCC. S100 showed a similar pattern, although staining fewer cells. Moderate rather than extensive expression of CK7 may help to distinguish NSM from MEC. CONCLUSION: Identification of myoepithelial cells and CK7 expression may help to distinguish NSM from its mimics.     

The role of the VEGF-C/-D/flt-4 autocrine loop in the pathogenesis of salivary neoplasms

Salivary gland cells produce and secrete VEGF under normal conditions, but this property has not been studied in salivary gland neoplasms. The aim of this study was to evaluate the expression of VEGF-C/VEGF-D/flt-4 in salivary gland tumors. Thirty-one salivary gland tumors (19 with and 12 without myoepithelial differentiation) were examined. Immunostaining for VEGF-C/VEGF-D/flt-4, p63 and SMA was carried out. The chi-square distribution and the Pearson correlation were applied. A statistically significant relationship (p<0.05) was found in the group of tumors with myoepithelial differentiation regarding simultaneous positive staining for VEGF-C/VEGF-D and flt-4. All pleomorphic adenomas (PA) exhibited a statistically significant coexpression of the three antibodies. p63 and SMA were strongly expressed in the same areas as VEGF-C, VEGF-D and flt-4. The cells responsible for the strong expression of VEGF-C, VEGF-D and flt-4 in PAs are myoepithelial cells. Coexpression of flt-4 and its ligands in all PAs suggests the presence of a dominant VEGF-C/VEGF-D/flt-4 axis in this tumor.     

An immunohistochemical study of pleomorphic adenomas of the salivary gland: glial fibrillary acidic protein-like immunoreactivity identifies a major myoepithelial component

An immunohistochemical study of 34 pleomorphic adenomas of the major salivary glands demonstrated phenotypic differences among the various morphologic regions in these tumors. The phenotypes expressed were comparable to those of normal salivary gland cells. In the normal glands, myoepithelial cells were immunoreactive for glial fibrillary acidic protein (GFAP), S-100 protein, and keratin; acinic cells exhibited strong, predominantly nuclear S-100 staining and weaker keratin staining; intercalated ducts had both cytoplasmic and nuclear S-100 positivity; and several epithelial antigens were observed throughout the ductal system. In the tumors, the presence of classic epithelial markers (including carcinoembryonic antigen, epithelial membrane antigen, secretory component, and keratin) in the luminal cells of ducts and the intense immunoreactivity with GFAP (with weaker keratin and S-100 staining) in periductal and stromal cells indicated distinct epithelial and myoepithelial differentiation. Solid epithelioid areas consisted phenotypically of intercalated duct/acinic cells and/or myoepithelial cells, the former exhibiting predominant nuclear S-100 positivity. The presence of GFAP-like immunoreactivity in normal myoepithelial cells strongly supports the extensive involvement of this cell in pleomorphic adenomas. The spectrum of phenotypes expressed adds weight to existing evidence for pleomorphism rather than a mixed origin of this tumor. The combination of keratin, S-100, and GFAP immunostaining is particularly useful in identifying the component cells in pleomorphic adenomas of the salivary glands.     

Epithelial myoepitheial carcinoma of minor salivary gland--low grade malignant tumor presenting with nodal metastasis

Epithelial myoepithelial carcinoma (EMC) is a rare low grade malignant salivary gland neoplasm that most commonly occurs in the parotid gland but can also arise in minor salivary glands. We report a case of primary epithelial myoepithelial carcinoma of minor salivary gland in a 25 year old women who presented with swelling left cheek of one year duration and bilateral submandibular lymphadenopathy. A mass causing erosion of mandible, thyroid cartilage and masseter muscle was identified on CT scan. This was excised and histological examination revealed a mixture of ductal structures consisting of inner dark cells and outer clear cells seen in solid sheets. Immunohistochemical analysis showed the clear cells to be weakly positive for S100 and smooth muscle actin (SMA) and ductal cells to be positive for cytokeratin (CK) and epithelial membrane antigen (EMA). The characteristic morphological and immunohistochemical features aided in the diagnosis of epithelial myoepithelial carcinoma.     

Immunophenotypic characterization of anal gland carcinoma: loss of p63 and cytokeratin 5/6

Anal gland carcinoma (AGC) is a rare perianal invasive cancer composed of tubular glands lined by cuboidal epithelium. The clinical features and histogenesis of AGC are not well understood and its origin from anal glands is often difficult to prove. Little is known about immunophenotypic features of AGC that could be useful in establishing the diagnosis. This study evaluated the immunohistochemical profile of 2 cases of AGC in comparison to anal glands from 11 hemorrhoidectomy specimens. Sections from the specimens were routinely processed and immunostained using commercial antibodies to cytokeratin (CK) 7, CK20, CK5/ 6, p63, CDX2, smooth muscle actin, calponin, heavy chain smooth muscle myosin, p53, and p16. In case 1 of AGC, radiation and chemotherapy preceded an abdominoperineal resection. In biopsies from this case, the neoplastic anal glands had a tubular pattern, whereas most glands in the resection specimen exhibited mucinous features. The histologic pattern in case 2 was tubular. Normal anal glands showed immunoreactivity for myoepithelial and basal cell markers CK5/6 and p63 in basal and parabasal cell layers and for CK7 in superficial cell layers. In contrast, both cases of AGC were negative for CK5/6 and p63 and were diffusely positive for CK7. Normal glands and both cases of AGC were negative for the intestinal differentiation marker CDX2, CK20, smooth muscle actin, calponin, smooth muscle myosin heavy chain, p16, and p53. Our data suggest that loss of p63 and CK5/6 expression is a feature of AGC. Anal gland carcinoma shares negativity for CDX2 and CK7+/CK20- profile with normal anal glands. No evidence of myoepithelial cells was found in normal or malignant anal glands. These data may be useful in establishing the diagnosis of AGC.     

The myoepithelial immunophenotype in 135 benign and malignant salivary gland tumors other than pleomorphic adenoma.

BACKGROUND: We have previously studied the immunoreactivity of 3 novel smooth muscle-specific proteins, alpha-smooth muscle actin, smooth muscle myosin heavy chains, and calponin, to assess myoepithelial differentiation in pleomorphic adenomas. OBJECTIVE: To further expand our knowledge of myoepithelial differentiation in other benign and malignant salivary gland tumors. DESIGN: Formalin-fixed paraffin sections of 135 salivary gland tumors with associated normal glands were stained with monoclonal antibodies using the avidin-biotin complex immunoperoxidase method and enzymatic and microwave heat-induced epitope retrieval. RESULTS: In adenoid cystic carcinomas and epithelial-myoepithelial carcinomas, all 3 markers exclusively highlighted the myoepithelial cell components and the epithelial cells were entirely negative. No immunostaining was detected in canalicular adenomas, oncocytomas, Warthin tumors, acinic cell carcinomas, mucoepidermoid carcinomas, squamous cell carcinomas, and polymorphous low-grade adenocarcinomas. Salivary duct carcinomas and adenocarcinomas, not otherwise specified had a distinctive pattern of uniform periductal staining of reactive myofibroblastic cells, and in salivary duct carcinomas some ducts retained a peripheral immunoreactive myoepithelial cell layer. CONCLUSION: Immunoreactivity for these 3 smooth muscle-specific proteins confirms the known neoplastic myoepithelial component of adenoid cystic carcinomas and epithelial-myoepithelial carcinomas. The consistently positive staining pattern in adenoid cystic carcinomas may be diagnostically useful in discriminating histologically similar but consistently negative polymorphous low-grade adenocarcinomas. Periductal linear staining in adenocarcinoma, not otherwise specified and salivary duct carcinomas is distinctive and appears to represent a tight cuff of myofibroblasts associated with the infiltrating glands.     

Plasmacytoid cells in salivary-gland pleomorphic adenomas: evidence of luminal cell differentiation

To determine the cellular origin of plasmacytoid cells in salivary gland adenomas, immunohistochemistry was performed on sections from 12 pleomorphic adenomas rich in these cells. In normal salivary glands included in these sections, the myoepithelial cells (MECs) expressed -smooth muscle actin (SMA) and smooth muscle myosin heavy chain (SMMHC), whereas the duct luminal cells expressed keratins 19, 18 and 8. Some of the salivary duct basal cells expressed these keratins, and the acinar cells expressed keratins 18 and 8. The expression profile was similar in rat salivary glands not only after but also during development. The immature MECs never expressed the keratins nor did the immature duct cells express SMA. In seven cases, up to 60% of the plasmacytoid cells expressed keratin 19. In three of these cases, about 10% of the plasmacytoid cells expressed keratin 18. No plasmacytoid cells expressed SMA, SMMHC or keratin 8. These results indicate that plasmacytoid cells originate from luminal cells and not from MECs. Furthermore, in addition to the luminal tumor cells, the non-luminal cells could express keratins 19, 18 and 8. Therefore, it is necessary to re-evaluate the prevailing notion that non-luminal cells are modified MECs. Keratin 14, basic calponin, vimentin and p63 were bi-specific for the MECs and the duct cells. Therefore, expression of these proteins by significant numbers of the non-luminal tumor cells and the plasmacytoid cells never denied the above notion.     

Myoepithelial carcinoma of pharynx expressing KIT and PDGFRA

KIT and PDGFRA expression has rarely been examined in myoepithelial carcinoma (MC) of the salivary glands. An 89-year-old Japanese woman presented with a pharyngeal mass. Gross and imaging examinations revealed an elevated mass in the middle pharynx next to the oral cavity. A biopsy revealed atypical cells, and tumorectomy was performed. The tumor was composed of atypical epithelioid cells arranged in solid nests, cords, and vague acinar patterns. Mitotic figures were recognized in 3 per 50 high power fields. Immunohistochemically, the tumor cells were positive for myoepithelial markers including cytokeratin (CK) 14, α-smooth muscle antigen, S100 protein, and p63. They were also positive for KIT, PDGFRA, pancytokeratin AE1/3, CK34βE12, CK5/6, vimentin, p53, and Ki-67 (labeling=28%). They were negative for neuron-specific enolase, CD45, CD34, CD56, chromogranin, synaptophysin, melanosome, desmin, epithelial membrane antigen, CK18, CK20, pancytokeratin (CAM5.2). A pathologic diagnosis of myoepithelial carcinoma arising from minor salivary glands was made. No metastatic lesions were found by various imaging techniques. The patient is now receiving palliative radiation therapy 2 months after the operation. The present case showed that MC can express KIT and PDGFRA.