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At least 343 records · Page 19Linked to original sources
PubMedDate not supplied

Endogenous avidin-binding activity in epithelial cells of the ducts of human salivary glands.

Avidin-biotin (AB) systems are commonly employed to investigate salivary gland sections either in immunohistochemistry or in immunofluorescence techniques. We noted non-specific staining in the ductal epithelium of minor salivary gland (SG) sections from 5 Sjögren's syndrome (SS), 5 chronic sialoadenitis (CS), and one normal parotid gland (NP) when incubated with AB peroxidase complex. Inhibition of endogenous peroxidase did not prevent the staining while saturation of supposed biotin-like molecules in the tissue with added avidin led to the loss of this non-specific staining. These results demonstrate the presence of endogenous avidin binding activity (EABA) in the epithelial cells of salivary gland ducts. We suggest that the avidin and streptavidin systems should not be used for immunohistological examination of the ductal epithelium of salivary glands.

Avidin↗
PubMed1991

Terminal parotid duct carcinoma.

Terminal duct carcinoma of salivary glands is an uncommon, histologically distinctive, low grade malignant neoplasm arising from the intercalated salivary duct. We present a case arising eight years after removal of a parotid tumour reported as a pleomorphic adenoma. We describe the clinico-pathological features of the present tumour, illustrate the difficulties that may be encountered in differentiating it from other salivary gland tumours, and discuss the possible significance of the previous tumour.

Adenoma, Pleomorphic↗
PubMed1988

Small-cell carcinoma of the parotid gland with neuroendocrine features.

An 82-year-old woman had a small-cell carcinoma of the parotid gland with cells containing neuroendocrine secretory granules. To our knowledge, these dense-core granules have been identified in only three other major salivary gland small-cell carcinomas. The findings of histologic and ultrastructural evaluations of this neoplasm suggested a salivary duct cell origin. The tumor appears to arise from cells of the salivary duct system that differentiate into cells with either neuroendocrine or epithelial features. Electron microscopy to determine the type of small-cell carcinoma should be performed, as this may have prognostic significance. Aggressive therapy should be undertaken, since small-cell carcinomas of the major salivary glands appear to have a better prognosis than bronchogenic or laryngeal small-cell carcinomas have.

Aged↗
PubMed1987

Salivary gland adenocarcinomas: a clinicopathologic analysis of three distinctive types.

Myoepithelial cells play an important role in the histogenesis of adenocarcinomas arising from the salivary duct unit nearest the acini. Prototype adenocarcinomas arising from the intercalated duct are the terminal duct carcinoma and the epimyoepithelial carcinoma, both typically low-grade malignancies. Those salivary adenocarcinomas arising from the larger nonintercalated excretory ducts do not manifest myoepithelial cells in their composition. A prime example is the salivary duct carcinoma, which is a high-grade malignancy. These adenocarcinomas have distinctive clinical and pathologic features and they should be recognized by the examining pathologist. Because of the potential clinical confusion between terminal duct carcinoma and salivary duct carcinoma when rendered as a diagnosis, each should be further qualified, eg, by adding high or low grade.

Adenocarcinoma↗
PubMed1992

Immunoreaction of keratin, actin, S-100 protein and rat-EGF in duct-ligated rat salivary glands.

Duct-ligated submandibular and sublingual glands of rats were evaluated immunohistochemically for changes in keratin (MoAb 1164), actin, S-100 protein and rat-EGF (rEGF). Normal salivary glands were reactive for keratin, S-100 protein and rEGF in the granular convoluted tubule (GCT) and duct cells, and for actin in the myoepithelium. Submandibular glands showed a marked reduction of S-100 protein and rEGF staining following duct ligation, and no increased staining of proliferating epithelial cells of the late stage in duct ligated glands. Sublingual glands revealed no marked changes for actin staining in myoepithelial cells, irrespective of atrophic changes occurring in acinar and duct cells after duct ligation. Immunohistochemical patterns differed for each type of gland; changes associated with the obstructive lesion were more prominent in the submandibular gland.

Actins↗
PubMed1980

Saliva from patients with cystic fibrosis inhibits amiloride-sensitive sodium transport.

A factor is present in the saliva and sweat from patients with cystic fibrosis (CF) which inhibits the reabsorption of sodium in the ducts of the salivary and sweat glands. Inasmuch as the physiology of sodium absorption is similar in salivary ducts and the distal colon, we have examined the sensitivity of the sodium absorption in the rat colon to saliva from CF patients. Sodium absorption by the rat colon, estimated as the shortcircuit current, was inhibited by saliva from both patients with CF and normal volunteers. However, only with CF saliva was the inhibition consistently proportional to the saliva concentration. Furthermore, the inhibitory activity of CF saliva was greater than the inhibition observed with saliva from age- and sex-matched controls (percentage of inhibition: CF = 20.1 +/- 2.2, and controls = 14.9 +/- 2.1; P < 0.02), and the inhibition of the colonic shortcircuit current was proportional to the activity measured by the ductal retrograde perfusion assay with the rat parotid gland (linear correlation coefficient = 0.634; P < 0.005). This latter assay is an accepted assay for CF factor activity. We conclude that the CF factor present in saliva probably interacts in a reversible manner with the amiloride-sensitive sodium transport system which is present in all sodium scavenging epithelia. The rat colon is a promising assay system for CF factor activity because the electrical measurements permit a rapid quantitative estimate of activity and a single piece of tissue can be used to measure the activity of several saliva samples.

Amiloride↗
PubMed1993

Use of the carbon dioxide laser to locate small sialoliths.

Six cases of small salivary duct sialoliths were treated using the carbon dioxide laser as a surgical dissector. When the laser beam encountered the small sialolith (3 mm or less), a light-scattering effect (flash or burst) was observed, thus enabling an almost immediate localization of the stone in the salivary duct or in the surrounding tissue. Stone extirpation is more rapid, with less surgical trauma, using this technique.

Adult↗
PubMedDate not supplied

Expression of TNF-related apoptosis inducing ligand (TRAIL) on infiltrating cells and of TRAIL receptors on salivary glands in patients with Sjögren's syndrome.

BACKGROUND: Tumor necrosis factor-related apoptosis inducing ligand (TRAIL) induces apoptosis of tumor cells but not normal cells; its role in normal non-transformed tissues is unknown. OBJECTIVE: To evaluate the role of apoptosis mediated by TRAIL and TRAIL-receptor (TRAIL-R) system in lymphocytic sialadenitis in patients with Sjögren's syndrome. METHODS: The expression of TRAIL and TRAIL-R1, 2, 3 and 4 in lymphocytic sialadenitis was examined by immunoperoxidase staining in patients with Sjögren's syndrome and in normal subjects. To elucidate the mechanism of de novo expression of TRAIL-R1 antigen, we quantitatively investigated its induction by cytokines in human salivary duct cell line (HSG) by cell enzyme-linked immunosorbent assay. In human salivary duct cells stimulated by cytokines, we investigated the induction of apoptotic cell death by recombinant TRAIL protein. RESULTS: In patients with massive mononuclear cell infiltration, some infiltrating cells showed TRAIL. In patients with severe lymphocytic sialadenitis, TRAIL-R1, TRAIL-R2, or both were strongly expressed on the ductal epithelial cells. Neither TRAIL-R3 nor R4 were observed on ductal epithelium. In contrast, TRAIL-R1 and R2 were not found in the minor salivary glands of normal subjects or patients with mild lymphocytic sialadenitis. Unstimulated HSG cells did not express TRAIL-R1. Interferon-gamma (IFN-gamma) consistently upregulated levels of TRAIL-R1. In contrast, tumor necrosis factor-alpha (TNF-alpha), interleukin 1-beta (IL-1 beta), IL-2, and IL-4 had no effect on TRAIL-R1 levels. HSG cells expressing TRAIL-R1 in response to IFN-gamma were susceptible to apoptosis by recombinant TRAIL protein. CONCLUSION: Our findings suggest that TRAIL and TRAIL-R system may play a role in the pathogenesis of lymphocytic sialadenitis in patients with Sjögren's syndrome.

Adult↗
PubMed1985

[Adenocarcinoma of the salivary glands. The pathohistology and subclassification of 77 cases].

Seventy-seven adenocarcinomas of the salivary glands recorded in the Salivary Gland Register between 1965 and 1984 were analysed and classified histopathologically. The following results were obtained: 1. 2% of all salivary gland tumours and 10% of all malignant epithelial salivary gland tumours were allotted to the group of adenocarcinomas. The age peak lies in the 7th to 8th decade. 60% occurred in women, 58.5% were localized to the parotid gland, 28.5% to the minor salivary glands (palate, lips, and cheek), 11.5% to the submandibular gland and only 1.5% to the sublingual gland. 2. Solid, tubular and papillary adenocarcinomas can be distinguished. Additional criteria are microcysts, mucus production and grade of differentiation. 3. The solid adenocarcinoma (13%) is predominantly localized in the parotid gland and characterized by a low differentiation, invasive growth and metastases. 4. 62.5% of tubular adenocarcinomas (52%) are localized in the parotid gland, 27.5% to the minor salivary glands and 10% to the submandibular gland. Most of the tumours are highly differentiated. A distinct mucus production is present in 40% of the cases. Microcysts are very frequent. 5. Papillary adenocarcinomas (28.5%) are localized in almost 50% of cases to the minor salivary glands, 45% to the parotid and only 5% to the submandibular gland. Microcysts and mucus production can be observed in 50% of the cases. 6.5% of the cases have a mixed tubular papillary structure. 6. In differential diagnosis, thyroid gland carcinomas and metastases of other adenocarcinomas must be distinguished, the former by negative result of the thyroglobulin reaction, and absent mucus production. 7. Adenocarcinomas arise from the salivary duct system. Solid or tubular adenocarcinomas imitate stages of the embryonal development of the salivary ducts.

Adenocarcinoma↗
PubMed1991

Terminal duct adenocarcinomas of salivary tissues.

Terminal duct adenocarcinoma is recommended as an encompassing diagnostic designation for a preponderantly intraoral salivary gland carcinoma that has also gone under the names of polymorphous low-grade adenocarcinoma, lobular carcinoma, and low-grade papillary adenocarcinoma. The carcinoma is biologically low grade, with its papillary phenotype manifesting a more aggressive behavior than nonpapillary forms.

Adenocarcinoma↗
PubMed2006

Implications of methylation patterns of cancer genes in salivary gland tumors.

PURPOSE: We investigated the methylation status and protein expression of four tumor suppressor genes to determine their role in salivary gland tumorigenesis. EXPERIMENTAL DESIGN: We performed methylation-specific PCR and protein analyses of 29 normal salivary glands, 23 benign, and 79 malignant salivary gland neoplasms to determine the pattern and potential diagnostic and/or biological role of the RASSF1, RARbeta2, DAPK, and MGMT tumor suppressor gene methylation in these tumors. RESULTS: No methylation was detected in the normal tissues. Methylation occurred in 9 of 23 (39.1%) benign tumors; 3 (25.0%) pleomorphic adenomas and 6 (66.7%) Warthin's tumors at the MGMT, DAPK, or RASSF1 genes. Methylation occurred in 33 of 79 (41.8%) malignant tumors; 8 (30.8%) adenoid cystic carcinomas, 6 (33.3%) mucoepidermoid carcinomas, 6 (42.9%) acinic cell carcinomas, and 13 (62.0%) salivary duct carcinomas. RASSF1 and RARbeta2 represented 75.8% of methylation events occurring most frequently in salivary duct and acinic cell carcinomas. Overall, we found no significant correlation between protein expression and methylation status of individual genes, but observed low or absent protein expression in several methylated tumors. Significant correlations were found between methylation and aggressive malignant phenotypes (P = 0.0004) and age (P = 0.05). CONCLUSIONS: (a) Benign and malignant salivary tumors differed in the frequency and pattern of gene methylation; (b) high-grade carcinomas were significantly methylated compared with low-grade phenotypes; (c) RASSF1 and RARbeta2 were highly methylated in malignant tumors and can be targeted for therapy; and (d) methylation pattern may serve as a diagnostic and biological marker in assessing these tumors.

Adolescent↗
PubMed2002

Expression of type 2 nitric oxide synthase and p53 in Warthin's tumour of the parotid.

Although the pathogenesis of Warthin's tumour is not fully understood, it is generally thought that the tumour arises from heterotopic salivary ducts within pre-existing lymphoid tissue. Prolonged nitric oxide (NO) production by the enzyme type 2 nitric oxide synthase (NOS2) has been implicated in the pathogenesis of many solid tumours, but not in Warthin's tumour. Since NO and NOS2 are known to be associated with p53, the immunohistochemical expression of both NOS2 and p53 was investigated in 23 cases of Warthin's tumour. Widespread diffuse cytoplasmic immunostaining for NOS2 was found in tumour epithelial cells of all 23 cases studied, and it was additionally expressed in normal salivary duct epithelium. p53 staining was localised to the nuclei of tumour epithelium in 16 cases, with a similar pattern of distribution to tumour NOS2 expression. A significant correlation was found between NOS2 and p53 staining in the tumours (P < 0.001). In contrast to NOS2, p53 was not expressed by normal salivary ductal cells in any of the cases studied. NOS2 is widely expressed by the tumour epithelium of Warthin's, and its association with p53 expression is discussed. The role of NO in the pathogenesis of Warthin's tumour remains to be established.

Adenolymphoma↗
PubMed1989

Sialocysts of the parotid glands.

Sialocysts of salivary glands are outnumbered greatly by pseudocystic lesions, exemplified by mucoceles. In the major salivary glands, sialocysts are preponderantly lesions of the parotid glands, where they are classified as 1) salivary duct cysts, 2) lymphoepithelial cysts, or 3) dysgenetic or congenital cysts. All arise from salivary ducts and have no relation with the branchial apparatus.

Cysts↗
PubMed1998

Regulation of bHLH-PAS protein subcellular localization during Drosophila embryogenesis.

The Drosophila Single-minded and Tango basic-helix-loop-helix-PAS protein heterodimer controls transcription and embryonic development of the CNS midline cells, while the Trachealess and Tango heterodimer controls tracheal cell and salivary duct transcription and development. Expression of both single-minded and trachealess is highly restricted to their respective cell lineages, however tango is broadly expressed. The developmental control of subcellular localization of these proteins is investigated because of their similarity to the mammalian basic-helix-loop-helix-PAS Aromatic hydrocarbon receptor whose nuclear localization is dependent on ligand binding. Confocal imaging of Single-minded and Trachealess protein localization indicate that they accumulate in cell nuclei when initially synthesized in their respective cell lineages and remain nuclear throughout embryogenesis. Ectopic expression experiments show that Single-minded and Trachealess are localized to nuclei in cells throughout the ectoderm and mesoderm, indicating that nuclear accumulation is not regulated in a cell-specific fashion and unlikely to be ligand dependent. In contrast, nuclear localization of Tango is developmentally regulated; it is localized to the cytoplasm in most cells except the CNS midline, salivary duct, and tracheal cells where it accumulates in nuclei. Genetic and ectopic expression experiments indicate that Tango nuclear localization is dependent on the presence of a basic-helix-loop-helix-PAS protein such as Single-minded or Trachealess. Conversely, Drosophila cell culture experiments show that Single-minded and Trachealess nuclear localization is dependent on Tango since they are cytoplasmic in the absence of Tango. These results suggest a model in which Single-minded and Trachealess dimerize with Tango in the cytoplasm of the CNS midline cells and trachea, respectively, and the dimeric complex accumulates in nuclei in a ligand-independent mode and regulates lineage-specific transcription. The lineage-specific action of Single-minded and Trachealess derives from transcriptional activation of their genes in their respective lineages, not from extracellular signaling.

Animals↗
PubMed1979

Sicca complex and cholangiostatic jaundice in two members of a family probably caused by thiabendazole.

An entire family (father, mother, and three daughters) were given thiabendazole because one of the children had acquired pinworm infestation. The mother and one daughter (non-infected) developed a sicca complex (keratoconjunctivitis sicca and xerostomia) accompanied by cholangiostatic jaundice. Sjögren's syndrome is an autoimmune disease and presents many immune mechanism aberrancies. An association between autoimmune liver disease and sicca complex has been reported. Labeled mitochondrial antibodies bound to the parotid duct have been noted in patients with autoimmune cholangiostatic jaundice and such antibodies may be similar to the antibody against salivary duct found in Sjögren's syndrome. It is suggested that in these two patients, thiabendazole may have acted as a hapten and by binding to the body protein induced the production of autoantibodies which may have acted against the biliary epithelium, the salivary duct epithelium, and the lacrimal gland ducts.

Adolescent↗