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Unilateral multiple adenolymphomas originating in the parotid gland: a clinicopathological study.

The validity of Seifert's hypothesis about growth pattern of adenolymphomas has been evaluated in three of five patients with adenolymphomas of the parotid gland, who at the time of a parotidectomy, were found to have multiple unilateral adenolymphomas in the intraglandular lymph nodes. This evaluation, which was based on assessing the epithelial: lymphoid tissue ratio in excised adenolymphomas and the growth in tumor size, showed that there was no association between the histological changes in the epithelial:lymphoid tissue and the tumor size. Adenolymphomas seem to have no consistent growth pattern and develop independently. However, as multiple tumors were detected histopathologically in lymph nodes as small as 5 mm in diameter the importance of a detailed examination of patients with adenolymphomas is stressed, so that other tumours are not overlooked.

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Smoking predisposes to parotid adenolymphoma.

Of 574 patients with previously untreated, unremarkable parotid lumps, 194 proved to have pleomorphic adenomas and 73 adenolymphomas. ABO blood group details were available in 59 and 85 per cent of patients respectively. Smoking details were available in 84 per cent of a randomly chosen 46 per cent subgroup of patients with pleomorphic adenomas and in 86 per cent of all those with adenolymphomas. The incidences of smoking and of the ABO blood groups in these two diagnoses were compared with standard sources. There was no evidence that either histological diagnosis of parotid tumours was linked to an abnormal pattern of ABO blood groups. However, there was a much greater incidence of smoking among the adenolymphoma than in the pleomorphic adenoma group: only one of 63 patients with adenolymphoma as opposed to 31 of 75 with pleomorphic adenoma had never smoked, while the mean number of cigarettes smoked by each patient with an adenolymphoma was estimated to be 300,000 as opposed to 80,000 for those with pleomorphic adenoma.

ABO Blood-Group System↗

Difference of immunohistochemical reactions in epithelial cells of adenolymphoma.

An immunoperoxidase staining technique was used for detecting alpha one-antichymotrypsin (alpha 1-ACT), alpha one-antitrypsin (alpha 1-AT), lactoferrin and transferrin in routine histological paraffin sections of 30 adenolymphomas, as well as in normal salivary gland tissue. Microscopically, the epithelial, component of adenolymphomas consisted of tall columnar luminal cells and irregularly shaped basal cells. alpha 1-ACT was detected in the luminal layer of epithelium in 27 (90%) of 30 adenolymphomas, while the basal layer was positive in 4 cases (13%). Lactoferrin could be observed in the columnar cells of 21 cases (70%) and was positive in the basal cells of 2 cases (7%). In normal salivary gland tissue, alpha 1-ACT and lactoferrin were observed in the intercalated duct and serous acinar cells. The staining pattern of alpha 1-AT in adenolymphoma was similar to those of alpha 1-ACT and lactoferrin, however, the number of positive cases for alpha 1-AT was fewer than in the alpha 1-ACT and lactoferrin. alpha 1-AT was not found in the normal salivary gland. On the contrary, the localization of transferrin in the epithelial component of adenolymphomas was exclusively different from those of alpha 1-ACT, alpha 1-AT and lactoferrin. Transferrin was found more often in the basal cells than in the tall columnar apical cells. The staining pattern of transferrin in the normal salivary gland was different from alpha 1-ACT and lactoferrin, and transferrin was positive in the cytoplasm of intercalated ducts, serous acinar and myoepithelial cells.(ABSTRACT TRUNCATED AT 250 WORDS)

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[The mechanism of positive scintigraphy with 99mTc-pertechnetate in adenolymphomas of the parotid grand].

In order to clarify the mechanism of positive scintigraphy with Tc pertechnetate in adenolymphomas of the parotid gland, 10 cases of adenolymphoma were studied morphologically and from a functional view point. Salivary tissue obtained from normal parotid glands were also investigated for comparison with the tumor. In morphological studies, rapid tissue fixation by microwave irradiation produced very good results for examining mitochondria by high resolution light microscopy. A number of mitochondria were found both in the epithelial cells of adenolymphoma and in the striated duct cells of the parotid gland. In functional studies, the one-step method of enzymatic histochemistry was used for detecting Na-K ATPase. Na-K ATPase was found on the baso-lateral side of the epithelial cells of adenolymphoma and the striated duct cells of the parotid gland, and this activity of Na-K ATPase may enhance the accumulation of Tc pertechnetate in these cells. These observations may provide evidence for the bi-cellular theory which indicates that adenolymphoma originated from immature intercalated duct reserve cells.

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[Immunohistological investigation of epithelial components of adenolymphoma of the parotid gland].

In order to develop a more objective method of evaluating the origin of adenolymphoma, we immunohistochemically investigated the expression of cytokeratins, vimentin, S-100 protein, and alpha-smooth-muscle actin using the avidin-biotin-peroxidase (ABC) method in ethanol-fixed paraffin-embedded specimens from 8 adenolymphomas. Several kinds of monoclonal antibodies which react monospecifically with each subclass of cytokeratins were used. Results were compared with specimens of 8 normal parotid glands by radical neck dissection in patients with other diseases who had not undergone radiotherapy. In the adenolymphoma specimens, basal cells were strongly positive for CK-6, but reactivity of columnar cells was apparently reduced. In contrast, columnar cells were strongly positive for CK-7, but reactivity of basal cells was reduced. In normal parotid gland specimens, CK-7 was also detected in all columnar cells in the ductal system, although some duct cells around the columnar cells, which showed strong CK-6 expression, showed poor CK-7 expression. alpha-smooth-muscle actin was present in myoepithelial cells in normal parotid gland specimens, but not in basal cells of adenolymphoma or of the normal ductal system, which were CK-6-positive. As these characteristic findings were consistently observed in all specimens, the demonstration of CK-6, CK-7, and alpha-smooth-muscle actin may be useful in the recognition and classification of columnar and basal cells. CK-8 was present in both columnar and basal cells of adenolymphoma and of the normal duct, but in the normal parotid gland, acinus cells were also strongly positive for CK-8.(ABSTRACT TRUNCATED AT 250 WORDS)

Actins↗

[Adenolymphoma and microadenolymphoma. Histomorphogenetic considerations].

Histomorphogenetic considerations. Seventy three consecutive cases of parotid adenolymphoma were studied. Clinical data (age, sex, site, diagnostic hypothesis, type of surgery), macroscopy (examination of all nodules associated with adenolymphoma and related topography), microscopy (morphological analysis by means of conventional stainings, histochemistry, immunohistochemistry, semiquantitative and morphometric evaluations), with special regard to the lymphoid stroma, were correlated in order to investigate histo-morphogenetic aspects. In 44 cases, lymph nodes were detected (156:83 intraparotid and 73 periparotid). In 18 cases the adenolymphoma resulted multifocal. In 14 of them multifocality was due to the presence of only microscopic (clinically unsuspected) additional adenomas in intraparotid lymph nodes (20 microadenolymphomas). A further microadenolymphoma with 6 associated lymph nodes was occasional finding in a case of sialadenitis. Inclusions of salivary epithelium were observed in 46 intraparotid lymph nodes, were metaplastic (different types of metaplasia) in 23 of them, and were associated with 16 microadenolymphomas. Inclusions and microadenomas were both absent in periparotid lymph nodes. This study strongly supports the intralymphonodal histogenesis of the adenolymphoma and emphasizes the role of the ductal metaplastic changes of the salivary inclusions in the development of the adenomatous proliferation. A model of morphogenetic evolution (with related diagnostic problems) from intralymphonodal inclusions to microadenolymphoma and successively to clinical tumour (macroadenolymphoma) is proposed on the basis of the sequential rearrangement of the various morphological and morphofunctional observations. With special reference to the characteristics of the lymphoid stroma, a minor role of specific immunological mechanisms in the etiopathogenesis of the adenolymphoma is suggested.

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Adenolymphoma of the parotid: aetiology, diagnosis and treatment.

In order to study the changing clinical pattern, diagnosis and surgical treatment of adenolymphoma, the records of all 57 patients with a confirmed histological diagnosis, made at Bristol Royal Infirmary between 1951 and 1984, were reviewed; in 3 patients (5 per cent) bilateral lesions had been found. No characteristics emerged in a review of the history and clinical examination which would have enabled a correct preoperative diagnosis to be made. During the period of study the incidence of adenolymphoma increased 24-fold. (Parotid pleomorphic salivary adenomas increased in incidence by only 42 per cent over the same period). Before 1965 all patients were men; between 1965 and 1975 the male to female ratio was 3:1; between 1975 and 1985, 1.6:1. Of the 48 patients who had a relevant history taken 45 were smokers (93.8 per cent). It is postulated that tobacco consumption is important in the development of adenolymphoma, and has produced the changes in incidence and sex ratio. Fine needle aspiration biopsy cytology (FNAB) afforded the only method of achieving a pre-operative diagnosis. This was successful in 64.7 per cent. Superficial parotidectomy induced a 43 per cent incidence of facial nerve neurapraxia. Controlled enucleation reduced this to 8 per cent. Enucleation is the procedure of choice for adenolymphoma but can only be employed with confidence if an exact pre-operative diagnosis is made.

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Malignant adenolymphoma.

Adenolymphoma (Warthin's tumor) is a well studied benign tumor of the salivary gland. Malignant transformation of such a tumor is rare and not well documented in the literature. The light microscopic and ultrastructural features of an undifferentiated carcinoma arising in an adenolymphoma in the parotid gland of a middle aged male are described, and the relevant literature is reviewed. Similarities between the benign adenolymphoma and the undifferentiated malignant tumor, such as the presence of interstitial lymphoplasmacytic cell infiltrates, dark and light epithelial cells, similar cytoplasmic organelles, and nuclear morphology, suggest a malignant transformation of a previously existing benign adenolymphoma.

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Heterogeneity of keratin expression in epithelial tumor cells of adenolymphoma in paraffin sections.

Immunohistochemical expressions of keratin polypeptides detected by monoclonal antibodies were described in tumor cells of adenolymphoma, and the possibility of intercalated duct and ductal basal cells in the salivary glands being the progenitors was discussed. Basal cells in the tumor showed positive staining for keratin nos. 8, 13, 16, 18 and 19 detecting for monoclonal keratin antibodies (PKK 1, K 4.62, K 8.12, K 8.13), columnar tumor cells displayed strongly positive reactions with RPN 1164 and K4.62 suggesting keratin nos. 8 and 19. Great heterogeneity of distribution for keratin polypeptides was displayed by epithelial cells of adenolymphoma. Intercalated duct cells of normal salivary glands reacted with RPN 1164, RPN 1165, K 4.62 and K 8.13 monoclonal antibodies, which indicates the presence of keratins 8 and 19; and ductal basal cells reacted with PKK 1, K 4.62 and K 8.12, suggesting nos. 8, 13, 16, 18 and 19 keratins. Distribution of involucrin was variable in tumor epithelium of adenolymphoma, and was negative in the normal gland. The immunohistochemical distribution of keratin types between basal tumor cells of adenolymphoma and ductal basal cells of the normal salivary gland was compared.

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Adenolymphoma and non-Hodgkin's lymphoma of the salivary glands and oral cavity in immunocompetent patients are not associated with latent Epstein-Barr virus.

The presence of Epstein-Barr virus (EBV) was studied in specimens of 50 primary non-Hodgkin's lymphomas (NHL) of the salivary gland and the oral cavity and 11 solitary adenolymphomas of the parotid gland, using EBER-1/2 in situ hybridisation and by immunohistochemistry for the detection of latent membrane-protein-1 (LMP-1). None of the patients were tested for HIV-infection, nor were there any clinical signs to suspect HIV-infection. In one adenolymphoma, few reactive EBER-1/2 positive cells were detected. In this case staining for LMP-1 was negative. In one oral B-cell NHL, EBER-1/2 positive lymphoma cells were identified; these cells also expressed LMP-1. None of the 31 oral (30 B-cell and one T-cell) and 18 salivary gland (all B-cell) NHLs and none of the 10 adenolymphomas were EBER-1/2 positive or expressed LMP-1. These results indicate that EBV is not involved in the pathogenesis of oral and salivary gland primary NHL and adenolymphoma in immunocompetent patients.

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Multifocal nature of adenolymphoma of the parotid.

The multifocal nature of adenolymphoma of the parotid salivary gland was studied in 24 patients who underwent parotidectomy. Twenty-six resected specimens were examined by a step-serial whole-organ sectioning technique; multiple adenolymphoma was found in 13. The maximum number of synchronous tumours in any gland was four. Salivary epithelial elements were found embedded within lymph nodes in nine resected specimens. Synchronous or metachronous bilateral tumours were found in eight patients. The multifocal nature of adenolymphoma of the parotid gland is demonstrated.

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[Adenolymphoma of parotid gland--analysis of 75 cases].

The authors present a clinical analysis of the group of 75 patients, who was treated in Department of Otolaryngology in the years 1986-2000 and who was diagnosed as adenolymphoma. The frequency of incidence of Warthin's tumour is 17,6% of all 426 cases of parotid gland's tumours. In 72 cases (96%) the tumour was localized in the superficial part, only in 3 cases (4%)--in the deep part of the gland. In one patient we observed recurrence of adenolymphoma. In one case adenolymphoma coexisted with carcinoma planoepitheliale of parotid gland.

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Squamous cell carcinoma arising in benign adenolymphoma (Warthin's tumor) of the parotid gland.

Adenolymphoma of the parotid gland is a benign tumor occurring primarily in middle-aged males. Major texts of surgery and pathology state that this tumor is not malignant nor does it undergo malignant degeneration. This report demonstrates squamous cell carcinoma arising in a parotid adenolymphoma in a patient with no other malignancy or previous irradiation to the head and neck.

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Pleomorphic adenomas, adenoid cystic carcinomas and adenolymphomas of salivary glands analysed by a monoclonal antibody against myoepithelial/basal cells. An immunohistochemical study.

Myoepithelial and basal cells were identified by a monoclonal antibody raised against keratin. This antibody (CK B1) which detects myoepithelial cells in normal salivary glands, labels spindle shaped and polygonal cells in pleomorphic adenomas. Most cells in adenoid cystic carcinomas and some basal cells in adenolymphomas were also positive for this antibody. The oncocytic epithelium of adenolymphoma was negative. An inverse reaction was seen with an antibody against cytokeratin 18. The antibody CK B1 seems to be of interest for the detection of myoepithelial/basal cells in salivary glands and salivary gland tumours.

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Adhesion molecules and lymphocyte recruitment in lymphocytic thyroiditis, thyroid papillary carcinoma and parotid adenolymphoma.

Lymphocytic infiltrates are usually present in chronic lymphocytic thyroiditis, thyroid papillary carcinoma and parotid adenolymphoma. We selected these conditions to investigate the mechanisms of recruitment and organization of lymphocytic infiltrates in extranodal tissues. MoAbs in immunoperoxidase were used to identify the expression of ICAM-1 and VCAM-1 on endothelial cells (EC), and of their ligands LFA-1 and VLA-4 on lymphocytes and accessory cells. VCAM-1 positive EC were rarely observed in thyroids devoid of lymphocyte infiltration. Conversely, EC in chronic lymphocytic thyroiditis and in papillary carcinoma showed positive immunostaining for VCAM-1 and ICAM-1. These findings were associated with the presence of lymphocytes positive for the ligands VLA-4 and LFA-1. The upregulated expression of VCAM-1 on perifollicular capillaries was co-distributed with an accumulation of VLA-4 positive lymphocytes. In adenolymphoma, all EC were ICAM-1 positive, whereas the majority of vessels were VCAM-1 negative. Consequently the majority of lymphoid cells were LFA-1 positive and VLA-4 negative. We suggest that ICAM-1 and VCAM-1 expression on EC play a role in the recruitment of lymphocyte infiltration in chronic lymphocytic thyroiditis and papillary carcinoma. Furthermore, the upregulation of VCAM-1 and VLA-4 in thyroid reactive and neoplastic conditions may be linked to an immune response possibly related to thyroid tissue antigens.

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