The Expression of a Vascular Smooth-Muscle Actin in Salivary Gland Tumors

Hirano, Toshikazu; Gluckman, Jack L.; deVries, Egbert J.

doi:10.1001/archotol.1990.01870060050008

Cited by 31 publications

(9 citation statements)

References 17 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…It has been often difficult to identify vimentin immunostaining in MECs [18,24,33,37], probably due to its restricted distribution in the cytoplasm [19,23]. Despite this difficulty, the present and the previous [6,24,25] studies observed distinct vimentin staining in MECs. In this context, some authors have recommended this protein as a MEC marker [2,3,33].…”

Section: Discussionmentioning

confidence: 60%

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

et al. 2003

View full text Add to dashboard Cite

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 alpha-smooth muscle actin (alphaSMA) 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 alphaSMA. 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 alphaSMA, 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.

show abstract

Section: Discussionmentioning

confidence: 60%

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

et al. 2003

View full text Add to dashboard Cite

show abstract

“…Therefore, coexpression of keratin 14 and a-smooth muscle actin (aSMA) has been the most widely used marker for identification of MECs [6-8, 14, 21, 22, 29, 31, 48, 50, 55]. Tumor cells with keratin 14 are more abundant than are those with aSMA in certain tumors, such as pleomorphic adenoma and adenoid cystic carcinoma [6,8,22,31,34,48,55,56,60]. By definition, the neoplastic cells expressing keratin 14 alone (without aSMA) are not necessarily derived from MECs.…”

Section: Introductionmentioning

confidence: 99%

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

et al. 2000

View full text Add to dashboard Cite

Our recent study of developing myoepithelial cells (MECs) in rat salivary glands demonstrated that developing MECs begin to express alpha-smooth muscle actin (alphaSMA) 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 alphaSMA, 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 alphaSMA 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 (alphaSMA 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.

show abstract

“…Later, alphasmooth muscle actin (ct-SMA) was demonstrated in normal MEC of a salivary gland, and turned into its standard marker, even in neoplasms. Nevertheless, later studies showed that neoplastic MEC may not express oc-SMA [4][5][6][7][8][9]. Vimentin has also been used as a neoplastic MEC marker [10][11][12][13][14][15], and was indicated as an early marker of myoepithelial differentiation, being present in all morphologic types that the MEC may assume [9,16,17].…”

mentioning

confidence: 99%

Myoepithelial Cell Markers in Salivary Gland Neoplasms

Furuse

Sousa²,

Nunes³

et al. 2005

Int J Surg Pathol

View full text Add to dashboard Cite

We compared the immunoexpression of 5 myoepithelial cell (MEC) markers (alpha-smooth-muscle actin, calponin, h-caldesmon, vimentin, and S-100-protein) using 16 pleomorphic adenomas (PA), 15 adenoid cystic carcinomas (ACC), and 3 epithelial-myoepithelial carcinomas (EMC) of salivary glands. The alpha-smooth-muscle actin was useful for identification of MECs, especially in cribriform and tubular ACC, followed by EMC. Calponin was similar to alpha-smooth-muscle actin, except for polygonal and plasmacytoid cells of PA and for solid ACC, which showed alpha-smooth-muscle actin negative and calponin positive. H-caldesmon was negative. Vimentin immunostained all MEC types, and was negative in luminal cells. S-100 protein was expressed both in the nuclei and cytoplasm of MECs and luminal cells, especially in PA. The best way to identify MEC is using alpha-smooth-muscle actin or calponin, plus vimentin, since in tumors MECs are hardly ever fully differentiated.

show abstract

The Expression of a Vascular Smooth-Muscle Actin in Salivary Gland Tumors

Cited by 31 publications

References 17 publications

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

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

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

Myoepithelial Cell Markers in Salivary Gland Neoplasms

Contact Info

Product

Resources

About