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Biomedical subjects

J W Eveson

Publications and source records attributed to J W Eveson.

At least 19 recordsLinked to original sources
PubMed2002

Parotid Warthin's tumour Bristol Royal Infirmary (1985-1995): a study of histopathology in 33 cases.

This is a study of 33 (32 patients) confirmed Warthin's tumours (adenolymphomas) treated surgically at Bristol Royal Infirmary (1985--1995) focussing specifically upon 17 salient histopathological features together with capsular measurement by micrometry. Twenty-four out of 33 tumours had 'thin' capsules (< or = 200 microm), whereas 5/9 'thick' capsules were associated with gross tumour degeneration. The degenerative features including cystic change, squamous metaplasia, corpora amylacea like bodies, etc. were quantified. Tumours were classified into subtypes (typical, stroma poor, etc). These variations were not associated with age or sex. In 20/33 tumours a marginal sinus suggested a lymph node origin. Fine needle aspiration cytology (FNA) smears showing degeneration features are a diagnostic problem, but histopathological features are reflected in such smears and their recognition enhances diagnostic precision, enabling controlled surgical enucleation, the ideal operation, to be performed in most cases. In this study only 12 tumours were so treated; 11 others received parotidectomy. The theories of histogenesis are reviewed and discussed.

Adenolymphoma↗
PubMed2001

Overexpression of JunB in undifferentiated malignant rat oral keratinocytes enhances the malignant phenotype in vitro without altering cellular differentiation.

Our study examined the expression of AP-1 family members in keratinocytes derived from the rat-4NQO model of oral carcinogenesis in which extremes of epithelial differentiation and tumour cell aggressiveness are evident. The constitutive expression of JunB was diminished in the undifferentiated, more aggressive tumour phenotype compared with the well-differentiated, less aggressive keratinocytes, whereas the expression of other AP-1 family members (c-jun, junD, c-fos, fra1, fra2 and fosB) was either very weak or variable. After transfection of the undifferentiated keratinocytes with junB cDNA, clonal populations were isolated that expressed similar levels of JunB protein as the well-differentiated cells. Both untransfected and transfected cell lines were keratin negative and vimentin positive. Increased expression of JunB in the transfected cells resulted in up-regulation of c-Jun and Fra1 and an enhanced AP-1 activity as demonstrated by transcriptional activation of the prototypic AP-1 dependent promoter, MMP-1. JunB transfected cells grew more quickly than vector-only controls and were refractory to the growth inhibitory effects of TGF-beta1. Over-expression of JunB resulted in the elevated expression of the AP-1 dependent proteinase, MMP-9, whereas the expression of the AP-1 independent enzyme, MMP-2, was unaffected. JunB transfected keratinocytes were highly invasive in an in vitro assay of tumour cell invasion compared with vector controls. The results indicate that increased expression of JunB above baseline levels in undifferentiated rat keratinocytes does not alter epithelial differentiation but enhances the malignant phenotype in vitro, possibly by altering the dynamics of the AP-1 complex.

3T3 Cells↗
PubMed2001

Pleomorphic adenomas of the major salivary glands: a study of the capsular form in relation to surgical management.

This was a retrospective study of 126 primary pleomorphic adenomas to correlate capsular characteristics with tumour histopathology in relation to current surgical debate (parotidectomy versus local excision). Capsular thickness was measured by micrometry and tumours classified into subtypes (1-4). Evidence of fine needle aspiration damage (needle tracks, infarction) was sought. Minimal changes were seen in eight tumours. Tumour growth features (bosselations, enveloping) were present in 57% and 33%, respectively, also microinvasion (42%) and tumour 'buds' (12%). Parotid lesions possessed thicker capsules than submandibular tumours. There was little correlation between capsular thickness and cellular structure. The significant exception was large (> 25 mm) hypocellular parotid tumours which had thinner capsules and could be vulnerable to operative rupture. In 110 standard operations (parotidectomy, submandibular gland excision), capsular exposure was evident in 81%. Field irrigation is recommended to lessen the risk of tumour seeding. This study reaffirms many elements of capsular weakness and suggests that parotidectomy is the operation of choice.

Adenoma, Pleomorphic↗
PubMed2000

Oral mucosal non-Hodgkin's lymphoma--a dangerous mimic.

Reports of T-cell lymphomas in the oral cavity are rare. Most have presented as a persisting ulcerated swelling. This paper reports two men, one of whom presented with a short history of increasing facial swelling and pain apparently related to a lower premolar tooth, and the other who had recurrent oral ulceration in several sites over a period of years. These types of cases are likely to present initially to general dental practitioners.

Aged↗
PubMed2000

Endogenous TGF-beta1 inhibits the growth and metastatic dissemination of rat oral carcinoma cell lines but enhances local bone resorption.

This study examined the effect of stable transfection of latent transforming growth factor-beta1 (TGF-beta1) cDNA into a predominantly polygonal, 4 nitroquinoline N-oxide (4NQO)-induced rat oral keratinocyte cell line. Seven polygonal and five spindle clonal populations were isolated that overexpressed TGF-beta1 protein by approximately two- to four-fold compared to vector-only transfected controls. Neutralisation experiments indicated that the majority of protein was in the latent form. There was no change in the proportion of polygonal and spindle cells in vitro after transfection with TGF-beta1 cDNA. Polygonal and spindle cells that overexpressed TGF-beta1 produced similar amounts of protein and grew more slowly in vitro than controls. The parent cell line and all transfected cells were growth inhibited (60-75%) by exogenous TGF-beta1. Orthotopic transplantation of the parent and the vector-only control cell lines resulted in primary tumours in the floor of the mouth in almost 100% (20/21) of athymic mice, with no evidence of bone resorption at the site of the primary tumour and pulmonary metastatic tumour deposits in some 40% (7/20) of these animals. The polygonal and spindle cells that overexpressed TGF-beta1 behaved similarly following orthotopic transplantation. A 96% (23/24) primary tumour take was evident following transplantation of cells that overexpressed TGF-beta1, with a significantly (P<0.02) higher number of animals showing bone resorption at the site of the primary tumour (35%; 8/23) compared to controls. By contrast, there was a significant (P<0.03) decrease in the number of animals with pulmonary metastases (4%; 1/23) following transplantation of TGF-beta1 overexpressing cells compared to controls. Overexpression of TGF-beta1 did not alter tumour cell differentiation in vivo. The results demonstrate that endogenous TGF-beta1 functions as a tumour suppressor in the rat-4NQO model of oral carcinogenesis without altering tumour cell morphology or differentiation but can also act to promote local bone resorption.

Animals↗
PubMed1999

Salivary duct carcinoma in five cats.

Carcinomas of salivary gland ducts are described in five cats. The typical histological pattern was the formation of large cell aggregates resembling dilated ducts, often with central necrosis and a looping pattern. All tumours were labelled with antibody to cytokeratins (CKs) 5, 6, 8, 14, 17 and 19. Labelling of tumour cells with CK14 suggested basal cell differentiation. All tumours stained with Jack bean (Canavalia ensiformis) agglutinin (Con A); this is a feature of normal salivary gland ducts but is seen in other salivary gland tumours. Staining of tumour cells at the luminal surface of ductal structures with wheat germ (Triticum vulgaris) agglutinin (WGA) in the cat tumours was similar to that seen in ducts of normal cat salivary glands but occurs in other cat tumours. Other immunohistochemical staining results were unremarkable. 1999 Harcourt Publishers Ltd.

Adenocarcinoma↗
PubMed1999

Loss of differentiation of 4NQO-induced rat malignant oral keratinocytes correlates with metastatic dissemination and is associated with a reduced cellular response to TGF-beta1 and an altered receptor profile.

This study examined the metastatic capacity of clonal populations of 4NQO-induced rat malignant oral keratinocytes following orthotopic transplantation to athymic mice. Polygonal and spindle cells formed well-differentiated squamous cell carcinomas (keratin positive and vimentin negative) and undifferentiated spindle cell tumours (keratin negative and vimentin positive), respectively, in almost 100% of animals at the site of inoculation (floor of mouth). Transplantation of 5x 10(6) cells of either cell type at high cell density resulted in approximately 50% of animals forming pulmonary metastases. By contrast, inoculation of 2x 10(6) differentiated polygonal cells resulted in the formation of significantly fewer pulmonary metastases than the undifferentiated spindle cells. A single well-differentiated clone of polygonal cells and 3 of 4 of the undifferentiated spindle cell lines produced comparable levels of TGF-beta1. One undifferentiated spindle cell line expressed significantly more TGF-beta1 and, following transplantation orthotopically, fewer animals formed pulmonary metastases despite the formation of primary tumours in almost all grafted animals, suggesting that TGF-beta1 can act as a tumour suppressor in this cell type. All cell lines produced comparable amounts of TGF-beta2. The clones of polygonal cells were markedly inhibited and the spindle cells were only partially inhibited by exogenous TGF-beta1. Both cell types expressed high-affinity TGF-beta cell surface receptors; the ratio of type I to type II TGF-beta receptors was 1.0:<3.0 in the spindle cells and 1.0:17.9 in the polygonal clone. The results suggest that differentiated rat malignant oral keratinocytes are less aggressive and have a decreased potential to metastasise than their undifferentiated spindle cell counterparts. This may be attributable, in part, to a change in TGF-beta receptor profile leading to the partial loss of response to exogenous TGF-beta1.

4-Nitroquinoline-1-oxide↗
PubMed1999

Adenosquamous carcinoma of the mouth: a rare variant of squamous cell carcinoma.

Adenosquamous carcinoma is a rare tumour in the oral cavity and is characterised histologically by carcinomatous change in surface epithelium, in association with adenocarcinoma affecting the ducts of minor salivary glands. Only a dozen cases have previously been reported in the oral cavity, but all have shown an aggressive course with 60% of patients dying of disease. We report three further cases and review the literature, which suggests that this lesion should be regarded as a high-grade variant of squamous cell carcinoma.

Aged↗
PubMed1998

Langerhans cell histiocytosis presenting as bilateral eosinophilic granulomata in the molar region of the mandible. A case report.

Eosinophilic granuloma represents one of a triad of lesions encompassing a disease under the generic name, histiocytosis X or Langerhans cell histiocytosis. Localised eosinophilic granuloma, multifocal eosinophilic granuloma, Hand-Schüller-Christian disease, and the most malignant form of histiocytosis, Letterer-Siwe disease, can all present as destructive bony lesions of the jaws. The present case was a 30-year-old man who presented with almost total destruction of the periodontal support to the left and right mandibular, 1st and 2nd molars. Whereas the radiographic features were typical of eosinophilic granuloma, the clinical appearance and mirror image presentation were unusual.

Adult↗
PubMed1997

Overexpression of autocrine TGF-beta 1 suppresses the growth of spindle epithelial cells in vitro and in vivo in the rat 4NQO model of oral carcinogenesis.

We examined the effect of the stable transfection of latent TGF-beta 1 cDNA, under the control of a cytomegalovirus promoter in the expression vector pcDNA3, into a 4NQO-induced clonal rat oral keratinocyte cell line that formed undifferentiated spindle cell tumours following subcutaneous transplantation to athymic mice. Test cells containing latent TGF-beta 1 cDNA produced a 2.3-fold increase in TGF-beta 1 protein compared to pcDNA3 controls as demonstrated by ELISA. Neutralisation experiments indicated that the majority of the protein was in the latent form. Untransfected and transfected (containing either TGF-beta 1 cDNA or pcDNA3) cell lines were keratin negative and vimentin positive. Cells transfected with TGF-beta 1 were inhibited more than pcDNA3 controls when cultured in an anchorage dependent or independent environment. Subcutaneous transplantation of cells overproducing TGF-beta 1 resulted in tumours of significantly smaller volume than vector-only controls. Further, orthotopic transplantation of cells containing TGF-beta 1 cDNA to the floor of the mouth in athymic mice markedly inhibited the development of pulmonary metastases compared to vector-only controls. Both test and control cell lines in athymic mice formed undifferentiated tumours with a complete absence of keratin elaboration. Subcutaneous xenografts were recultured and cells containing the TGF-beta 1 cDNA produced a similar amount of TGF-beta 1 peptide as the cells containing pcDNA3 only. The production of TGF-beta 1 by both of the xenograft-derived cell lines was significantly less than the parent, pre-transplanted cell lines and the untransfected cell line. All of the cell lines were inhibited by exogenous TGF-beta 1. Our results demonstrate that autocrine TGF-beta 1 functions as a tumour suppressor in vitro and in vivo in 4NQO-induced spindle tumour cells that are growth inhibited by the ligand. Furthermore, tumour formation in athymic mice is associated with selection for a cell phenotype with diminished autocrine TGF-beta 1 production.

4-Nitroquinoline-1-oxide↗
PubMed1997

Early genetic and functional events in the pathogenesis of oral cancer.

Oral squamous cell carcinoma (SCC) is a major world health problem, but the changes leading to the development of malignancy remain essentially unknown. Early changes are thought to include the loss of tumour suppressor genes on chromosomes 3p, 9p, and 17p. Although what genes are involved on chromosome 3 remains speculative, p16 (9p21) and p53 (17p13) are inactivated in a high proportion of oral dysplastic lesions and carcinomas. SCC-derived cell lines are immortal, have decreased growth requirements in vitro, and show a variable capacity to form tumours in athymic mice. Normal oral keratinocytes and cells from potentially malignant lesions invariably senesce at early culture passage, have strict growth requirements in vitro, and are nontumorigenic in vivo. By contrast to normal oral keratinocytes, cells from potentially malignant lesions are defective in their capacity to terminally differentiate in suspension culture. Loss of cellular senescence and gain of the immortal phenotype is associated with inactivation of p16 and p53.

Animals↗
PubMed1997

Adenoid cystic carcinoma of the sublingual salivary gland in a 16-year-old female--report of a case and review of the literature.

Tumours of the sublingual salivary gland are exceptionally rare. The present case report describes an adenoid cystic carcinoma of the sublingual salivary gland occurring in a 16-year-old girl, in itself an uncommon event. In addition, an interesting feature of the presentation was obstruction of the ipsilateral submandibular gland due to involvement of Wharton's duct.

Adolescent↗
PubMed1996

Molecular changes in oral cancer may reflect aetiology and ethnic origin.

Oral cancer, although uncommon in the Western world, accounts for up to 40% of all malignancies in parts of India and South East Asia. Recognised aetiological agents of oral cancer include tobacco and alcohol. This paper reviews the spectrum of molecular changes found in oral squamous cell carcinomas from Western (U.K., U.S.A., Australia) and Eastern (India, S.E. Asia) countries. p53 mutations are common in tumours from the West (47%) but are infrequent in the East (7%). Tumours from India and South East Asia are characterised by the involvement of ras oncogenes, including mutation, loss of heterozygosity (H-ras) and amplification (K- and N-ras), events which are uncommon in the West. The possibility that these genetic differences reflect aetiology and/or ethnic origin is discussed.

Carcinoma, Squamous Cell↗
PubMed1996

Polymorphous low-grade adenocarcinoma of parotid gland.

A case of polymorphous low-grade adenocarcinoma arising within the parotid gland is described. This appears to be only the second case of this distinctive neoplasm to have arisen ab initio within a major salivary gland. It displayed the relatively indolent course associated with this adenocarcinoma subtype and emphasises that this diagnosis now has to be considered in tumours of major salivary glands.

Adenocarcinoma↗
PubMed1996

Granulomatous disorders of the oral mucosa.

A wide variety of granulomatous disorders can involve the orofacial tissues. As in other sites, appropriate clinicopathologic correlations are needed to reach a definitive diagnosis. The clinical and pathologic features of some of the more common oral granulomatous disorders are considered, including idiopathic conditions, foreign body lesions, and infectious lesions.

Crohn Disease↗
PubMed1995

Munchausen's syndrome: oral presentations.

Munchausen's syndrome is a rare psychiatric disorder in which patients repeatedly confabulate so as to cause unnecessary investigations and operative treatments to be carried out on them. Two cases are reported and the literature reviewed. The first patient complained of repeated dental pain and subsequently underwent repeated endodontic treatment; the second had salivary gland pain and glossopharyngeal neuralgia. Munchausen's syndrome can only be diagnosed by the exclusion of organic and other disease.

Adult↗
PubMed1995

Loss of expression of basement membrane proteins reflects anomalies of chromosomes 3 and 12 in the rat 4-nitroquinoline-N-oxide model of oral carcinogenesis.

This study examined the cytogenetic characteristics of keratinocyte cell lines derived from rat oral tissues treated in vivo with the carcinogen 4-nitroquinoline-N-oxide. A parent tumour with a spectrum of differentiation was used to establish clonal subpopulations that formed differentiated (squamous cell carcinomas; SCCs) and undifferentiated (spindle cell phenotype) tumours following transplantation to athymic mice. By contrast to spindle cell tumours, SCCs elaborated basement membrane proteins (laminin and collagen IV). Both diploid and tetraploid subpopulations formed either SCCs or spindle cell tumours. An unbalanced 10q+ translocation was common to all cell lines. Anomalies of chromosomes 3 and 12 (gain, loss, deletions, translocations) were present only in cell lines that formed spindle cell tumours and were absent in keratinocytes forming SCCs. The results suggest that proto-oncogenes and/or tumour suppression genes located to rat chromosomes 3 and 12 may control tumour cell differentiation.

3T3 Cells↗