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At least 19 recordsLinked to original sources
PubMed2006

Expression of betacatenin in carcinoma in pleomorphic adenoma, pleomorphic adenoma and normal salivary gland: an immunohistochemical study.

OBJECTIVES: Pleomorphic adenomas are the most frequent type of epithelial salivary gland neoplasms, and their malignant counterpart, the carcinoma in pleomorphic adenomas, is much less common. Beta-catenin is a cell adhesion molecule associated with the invasion and metastasis of carcinomas of the head and neck, esophagus. The objective of this study was to detect the expression of beta-catenin in pleomorphic adenomas, carcinomas in pleomorphic adenomas and normal salivary glands to discuss its role in the development of these two lesions. STUDY DESIGN: The expression of beta-catenin (BD Transduction Laboratories) was analyzed by immunohistochemistry in formalin-fixed, paraffin embedded specimens by the avidin-biotin-peroxidase complex method in 16 pleomorphic adenomas (12 from minor salivary glands), 3 carcinomas in pleomorphic adenomas (all from palate) and 10 normal salivary glands as control group (5 from major and 5 from minor salivary glands). RESULTS: All cases of glands, adenomas and carcinomas in pleomorphic adenomas have membranous and cytoplasmic immunostaining. Nuclear beta-catenin immunostaining was not observed. The antibody presented a fine granular arrangement in the cytoplasm and cellular membrane of duct and acinic cells. Higher beta-catenin index rates were seen mainly in salivary gland ducts and in ductal structures in the adenomas and carcinomas in pleomorphic adenomas. There was protein loss in pleomorphic adenomas and cytoplasmic accumulation in carcinoma in pleomorphic adenomas. CONCLUSIONS: The present study showed participation of the loss of beta-catenin adhesion molecule in the development of pleomorphic adenoma, and that the cytoplasmic accumulation of the molecule takes part in the malignant transformation of the pleomorphic adenoma into carcinoma in pleomorphic adenoma.

Adenoma, Pleomorphic↗
PubMed2004

Elevated expression of cyclooxygenase-2 in adenocarcinoma of the parotid gland: insights into malignant transformation of pleomorphic adenoma.

Pleomorphic adenoma, the most common type of tumor of the parotid gland, may transform into a malignant tumor. In the current study, we investigated whether the expression of cyclooxygenase-2 (COX-2) is elevated in adenocarcinoma as compared to pleomorphic adenoma. Ten pleomorphic adenomas and 10 adenocarcinomas were examined. The tumor specimens were immunohistochemically stained with antibodies against COX-2 and Ki-67. The labeling indices of COX-2 in pleomorphic adenoma and adenocarcinoma were 6.0% +/- 4.1% and 16.1% +/- 4.6%, respectively, and those of Ki-67 in pleomorphic adenoma and adenocarcinoma were 0.77% +/- 0.62% and 6.9% +/- 6.6%, respectively. The labeling indices of both COX-2 and Ki-67 were significantly greater (p < .001) in adenocarcinoma than in pleomorphic adenoma. Together with the biological effects of COX-2, these results suggest that overexpression of COX-2 plays a crucial role in the pathogenesis of malignant transformation of pleomorphic adenoma in the parotid gland.

Adenocarcinoma↗
PubMed2004

Lumican expression is associated with the formation of mesenchyme-like elements in salivary pleomorphic adenomas.

Pleomorphic adenomas are the most common salivary gland tumour. Although this tumour is considered to be of epithelial origin, it contains 'mesenchyme'-like elements histologically. Lumican is a keratan sulphate proteoglycan that belongs to the small leucine-rich repeat (LRR) proteoglycans and has been reported to be associated with cartilage formation. These findings suggest that lumican expression may be related to the chondroid component in pleomorphic adenomas. To investigate this hypothesis, the present study investigated the expression and localization of lumican in 20 normal human salivary glands and 35 pleomorphic adenomas. Firstly, immunohistochemistry for lumican was performed with pepsin pretreatment. In normal salivary glands, lumican was deposited in the periductal regions. In pleomorphic adenomas, it was predominantly deposited in the hyaline (100%) and fibrous areas (89.4%). In 16 tumours (66.7%), lumican was also deposited in the chondroid areas. Without pepsin pretreatment, lumican was identified in myoepithelial cells in myxoid areas, lacuna cells in chondroid areas, and in the cytoplasm of inner ductal cells. In situ hybridization revealed lumican mRNA expression mainly in the inner cells, the neoplastic myoepithelial cells, and the lacuna cells. These results suggest that lumican is associated with the formation of 'mesenchyme'-like structures in pleomorphic adenomas. In conclusion, normal salivary glands express lumican, which appears to be related to stromal maintenance, and pleomorphic adenomas express lumican mRNA and protein, which may play important roles in the formation of 'mesenchyme'-like areas in this type of tumour.

Adenoma, Pleomorphic↗
PubMed2004

Expression and localization of cartilage-specific matrix protein chondromodulin-I mRNA in salivary pleomorphic adenomas.

Pleomorphic adenoma is the most common epithelial tumor in the salivary glands. This tumor frequently exhibits "mesenchyme"-like components, including myxoid or chondroid areas. Recently, using immunohistochemical techniques, we reported that cartilage-specific matrix protein, chondromodulin-I (ChM-I), was deposited on the inter-territorial matrix of the chondroid area in salivary pleomorphic adenomas and that ChM-I, which is also a strong angio-inhibitory factor, plays an important role in the avascular nature of the chondroid area and the chondroid formation in this type of tumor. To elucidate which cells express ChM-I mRNA in pleomorphic adenomas, we examined the expression and localization of ChM-I mRNA in this type of tumor using an in situ hybridization technique. Immunoreactivity for ChM-I was observed in the inter-territorial matrix of the chondroid area, especially around the lacunae, and in the cytoplasm of neoplastic myoepithelial cells of the myxoid element of pleomorphic adenomas. On in situ hybridization analysis, strong signals for ChM-I mRNA were detected in the cytoplasm of the lacuna cells of the chondroid element, and moderate to marked signals were observed in the cytoplasm of the neoplastic myoepithelial cells of the myxoid element. Signals for ChM-I mRNA were also seen in the cytoplasm of the spindle-shaped neoplastic myoepithelial cells in the transitional areas between the myxoid and chondroid elements of this tumor. Signals for ChM-I mRNA were not seen in the inner ductal cells or the fibrous element. These findings indicate that lacuna cells and neoplastic myoepithelial cells express ChM-I mRNA and that mature ChM-I, which lacuna cells and neoplastic myoepithelial cells translate, is deposited in the chondroid matrix of pleomorphic adenomas. In conclusion, lacuna cells and neoplastic myoepithelial cells express ChM-I mRNA ectopically in pleomorphic adenoma, and this plays an important role in chondroid formation and hypovascularity in this type of tumor.

Adenoma, Pleomorphic↗
PubMed1994

Familial occurrence of pleomorphic adenoma.

Pleomorphic adenoma is the most common neoplasm found in the parotid gland. The familial occurrence of any salivary gland neoplasm is rare. There are 8 previous reports in the literature of familial occurrence of salivary gland tumors. Two of these report the occurrence of pleomorphic adenoma of the parotid gland in siblings; all 4 patients were adults. We report here an 11-year-old male who presented with a left parotid mass and underwent parotidectomy. The mass proved to be a pleomorphic adenoma. His sister presented 9 years later at the age of 15 years with a similar mass also in the left parotid area. She underwent superficial parotidectomy which revealed the mass to be a pleomorphic adenoma. We believe these are the youngest siblings reported to date in which familial pleomorphic adenoma has occurred.

Adenoma, Pleomorphic↗
PubMed2001

[Subglottic pleomorphic adenoma].

Pleomorphic adenoma is the most common tumor of major salivary glands, but it is unusual into the larynx. The AA. expose a case of a 74-year-old man who consulted for dysphonia and diagnosed as having a subglottic pleomorphic adenoma. The patient needed an urgent tracheotomy owing to the dyspnoea. Removal of the tumor was made through direct laryngoscopy. Literature on pleomorphic laryngeal adenoma is reviewed.

Adenoma, Pleomorphic↗
PubMed1990

Metastatic salivary pleomorphic adenoma.

Pleomorphic adenomas of the salivary gland are usually regarded as benign tumours. We report a case in which a solitary pulmonary metastasis arose from a pleomorphic adenoma of the right parotid gland. The mechanism of metastasis is discussed.

Adenoma, Pleomorphic↗
PubMed1997

Ancient schwannoma masquerading as parotid pleomorphic adenoma.

Pleomorphic adenoma of the parotid gland is common. We report a typical case of a parotid gland swelling which clinically, radiologically and cytologically represented a pleomorphic adenoma. Only following surgical excision and histological examination however, was the true diagnosis of ancient schwannoma made. Benign peripheral nerve sheath tumours should always be considered in the differential diagnosis of parotid gland tumours.

Adenoma, Pleomorphic↗
PubMedDate not supplied

[Paranasal sinus pleomorphic adenoma].

Pleomorphic adenomas with atypical facial presentation, specifically, in the nasal sinus region, were studied. A patient who presented with malignant tumor of the nasal sinus was diagnosed as pleomorphic adenoma after histologic misdiagnosis. The surgical technique and outcome at one year are described.

Adenoma, Pleomorphic↗
PubMed2005

Loss of heterozygosity occurs predominantly, but not exclusively, in the epithelial compartment of pleomorphic adenoma.

Pleomorphic adenoma (PA), being the most common benign tumor of the salivary glands, is composed of epithelial and mesenchymal compartments. In this study, we analyzed 19 microsatellite markers from chromosomal arms 6q, 8q, 9p, 12q, and 17p in 31 PAs and 3 carcinoma ex pleomorphic adenomas (CXPAs) as well as 11 other non-PA-related carcinomas of the salivary gland for comparison. In our analysis, we differentiated between epithelial and mesenchymal tissues. Loss of heterozygosity (LOH) in PAs was most often found in 8q (32%) and 12q (29%). Two of the three CXPAs displayed allelic loss at all chromosomal arms investigated, whereas the results of the non-PA-related carcinomas were rather heterogeneous. LOH could not only be detected in the epithelial, but also in the mesenchymal, compartments of a subset of PAs, especially at chromosomal arm 8q. Concerning the CXPAs, we were able to demonstrate allelic losses not only in the malignant epithelial compartment, but also in the residual adenoma parts. Our data give further evidence that alterations in 8q may be an early event in PA tumorigenesis, whereas LOH in 12q may characterize cells with the potential to transform in CXPAs.

Adenoma, Pleomorphic↗
PubMedDate not supplied

[The recurrent multifocal pleomorphic adenoma].

Pleomorphic adenoma (P.A.), the most common tumor of the salivary gland, demonstrates a peculiar clinicopathological behaviour for numerous reasons: the high recurrence rate following primary surgery (up to 50%), the appearance of malignancy (2-9%), the reported number of distant metastases histologically identical to the primary P.A. From among 71 cases of benign parotid tumors treated from Nov. 89 to Nov. 92 in the ENT Department of "Regina Elena", the National Cancer Institute in Rome, six particular cases showed multiple force of P.A. recurring after primary surgery performed from 3 to 32 years previously and are object of discussion in this study. All of these six cases had multiple recurrences, usually manifest as nodular clusters in the parotid area, while in three cases appeared as well a recurrence in the soft tissue of the neck, far removed from the parotid space, with no involvement of neck nodes as was revealed through histological examination following neck dissection. A hypothetical mechanism of diffusion is discussed. The Authors agree with the opinion which holds the surgeon's inability to successfully eradicate primary tumors responsible for the high frequency of recurrences. The surgical technique of "enucleation" is, in fact, inadequate in P.A. excision owing the high risk of mishandling or rupturing the tumor capsule with a consequent seeding of the tumor onto the surgical bed. Lateral lobectomy, with identification of the facial nerve, or total conservative parotidectomy (for deep lobe adenoma) are correct techniques in treating primary P.A.. The Authors also discuss management of recurrent P.A. in relation to facial nerve involvement. Preservation of the seventh nerve with eventual post-operative radiation should be considered an alternative to nerve sacrifice in selected cases of recurrent pleomorphic adenoma.

Adenoma, Pleomorphic↗
PubMed2001

Pleomorphic adenoma.

Pleomorphic adenoma is the most common neoplasm of the salivary glands. Though a benign lesion, proper recognition and management of this process is needed to avoid increasing enlargement of the mass, facial nerve impairment, risk of malignant degeneration, and recurrence after surgical resection. The epidemiology, diagnosis, and treatment options for this neoplasm are discussed.

Adenoma, Pleomorphic↗
PubMed1994

[Cytogenetic subtyping of salivary gland pleomorphic adenoma and carcinoma in pleomorphic adenoma].

Current research on salivary gland pleomorphic adenoma is aimed at grouping the cases by cytogenetical aberrations into several subtypes. In this report, 21 cases of pleomorphic adenomas were analysed cytogenetically and divided into 4 subtypes following Bullediek's method; normal karyotype (6 cases), 8q12 rearrangement (8 cases), 12q13-15 rearrangement (5 cases) and other aberrations (2 cases). The average occurrence age of each group was examined. The 8q12 rearrangement group (37.2 y.o.) was younger than the normal karyotype (49.2 y.o.) and 12q13-15 rearrangement groups (52.4 y.o.). Histological subtyping based on Seifert's classification was made and its relationship with the above cytogenetic subtypes was studied. In the 8q12 rearrangement group, Seifert's type-1 was predominant (88%), while in the normal karyotype and 12r13-15 rearrangement groups, Seifert's type-2 was the most common (50% and 80% respectively). We also examined 2 cases of carcinoma in pleomorphic adenoma. Although both showed some cytogenetic abnormalities, no aberrations specific to pleomorphic adenoma (8q12 or 12q13-15 rearrangement) were found. This suggests that original adenomas of these carcinomas showed a normal karyotype or other types of aberrations.

Adenocarcinoma↗
PubMed2001

Histologic localization of PLAG1 (pleomorphic adenoma gene 1) in pleomorphic adenoma of the salivary gland: cytogenetic evidence of common origin of phenotypically diverse cells.

Pleomorphic adenoma gene 1 (PLAG1), a zinc finger transcription factor gene, is consistently rearranged and overexpressed in human pleomorphic adenomas of the salivary glands with 8q12 translocations. In this report, we describe the immunohistochemical localization of PLAG1 protein in pleomorphic adenomas of the salivary gland and corresponding normal tissue, in relation to cytokeratin, vimentin, and BCL-2 expression. Normal salivary gland tissue was not immunoreactive for PLAG1. In primary pleomorphic adenomas, cells strongly immunoreactive for PLAG1 were detected in the outer layer of tubulo-ductal structures, which are thought to be the origin of cells with bi-directional, epithelial, and mesenchymal phenotypes. In contrast, epithelial cells with abundant cytokeratin in the inner tubulo-ductal structures only sporadically expressed PLAG1. BCL-2 immunoreactivity was found mainly in the cells surrounding the tubulo-ductal structures and in the solid undifferentiated cellular masses, within the areas that had moderate PLAG1 immunoreactivity. The variability of PLAG1 expression in neoplastic cells seemed to reflect the morphologic heterogeneity that correlated with the stage of differentiation of the tumor cells. Immunohistochemical/cytogenetic evaluation of two pleomorphic adenomas with t(3;8)(p21;q12) or t(5;8)(p13;q12) translocations demonstrated the clonal nature of immunophenotypically diverse cells. This finding confirms the theory that pleomorphic adenoma cells share a common single-cell origin, most likely from the epithelial progenitor basal duct cells.

Adenoma, Pleomorphic↗
PubMed2005

PLAG1 gene alterations in salivary gland pleomorphic adenoma and carcinoma ex-pleomorphic adenoma: a combined study using chromosome banding, in situ hybridization and immunocytochemistry.

Pleomorphic adenoma is the most common benign tumor of the salivary glands. It has marked histological diversity with epithelial, myoepithelial and mesenchymal-type cells arranged in a variety of architectural and differentiation patterns. Pleomorphic adenoma gene 1 (PLAG1), shown to be consistently rearranged in pleomorphic adenomas, is activated by chromosomal translocations involving 8q12, the chromosome region that is most frequently affected in these tumors. In this study, we evaluated PLAG1 involvement in salivary gland tumorigenesis by determining the frequency of its alterations in a selected group of 20 salivary gland tumors: 16 pleomorphic adenomas and four carcinomas ex-pleomorphic adenoma, having in common the presence of karyotypic chromosome 8 deviations, either structural, with 8q12 rearrangements, or numerical, with gain of chromosome 8. PLAG1 status was analyzed using in situ hybridization techniques, on metaphase cells, by fluorescence detection and/or interphase cells in paraffin sections, by chromogenic detection. Except for one pleomorphic adenoma case (5%) that lacked PLAG1 involvement, 17 tumors (85%), (14 pleomorphic adenomas and three carcinomas ex-pleomorphic adenoma) showed intragenic rearrangements of PLAG1 and the remaining two cases (10%), (one pleomorphic adenoma and one carcinoma ex-pleomorphic adenoma), had chromosome trisomy 8 only. To further investigate the role of PLAG1 on pleomorphic adenomas tumorigenesis, as well as the putative morphogenesis mechanism, we attempted to identify the cell types (epithelial vs myoepithelial) carrying 8q12/PLAG1 abnormalities by a combined phenotypic/genotypic analysis in four cases (three pleomorphic adenoma and one carcinoma ex-pleomorphic adenoma) characterized by 8q12 translocations and PLAG1 rearrangement. In these cases, both cells populations carried PLAG1 rearrangements. This finding further supports the pluripotent single-cell theory, which postulates that the tumor-initiated, modified myoepithelial cell, evolves into the varied somatic cell phenotypes present in pleomorphic adenoma, and reinforces the role of PLAG1 on the tumorigenesis of benign and malignant pleomorphic adenoma.

Adenoma, Pleomorphic↗
PubMed2004

Pleomorphic adenoma and carcinoma ex pleomorphic adenoma: immunohistochemical demonstration of the association between tenascin expression and malignancy.

AIMS: To investigate tenascin expression in salivary gland tumours. Tenascin is a matricellular protein that has been studied in several tumour types. Its expression has been correlated with tumour morphogenesis as well as with local invasiveness and tumour metastatic behaviour. METHODS AND RESULTS: The distribution pattern of tenascin in a series of 63 pleomorphic adenomas (PA) and 20 carcinomas ex- pleomorphic adenoma (Ca ex PA) was studied immunohistochemically. Ten normal adult salivary glands were used as controls. Tenascin surrounded the excretory ducts of normal adult salivary gland tissue. It was absent in the basement membrane compartment of both benign and malignant mixed tumours. In the interstitial compartment of the extracellular matrix, the fibro-hyaline type expressed tenascin in a statistically significantly (P < 0.001) lower number of PA cases (25%) in comparison with both malignant and benign areas of Ca ex PA (75% and 90%, respectively). In the Ca ex PA group, a statistically significantly difference (P < 0.001) was found in the frequency of tenascin deposits around aggregates of neoplastic cells between metastasizing (73%) and non-metastasizing neoplasms (0%). CONCLUSIONS: These findings strongly support the hypothesis that tenascin deposition is involved in the mechanisms of malignant transformation of pleomorphic adenomas into carcinomas as well as being associated with clinical disease progression.

Adenocarcinoma↗
PubMed1994

c-erbB-2 oncoprotein expression and amplification in pleomorphic adenoma and carcinoma ex pleomorphic adenoma: relationship to prognosis.

The c-erbB-2 protooncogene has been shown to be overexpressed and/or amplified in carcinomas of the breast, ovary, pancreas, and other organs. Several studies of human breast carcinoma noted an association of c-erbB-2 overexpression and amplification with poor prognosis. Recent studies have demonstrated c-erbB-2 protein expression in a variety of salivary gland neoplasms, most notably pleomorphic adenoma (PA), carcinoma ex pleomorphic adenoma (CAexPA), and adenocarcinoma. In this study, we analyzed c-erbB-2 expression in 15 PAs and 13 CAexPAs, using immunohistochemistry. In addition, differential polymerase chain reaction was used to evaluate c-erbB-2 gene amplification in these tumors. Low-level c-erbB-2 immunoreactivity was detected in three of 15 PAs. Among the CAexPAs, low-, intermediate-, and high-level immunoreactivity was seen in two, three, and two cases, respectively. The only cases showing c-erbB-2 amplification were the two CAexPA cases with high-level immunoreactivity. Based on statistical analysis of the 10 CAexPA patients with known outcome, no significant association of prognosis with c-erbB-2 expression or amplification was apparent.

Adenoma, Pleomorphic↗