Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “pleomorphic”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

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

At least 595 records · Page 33Linked to original sources
PubMed2005

Carcinoma ex pleomorphic adenoma (CXPA): immunoprofile of the cells involved in carcinomatous progression.

AIMS: To characterize the cellular component in pleomorphic adenoma (PA) that undergoes malignant transformation in carcinoma ex pleomorphic adenoma (CXPA). METHODS AND RESULTS: A panel of antibodies against cytoskeletal proteins was applied in 16 cases of CXPA: intracapsular carcinoma (five cases), minimally invasive (four cases) and frankly invasive (seven cases). The CXPAs were classified into two main groups according to their predominant cellular component as detected by the panel of antibodies: (i) carcinomas with only epithelial differentiation (75% of the cases), and (ii) carcinomas with a myoepithelial component (25%). CXPA with only epithelial differentiation showed two types of malignant areas in the part of the tumour that was confined by the PA capsule: (i) intraductal carcinoma areas characterized by ductal structures containing both benign myoepithelial cells positive for alpha-smooth muscle actin (alpha-SMA), vimentin and cytokeratin (CK)14 and proliferating atypical luminal cells reactive for CK7, CK8 and CK19, and (ii) carcinoma areas composed only of epithelial cells reactive for CK7, CK8 and CK19. In the latter, the cells presented morphological and immunohistochemical characteristics similar to those found in areas of invasive carcinoma outside the PA capsule. CXPAs with a myoepithelial component were composed mainly or exclusively of cells that expressed vimentin and alpha-SMA. In this group, ductal structures reminiscent of PA filled by malignant cells were not identified. CONCLUSION: Most CXPAs consist only of epithelial cells that have an immunoprofile comparable to ductal luminal cells of PA. These malignant luminal cells arise in the duct-like structures as intraductal carcinoma and probably only at this early stage of development should the lesion be considered as a non-invasive carcinoma.

Actins↗
PubMed1992

Proliferative activity in normal salivary gland and pleomorphic adenoma. A study by argyrophilic nucleolar organizer region (AgNOR) staining.

Proliferative activity of the structural components of normal salivary glands (27 cases) and characteristic histological areas in salivary pleomorphic adenoma (51 cases) was examined by visualization of argyrophilic nucleolar organizer regions (AgNORs). In the normal salivary gland, there were clusters of cells, each with two or three AgNOR dots, within the intercalated ducts. The mean number of AgNORs in this portion was 1.80, which was significantly higher than in the other epithelial parts. This indicates vigorous proliferative activity of the intercalated ducts, and thus the ducts may play an important role as reserve cells in neoplastic transformation. In pleomorphic adenoma, solid nests had a high AgNOR count (1.61), showing a significant difference from the tumor cells scattered in the "stroma". Thus the decrease in proliferative ability might occur concurrently with formation of the extracellular matrix.

Adenoma, Pleomorphic↗
PubMed1995

Pleomorphic adenoma of the breast: case report and review of the literature.

A tumor of the right breast was noticed in a 70 year old female. The tumor was round, 1 x 1 cm, and was encapsulated with thin fibrous tissue. The boundary was clear. The cut surface showed a mosaic pattern of brown and white dots and the texture was gritty. Histologically, glandular structures, trabecular or solid epithelial cell nests, myxoid, cartilaginous and osteoid areas, and one ossifying focus were found. Round, polyhedral or fusiform myoepithelial cells proliferated around the glandular structures and were dispersing into the myxoid and cartilaginous tissue. Myoepithelial proliferation was especially marked around the small glandular structure. Immunohistochemically, S-100 protein was strongly positive for the myoepithelial cells around the glandular structures and in the cartilaginous tissue. Until now, 54 cases of pleomorphic adenoma of the breast have been reported. In those cases, the subareolar region was a common site for the tumor, and pleomorphic adenoma was thought to arise from large ducts in this region. No Oriental patients have been reported in the literature.

Adenoma, Pleomorphic↗
PubMed1995

Myoepithelial carcinoma in pleomorphic adenoma of salivary gland type, occurring in the mandible of an infant.

A rapidly growing mandibular tumor occurred in a 17 month old female infant. Tumor outgrowth showing a periosteal reaction was radiographically seen on the lower surface (base) of the mandible. Under the biopsy diagnosis of osteosarcoma, high-dose chemotherapy with methotrexate was performed, resulting in little effect. The right hemimandibulectomy specimen disclosed intraosseous infiltrative growth of pleomorphic adenoma of salivary gland type, associated with chondroid stroma and reactive bone formation. The highly proliferative small-sized cells retained immunohistochemical features of myoepithelial cells, with positive reactivity of cytokeratin, vimentin, S-100 protein, alpha-smooth muscle actin, epithelial membrane antigen, CA15-3, type IV collagen, laminin and p53 protein. No heterotopia of the salivary gland was identified within the bone tissue. The tumor recurred 2 months later. Due to uncontrollable local growth, the patient died 8 months after operation. At autopsy, reactive ossification was closely associated with malignant myoepithelial proliferation. No distant metastasis was noted. This osteosarcoma-like tumor can be regarded as myoepithelial carcinoma in pleomorphic adenoma, originating from intramandibular heterotopic salivary gland tissue.

Adenoma, Pleomorphic↗
PubMed1998

DNA analysis at p53 locus in carcinomas arising from pleomorphic adenomas of salivary glands: comparison of molecular study and p53 immunostaining.

Where and how frequently p53 abnormalities are involved in the development of pleomorphic adenoma (PA) and its malignant progression to carcinoma was investigated. The presence of p53 gene abnormalities was analyzed in eight patients with carcinoma in pleomorphic adenoma (CPA) by polymerase chain reaction (PCR)-based assays and immunohistochemistry. Normal salivary gland tissue, adenomatous, transitional and carcinomatous areas were microdissected from archival microslides and analyzed for allelic deletions of the p53 gene using two microsatellite markers at the p53 locus; dinucleotide (CA)n repeat and pentanucleotide (AAAAT)n repeat. Loss of heterozygosity (LOH) of the p53 gene was detected in 57% of adenomas, 86% of transitional lesions and 86% of carcinomas. In contrast, overexpression of p53 oncoprotein was noted immunohistochemically in 13% of adenomas, 50% of transitional areas and 75% of carcinomas. All of the tumors with immunoreactivity for p53 oncoprotein demonstrated LOH. Moreover, when LOH was present in adenomatous or transitional areas, the identical LOH was always detected in the corresponding carcinomatous areas in the same CPA tumors. These findings indicate that p53 gene mutation is an early event and occurs frequently at an early stage of precancerous lesions and may be responsible for most cases of malignant transformation of PA.

Adenoma, Pleomorphic↗
PubMed2006

Lipomatous pleomorphic adenoma of the ceruminous gland.

A case of lipomatous pleomorphic adenoma in the ceruminous gland is reported. A 69-year-old Japanese woman presented with a mass in the posterior wall of the cartilaginous external auditory canal. Light microscopic examination revealed a well-circumscribed tumor composed of tubular structures with apocrine secretion and ceroid deposition, extensive mature adipocytes, and spindle-shaped myoepithelial cells in the myxoid and fibrous stroma. This case demonstrates the peculiar location of a lipomatous pleomorphic adenoma in the external auditory canal.

Adenoma, Pleomorphic↗
PubMed2005

Pleomorphic adenoma of the lacrimal gland in a nine-year-old child.

A case of a 9-year-old child with pleomorphic adenoma of the lacrimal gland is described. This tumour is usually found in adults; cases younger than 10 years of age have proved to be extremely rare. Because of its age distribution, pleomorphic adenoma of the lacrimal gland is usually overlooked as a possible cause of unilateral proptosis in children. Also, the history of disease provided by the family may be incorrect, possibly leading to misdiagnosis by the ophthalmologist.

Adenoma, Pleomorphic↗
PubMed1987

'Benign' pleomorphic adenoma of the parotid.

A personal series of 141 surgically treated parotid tumours is reviewed. Of 112 parotid tumours in which a diagnosis of 'benign' pleomorphic adenoma or other benign tumour was made, 8% proved to be malignant on histological examination. Three patients were thought to demonstrate malignant change in long standing 'benign' parotid tumours. It is concluded that in otherwise healthy patients, discrete, mobile parotid tumours should be removed without undue delay because of the risk of misdiagnosis and the chance of late development of malignancy in pleomorphic adenomata. Malignant tumours simulate benign tumours often enough to warrant treating all as potentially malignant.

Adenoma, Pleomorphic↗
PubMedDate not supplied

The ultrastructural aspects of neoplastic myoepithelial cell in pleomorphic adenomas of salivary glands.

The purpose of this study has been to establish the major ultrastructural aspects of the myoepithelial cell and the myoepithelial-like cells proliferated in the pleomorphic adenomas of salivary glands. Thus, twelve benign pleomorphic adenomas of salivary glands have been studied by electron-microscopy transmission techniques. Our analysis has proved the proliferation of two major cellular populations, one of ductal type and one of myoepithelial type, which tried to reproduce the tubulo-acinar cytoarchitecture from the normal salivary glands. We have also noticed the key role of the so-called 'modified' myoepithelial cells from the periphery of the proliferating epithelial units in the genesis of the myxoid and chondromyxoid tumoral stromal areas. All these ultrastructural aspects have explained the great histological diversity of these salivary gland neoplasms as well as the key role of the myoepithelial cell in its histogenesis.

Adenoma, Pleomorphic↗
PubMed1988

Monoclonal antibody-detected vimentin distribution in pleomorphic adenomas of salivary glands.

To evaluate the participation of myoepithelial components in pleomorphic adenomas, an immunohistochemical study was carried out using monoclonal antibodies to vimentin. Of a total of 80 cases, 50 tumors gave positive staining, 5 tumors very slight, and 25 tumors negative staining for vimentin. Localization patterns for vimentin were divided into 3 classes: 1) vimentin staining in fibrous stromal tissue; 2) variable intensities of vimentin staining were found in the outer layers of tumor cells in tubulo-ductal structures (some of which were spindle cells connected to modified myoepithelial cells which also gave variable vimentin staining); and 3) modified myoepithelial cells and chondroidlike cells displayed strongly positive staining for vimentin. Typical histologic features of pleomorphic ademomas, i.e., tubulo-ductal or duct-like structures were characterized by positive vimentin staining in outer tumor cells and by a positive keratin reaction in the luminal tumor cells. In tumors devoid of stromal connective tissues and the near absence of well-developed, or modified myoepithelial cells, vimentin staining was absent.

Adenoma, Pleomorphic↗
PubMed1989

Coexpression of keratin and vimentin in salivary pleomorphic adenomas.

The coexpression of keratin and vimentin is described in 45 pleomorphic adenomas using an immunoperoxidase MAb method. Histopathologically, the outer layer of tubuloductal structures and peripheral tumor cells in solid masses, including modified or neoplastic myoepithelial cells, showed positive staining with monoclonal keratin antibody K8.12 and vimentin. This staining was found in the ratio of 10/26 (38.5%) in tubuloductal structures, 2/7 (28.6%) in peripheral tumor cells and 8/12 (66.7%) in modified myoepithelial cells. Concomitant staining of other keratin antibodies (PKK1, KL1) and vimentin did not exist. In addition, the ductal basal cells of normal salivary glands showed positive K8.12 labelling. The histogenesis of pleomorphic adenoma is discussed in relation to the differentiation of either ductal basal cells or ductal luminal cells from a single stem cell origin or the direct transformation of ductal basal cells to outer tumor cells and/or modified myoepithelial cells, both coexpressing K8.12 and vimentin.

Adenoma, Pleomorphic↗
PubMed1995

A fluorescence in situ hybridization (FISH) analysis with centromere-specific DNA probes of chromosomes 3 and 17 in pleomorphic adenomas and adenoid cystic carcinomas.

Aberrations of chromosomes 3 and 17 were studied by FISH using centromere-specific DNA probes in 11 salivary adenoid cystic carcinomas (ACC) and 8 salivary pleomorphic adenomas (PA), with 3 lymph nodes as controls. Two hybridized signals were detected in 92.8 +/- 2.7% of controls, 73.2 +/- 7.0% of PA and 66.8 +/- 7.9% of ACC cells for chromosome 3, and in 90.4 +/- 2.3% of controls, 59.5 +/- 25.0% of PA and 44.8 +/- 20.2% of ACC for chromosome 17. More than 3 hybridized signals, which indicate polysomy, were observed in 3.1% of controls, 15.5% of PA and 22.9% of ACC cells for chromosome 3, and in 1.2% of controls, 10.3% of PA and 23.1% of ACC cells for chromosome 17. A single hybridized signal was much more frequent for chromosome 17 than for chromosome 3. These findings suggest that polysomy of both chromosomes occurs during the development of salivary gland tumors, and its frequency is increased in adenoid cystic carcinoma as compared to pleomorphic adenoma. In addition, monosomy of chromosome 17 could possibly be significant in salivary gland tumors.

Adenoma, Pleomorphic↗
PubMed2004

Myxolipomatous pleomorphic adenoma: an unusual oral presentation.

The first case of a myxoid variant of lipomatous pleomorphic adenoma arising in the intraoral minor salivary gland is presented. A well-encapsulated tumor was composed almost entirely of myxolipomatous tissue with honeycomb-like spindled cellular areas, which contained only a scant glandular element. Immunohistochemistry confirmed the myoepithelial nature of spindle cells intimately admixed with mucoadipose component. We propose the term myxolipomatous pleomorphic adenoma for this peculiar lesion.

Adenoma, Pleomorphic↗
PubMed2005

Maspin expression in carcinoma ex pleomorphic adenoma.

AIMS: To investigate the presence and distribution of the protein maspin in carcinoma ex pleomorphic adenoma (CXPA). METHODS: Maspin expression was studied by means of immunohistochemistry in 16 cases of CXPA, using the labelled polymer method. RESULTS: According to the extent of invasion, the tumours were subdivided into: intracapsular (five cases), minimally invasive (four cases), and invasive (seven cases). Twelve patients had carcinoma with only epithelial differentiation, whereas four had a malignant myoepithelial component. Non-luminal cells in the duct-like structures of the remnant pleomorphic adenoma were strongly positive for maspin, whereas only a few luminal cells were immunopositive. A few positive cells were seen in the frequent hypocellular and hyalinised areas. Maspin was abundantly expressed, mainly in non-luminal cells, in transitional areas of CXPA with only epithelial differentiation. In frankly carcinomatous areas there was a gradual decrease in maspin expression. Almost all cells were maspin positive in CXPA with a myoepithelial component. When present, luminal cells were in general negative for maspin. CONCLUSIONS: When only epithelial cells undergo malignant transformation, maspin expression is gradually lost. In cases with a myoepithelial component, maspin expression is high, and this might be related to the tumour suppressor activity attributed to this cell.

Adenocarcinoma↗
PubMed2006

Oncocytic change in pleomorphic adenoma: molecular evidence in support of an origin in neoplastic cells.

BACKGROUND: Cells with oncocytic change (OC) are a common finding in salivary glands (SGs) and in SG tumours. When found within pleomorphic adenomas (PAs), cells with OC may be perceived as evidence of malignancy, and lead to a misdiagnosis of carcinoma ex pleomorphic adenoma (CaExPa). AIM: To describe a case of PA with atypical OC, resembling a CaExPa. A genomewide molecular analysis was carried out to compare the molecular genetic features of the two components and to determine whether the oncocytic cells originated from PA cells, entrapped normal cells, or whether these cells constitute an independent tumour. MATERIALS AND METHODS: Representative blocks were immunohistochemically analysed with antibodies raised against cytokeratin (Ck) 5/6, Ck8/18, Ck14, vimentin, p63, alpha-smooth muscle actin (ASMA), S100 protein, anti-mitochondria antibody, beta-catenin, HER2, Ki67, p53 and epidermal growth factor receptor. Typical areas of PA and OC were microdissected and subjected to microarray-based comparative genomic hybridisation (aCGH). Chromogenic in situ hybridisation (CISH) was performed with in-house generated probes to validate the aCGH findings. RESULTS: PA cells showed the typical immunohistochemical profile, including positivity for Ck5/6, Ck8/18, Ck14, vimentin, ASMA, S100 protein, p63, epidermal growth factor receptor and beta-catenin, whereas oncocytic cells showed a luminal phenotype, expression of anti-mitochondria antibody and reduced beta-catenin staining. Both components showed low proliferation rates and lacked p53 reactivity. aCGH revealed a similar amplification in both components, mapping to 12q13.3-q21.1, which was further validated by CISH. No HER2 gene amplification or overexpression was observed. The foci of oncocytic metaplasia showed an additional low-level gain of 6p25.2-p21.31. CONCLUSION: The present data demonstrate that the bizarre atypical cells of the present case show evidence of clonality but no features of malignancy. In addition, owing to the presence of a similar genome amplification pattern in both components, it is proposed that at least in some cases, OC may originate from PA cells.

Adenoma, Pleomorphic↗
PubMed2006

Lymphatic vascular density and lymphangiogenesis during tumour progression of carcinoma ex pleomorphic adenoma.

AIMS: To assess lymphatic vascular density (LVD) and lymph vessel endothelial proliferation in a series of carcinoma ex pleomorphic adenoma (CXPA) that represents the tumour in the different carcinogenesis phases and tumour progression. METHODS: In 8 cases of early CXPA (intracapsular and minimally invasive tumours), 8 of advanced CXPA (widely invasive tumours) and 10 of pleomorphic adenoma (PA) without malignant transformation, lymphatic vessels and proliferating cells were detected using the antibodies D2-40 and Ki-67 respectively. RESULTS: Comparing early tumours with advanced ones, LVD was not significantly different at the tumour margin. In contrast, regarding intratumoural lymphatics, PA without malignant transformation and early CXPA contained rare, if any, lymph vessels, whereas in widely invasive carcinomas they were more numerous. However, neither intratumoural nor peritumoural LVD were increased in comparison to adjacent normal salivary gland tissue. In no case did dual immunohistochemistry using D2-40 and the cell proliferation marker Ki-67 reveal the existence of proliferating lymphatics. Carcinomatous emboli were found in peritumoural as well as in intratumoural lymphatics only in advanced CXPA without myoepithelial differentiation. CONCLUSION: In CXPA, the lymphatic network is mainly composed of pre-existing lymphatics which are rare in tumours that have not infiltrated outside the confines of the original PA. In the widely invasive CXPA, intratumoural as well as peritumoural lymphatics are a conduit for carcinoma cells, but in carcinomas with myoepithelial differentiation, the neoplastic cells seem to have a lower invasion capacity.

Adenoma, Pleomorphic↗
PubMed1994

Simultaneous bilateral pleomorphic adenomas of the parotid glands with unilateral tyrosine rich crystalloids.

A case of simultaneous, bilateral pleomorphic adenoma of the parotid glands following irradiation to the head and neck for childhood Hodgkin's disease is presented. The tumour on the side given the highest radiation exposure contained so-called tyrosine rich crystalloids (TRCs). Simultaneous salivary gland neoplasms are rare; TRCs are also an unusual finding. Simultaneous pleomorphic adenomas with TRCs confined to one tumour have never been described, and any association between TRCs and irradiation has never been commented on. The precise nature of the TRCs remains obscure. Their unilateral distribution in this case supports the hypothesis that local factors are more important in their formation than systemic factors. In conjunction with other published work, this provides circumstantial evidence that irradiation may predispose to TRC deposition.

Adenoma, Pleomorphic↗
PubMed1991

Pleomorphic adenoma of the parotid gland.

A case of pleomorphic adenoma arising from the deep lobe of the parotid gland is presented. Controversy often surrounds the management of a parotid lump, and many investigations are of little help. The first operation cures most salivary tumours and the patient usually has no residual disability. There is no place for the use of radiotherapy, in the treatment of pleomorphic adenoma.

Adenoma, Pleomorphic↗