PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “SALIVARY GLAND NEOPLASMS”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 109 records · Page 6Linked to original sources

Demonstration of c-erbB-2 oncogene overexpression in salivary gland neoplasms by in situ hybridization.

The level of c-erbB-2 cellular mRNA in 18 salivary gland tumours and in 7 normal salivary glands was determined by in situ hybridization using [35S] labelled RNA probes. Computer assisted quantitation of the autoradiographic signal indicated a significantly higher c-erbB-2 expression in the tumour group (22.64 grains per cell +/- 3.79; 95% CI) as compared to the non-neoplastic salivary gland tissue (4.11 +/- 0.90; 95% CI). The c-erbB-2 expression as measured by grain counts per cell for the pleomorphic adenomas (16.29 +/- 1.87; 95% CI), mucoepidermoid carcinomas (31.52 +/- 0.08; 95% CI) and the acinic cell carcinomas (44.24 +/- 17.11; 95% CI) were significantly greater than the expression for the normal group. The acinic cell carcinomas exhibited the greatest level of expression. As observed at the individual cell level, the autoradiographic signal was distributed uniformly in the neoplastic tissues, regardless of the cell type. This study confirms the hypothesis that the c-erbB-2 oncogene is overexpressed at the mRNA level in salivary gland tumours.

Adenoma, Pleomorphic↗

[A rare salivary gland neoplasm: cystadenolymphoma].

The authors, after having examined three recent cases, explain some basic concepts about diagnostics and therapy in cystadenolymphoma of salivary glands. As a matter of fact this neoplasia, in spite of its low frequency, is very important because of its still controversial etiopathology and recent tendency in increasing its incidence in females. Today the diagnostic protocol, undertaken after clinical examination, which is necessary, consists of ultrasonography or computerized tomography. But only postoperative histological examination gives a sure diagnosis and can point out main histomorphological characteristics of tumour. Therapeutic approach can be limited to conservative treatment, which is able to respect the parotid gland, its vascularization and innervation.

Adenolymphoma↗

Salivary gland neoplasms as a late consequence of head and neck irradiation.

An increased occurrence of salivary tumors was observed in 1922 patients who received radiation to the tonsils and nasopharynx. Twenty-seven tumors, 19 benign and eight malignant, were found in this group as compared with an expected 0.2 malignant and less than 1 benign tumor. The latent period between the initial radiation treatment and diagnosis ranged from 7 to 32 years. After the first 15 years the incidence (77 cases/10(5) subjects/year) has remained constant and shows no indication of declining. Continued observation for salivary gland tumors is therefore indicated for subjects who received childhood irradiation.

Adult↗

Gamma knife stereotactic radiosurgical boost for patients treated primarily with neutron radiotherapy for salivary gland neoplasms.

OBJECT: To determine the feasibility of utilizing a Gamma Knife stereotactic boost for patients at high risk of local recurrence from minor salivary gland tumors invading the base of skull. METHODS: Eight patients with minor salivary gland tumors invading the base of skull were treated with primary neutron radiotherapy followed by a Gamma Knife radiosurgical boost to the base of skull. Patients had the following characteristics: (1) primary site of disease: paranasal sinuses (n = 3), nasopharynx (n = 3), hard palate (n = 1), pterygopalatine fossa (n = 1); (2) median age 59 years (range 37-80); (3) interval from completion of neutron radiotherapy to Gamma Knife boost 4 weeks (range 2-8 weeks); (4) median stereotactic dose delivered 10 Gy (prescribed to 50% isodose line, range 8-12 Gy), and (5) median number of isocenters treated 16 (range 14-21). Dosimetry from the neutron radiotherapy was used to determine both the volume boosted and the dose utilized. The median follow-up interval from the time of Gamma Knife treatment was 21.5 months (range 16-23 months). RESULTS: All patients tolerated the procedure well. Acute side effects were minimal and included 1 patient with a delayed fatigue reaction at 2 months, 1 patient with vertigo of limited duration, and a third patient with prolonged nausea requiring steroid use. All patients were placed on a tapering dose of steroids after the procedure. One patient suffered a local relapse, with a 2-year actuarial disease-free survival rate of 80%. CONCLUSIONS: Gamma Knife radiosurgical boost following primary neutron radiotherapy for patients with a high risk of local failure is feasible and well tolerated acutely. Careful attention must be given to the previously treated regions in regard to volume treated and dose delivered. Further follow-up will be necessary to determine the long-term effectiveness and complications of such a boost in these high-risk patients.

Adult↗

Beta-6 Integrin, tenascin-C, and MMP-1 expression in salivary gland neoplasms.

Beta-6 Integrin, tenascin-C, and MMP-1 (matrix metalloproteinase-1) are invasion-related proteins that are frequently overexpressed in many human malignancies. The objective of this study was to determine whether there is overexpression of these molecules in three types of salivary neoplasms showing markedly different behavior. A total of 55 formalin-fixed, paraffin-embedded archived specimens comprising 19 adenoid cystic carcinomas (ACC), 18 polymorphous low-grade adenocarcinomas (PLGA) and 18 pleomorphic adenomas (PA) were utilized in this study. A standard immunohistochemical technique was used to determine the expression levels of beta-6 integrin, tenascin-C, and matrix metalloproteinase-1 (MMP-1) proteins. Sections were assessed semiquantitatively, and tumors were divided into two groups, low-expressors (0-1+) and high-expressors (2-3+) for statistical analysis. Staining was graded as 0 (<1% positive tumor cells), 1+ (<25% positive tumor cells), 2+ (25-50% positive tumor cells), and 3+ (>50% positive cells). The results showed that the malignant tumors were higher expressors of beta-6 than the benign tumors. ACCs showed significantly higher expression of beta-6 than PAs (p=0.04). No significant difference was observed between ACCs and PLGAs. beta-6 expression was rarely seen in normal salivary gland epithelium and was occasionally present in mucosa overlying the tumors. PAs were high-expressors of tenascin-C with a significant difference relative to ACCs (p=0.03). A majority of tumors in all three tumor types showed high expression of MMP1 with expression significantly greater in the PAs compared to ACCs (p=0.008). We conclude that ACCs and PLGAs express beta-6, tenascin-C, and MMP-1, but that their expression patterns are not significantly different. beta-6 appears to be more closely associated with the malignant tumors, and MMP-1 more closely associated with the benign tumors. We believe that beta-6, tenascin-C, and MMP-1 proteins are part of the molecular repertoire used by salivary tumors for malignant invasion and benign tumor expansion.

Adenocarcinoma↗

Prostate marker immunoreactivity in salivary gland neoplasms. A rare pitfall in immunohistochemistry.

A 66-year-old man presented with a mass just behind the lower part of the left ear. A biopsy showed a moderately differentiated adenocarcinoma that was prostate-specific antigen (PSA)- and prostate-specific acid phosphatase (PSAP)-positive. This finding suggested a metastasis of a prostatic carcinoma. Extensive clinical and radiographical examination revealed no primary prostatic carcinoma or other metastases and serum levels of PSAP and PSA were not elevated. The reliability of the PSA and PSAP staining was studied in a series of 25 adenocarcinomas of various primary sites in females and in 26 salivary gland tumors in both males and females, because a primary adenocarcinoma of salivary gland seemed another possibility in this case. As expected, there was no immunoreactivity for PSA and PSAP in the adenocarcinomas from females, but 6 of 11 pleomorphic adenomas, 0 of 4 monomorphic adenomas, 1 of 6 mucoepidermoid carcinomas, and 1 of 2 adenocarcinomas not otherwise specified (NOS) of the salivary gland showed at least focal staining of both PSA and PSAP. The conclusion was that the patient had a primary salivary gland adenocarcinoma NOS. In males with PSA- and PSAP-positive adenocarcinoma without signs of primary prostatic carcinoma, a salivary gland origin should be considered.

Acid Phosphatase↗

Leukocyte mediated cytotoxicity of chemically induced rat salivary gland neoplasms.

Chemically induced tumors of the rat submaxillary glands were tested for the presence of tumor antigens by in vitro leukocyte mediated cytotoxicity assays. Since it has been reported that the saliva of humans with oral cancer contains markedly elevated levels of secretory antibody, the rats' saliva specimens were also tested for blocking and/or potentiating "antibody" activity. The results indicate that saliva from tumor-bearing animals potentiated tumor cell killing if either the tumor cells or leukocytes were pretreated. The effect was much more marked when tumor cells were pretreated. Furthermore, the addition of saliva to tumor cells imparted an immunologic cross reactivity which was not present with untreated tumor cells. Control saliva occasionally produced a similar effect, but not as consistently or with the potency of saliva from tumor-bearing animals. Heat inactivation did not abrogate this potentiation. It is inferred that this may indicate a new system of immunologic surveillance, i.e. arming or potentiation of leukocytes by soluble tumor antigens in glandular secretions.

Animals↗

Coexpression of intermediate-sized filaments in sialadenoma papilliferum and other salivary gland neoplasms.

The neoplastic cells present in a sialadenoma pappiliferum were found by immunoperoxidase method and immunofluorescent staining technique to co-express 3 different types of intermediate-sized filaments (IFs) defined by monoclonal antibodies to cytokeratin, vimentin and desmin. When other salivary gland tumors such as 18 pleomorphic adenomas, 15 adenolymphomas, 2 oxyphilic adenomas, 7 mucoepidermoid tumors, 5 acinic cell tumors, 8 adenoid cystic carcinomas and 6 adenocarcinomas were examined immunohistochemically for the expression of IFs, no tumors with all 3 types of IFs observed in sialadenoma papilliferum were found.

Adenocarcinoma↗

Myoepithelial cell markers in salivary gland neoplasms.

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.

Actins↗