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Query: UMLS:C0001430 (adenoma)
 21,222 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The histopathological diagnosis of minimal deviation adenocarcinoma (adenoma malignum) of the endocervix may be difficult. Two cases of minimal deviation adenocarcinoma (MDA) were examined using mucin histochemistry and immunocytochemistry with antibodies to epithelial membrane antigens (HMFG1, Ep1), low-molecular-weight cytokeratins (CAM 5.2), carcinoembryonic antigen (CEA), and alpha-amylase. The results were compared with those for normal endocervical glands. Reactivity for CEA in MDA was focal and would be unreliable for biopsy diagnosis. Both cases of MDA contained abundant neutral mucins and sialomucins, whereas sulfomucins were rarely detected; this pattern contrasted with that of normal endocervix. Neoplastic glandular epithelial cells in MDA consistently showed both luminal and cytoplasmic reactivity with Ep1 and HMFG1, whereas normal cervix showed luminal labeling only. Thus, mucin histochemistry and immunohistochemical detection of epithelial membrane antigens may distinguish between extremely well differentiated neoplastic glands in MDA and normal endocervical glands, and hence may aid diagnosis in biopsy specimens.
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PMID:Minimal deviation adenocarcinoma (adenoma malignum) of the endocervix: a histochemical and immunohistochemical study of two cases. 168 43

To study coexpression patterns in normal and adenomatous pituitaries, frozen (n = 4) and paraffin-embedded (n = 10), normal human glands and 34 pituitary adenomas were investigated, using immunoperoxidase and double-labeling immunofluorescence methods. Broad range monoclonal antibodies (mAB) against cytokeratins (CK) (lu-5, A45-B/B3, AE1/3, CAM 5.2) as well as anti-CK18 (DC10) and anti CK19 (A53-B/A2) were compared with mAB's against vimentin, epithelial membrane antigen (EMA), epithelial sialomucin (ESM 140 C1), GFAP (GF-2), neurofilament (2F11), Leu-7 (HNK-1) and polyclonal AB's against pituitary hormones (ACTH, FSH, LH, TSH, GH, PRL). CK and vimentin coexpressing endocrine cells, mainly of the ACTH type, were observed in the pars intermedia in 5 of 14 normal pituitaries. All hormone producing cells expressed CK. The mAB A53-B/A2 (CK19) stained selectively the folliculo-stellate cells in frozen and paraffin sections. EMA, sialomucin and Leu-7 antigen localized to different structures of normal pituitaries. 25 of 34 pituitary adenomas exhibited CK positive tumor cells. Coexpression of vimentin or neurofilament protein was rare (2 cases of each). 9 CK negative adenomas were also negative for other intermediate filament proteins. 6 hormone producing adenomas showed unusual positivity for CK19. Whereas EMA and sialomucin reactivity disappeared in adenoma tissues, an enhanced Leu-7 antigen expression in the GH and prolactin adenoma group was noted. The heterogeneity of antigen expression seen in normal and neoplastic pituitary cells calls for further functional studies and usage of a broad range of mAB's against intermediate filaments in immunohistochemical studies of the pituitary.
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PMID:Immunohistochemical studies on human pituitary gland and adenomas. 182 19

Following the diagnosis of nephrogenic adenoma in a bladder lesion, which was later interpreted as early clear cell adenocarcinoma, the morphological and immunocytochemical features of these two lesions were reviewed to see if differences could be established for future diagnostic application. The architecture, extent, cell type, nuclear pleomorphism, presence of mitotic figures and glycogen content were recorded in 28 nephrogenic adenomas and the clear cell carcinoma. Similarly, the immunoreactivity for CAM 5.2, LP34, EMA and CEA of 10 nephrogenic adenomas and the clear cell carcinoma were compared. Proliferation rate in five nephrogenic adenomas and the carcinoma was assessed by antibody M1B1. Many of the features showed differences in degree or extent (clear cell change, nuclear pleomorphism, CAM 5.2 and CEA positivity). The only features distinct to clear cell carcinoma were the presence of solid islands, mitoses greater than 1/10 HPF (HPF area = 0.4 mm2) and M1B1 counts in excess of 29/200 in clear cell carcinoma (range 30/200-83/200). Only the high M1B1 count was present in the first biopsy of the clear cell carcinoma.
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PMID:Vesical clear cell adenocarcinoma. V. Nephrogenic adenoma: a diagnostic problem. 755 5

Serous cystadenomas of the pancreas are uncommon benign neoplasms that occur most frequently in elderly females. Characteristically, the tumors have a spongy gross appearance and are composed of innumerable cysts lined by flat, cuboidal, and polygonal cells with clear to pale eosinophilic cytoplasm and round, hyperchromatic central nuclei. Macrocystic variants with an oligolocular gross appearance have also been described. In this report we describe a solid pancreatic neoplasm arising in a 70-year-old woman who remains well 5 years after a distal pancreatectomy. The well-circumscribed tumor measured 4.0 cm in maximal diameter and was formed by clear to pale polygonal to cuboidal cells arranged in nests, sheets, and trabeculae separated by thick fibrous bands. Although small acini with glandular spaces were present within the nests, cystic spaces were absent. Periodic acid-Schiff (PAS) and PAS-dismutase (PAS-D) stains revealed a large amount of cytoplasmic glycogen. The tumor cells were immunoreactive for CAM 5.2, epithelial membrane antigen, and neuron-specific enolase. The cytologic, histochemical, and immunohistochemical features of the tumor were indistinguishable from those of serous cystadenomas; therefore, we believe this solid serous adenoma represents a solid variant of serous cystadenoma. Recognition of this lesion is important because the vast majority of solid tumors in the pancreas are malignant. The differential diagnosis includes the rare primary clear-cell "sugar" tumor of the pancreas, clear cell carcinoma, clear cell islet cell tumor, and metastatic renal cell carcinoma.
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PMID:Solid serous adenoma of the pancreas. The solid variant of serous cystadenoma? 889 45

This article reports the clinicopathological and immunohistochemical findings of two cases of adenoma of the the rete ovarii (RO), one unilateral and the other bilateral, presenting with atypical histological features in the right ovary. Both tumors were incidental findings in 62- and 64-year-old patients presenting with metrorrhagia. The predominantly cystic lesions measured 2 cm and 3 cm in diameter and microscopically, they were tubulopapillary proliferations of regular columnar cells with clear cytoplasm. The stroma showed extensive differentiation of polygonal, Leydig-like cells which was associated in both cases with simple endometrial hyperplasia. In both cases rete and hilar mesonephric remnants were found in the vicinity of the lesion. The atypical lesion in one case had a complex papillary proliferation different in pattern and cellularity from a retiform Sertoli-Leydig cell tumor. It showed extensive areas of eosinophilic change, pleomorphism, and a few mitoses but did not invade the adjacent ovarian stroma. Its stroma also had steroidally active cells. The patient was alive and well after a follow-up interval of 3 years. Immunohistochemically, the lesions were diffusely positive for CAM 5.2, vimentin, epithelial membrane antigen, OC 125, OC 125, and progesterone receptors.
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PMID:Adenomas of the rete ovarii. 941 2

A 59-year old woman was diagnosed with a tumour in her right kidney. A nephrectomy was performed, and a 45 mm diameter tan-pink coloured tumour was found. Microscopy revealed small, dark cells in organized arrays of small round acini and tubules with glomeruloid infoldings. A diagnosis of metanephric adenoma was made. The tumour cells proved diploid on flow cytometry and immunohistochemical staining was positive for CAM 5.2 and AE-3. FISH analysis of three chromosomes did not reveal any abnormal karyotype. It is important to differentiate metanephric adenoma from renal cell carcinoma and adult Wilm's tumour, since it has a benign course.
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PMID:Metanephric adenoma. 1057 2

The present paper documents an investigation of the morphology, immunohistochemistry, and ultrastructure of Toker cells (TC), aiming for a better definition of these elements and better understanding of their histogenesis. We studied 12 nipples removed for nipple adenoma from twelve patients and a case of supernumerary nipple. In addition four cases of Paget's carcinoma (PC) restricted to the nipple without underlying tumor were studied for comparison. All cases were stained with hematoxylin and eosin (H&E), Alcian blue pH 2.5 and periodic acid-Schiff (PAS) preceded by diastase digestion and with immunohistochemistry using antisera anti cytokeratin 7, cytokeratin 20, protein S100, GCDFP-15, c-Erb-B2, CAM 5.2, and epithelial membrane antigen (EMA). Two cases from the nipple adenoma series were studied by electron microscopy. In seven cases within the series of 12 nipple adenomas as well as in the case of supernumerary nipple, keratin 7 antibody highlighted numerous cells located within the nipple epidermis which in three cases showed dendritic processes. These same elements were also positive with CAM 5.2. All these same elements were negative with Alcian Blue (AB), PAS and the other antisera employed. Ultrastructural examination demonstrated that these cells differed from keratinocytes while they presented the same features as the glandular cells seen in the related nipple adenoma. The cells constituting Paget's carcinoma showed more irregular nuclei and were more easily seen in the context of the epidermis. The immunocytochemical profile of the cancer cells was similar to that of TC, but in addition the neoplastic cells were c-Erb-B2 and EMA positive in all cases, and one case also displayed numerous cells immunoreactive with anti GCDFP-15 antibody. Keratin 7 highlighted dendritic cells in two cases and AB, PAS was negative in all patients. The immunocytochemical profile and the ultrastructural features of TC are similar to those of the glandular cells constituting the ducts and the adenoma. These findings together with the localization of TC near or around the openings of the lactiferous sinuses indicate that TC might be ductal cells with a dendritic aspect and migrate through the galactophorous ostia. PC cells not related to ductal carcinomas have a similar but not superimposable immunohistochemical profile to TC, and in two cases the neoplastic elements were also dendritic which suggests that these same cells are likely to be the neoplastic counterpart of TC.
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PMID:Toker cells are probably precursors of Paget cell carcinoma: a morphological and ultrastructural description. 1218

Pituitary GH secretion is regulated by hypothalamic hormones and peripheral factors. Cell-cell contact may also have an important role in regulating pituitary hormone expression and secretion. The role of pituicyte cell-cell contact mediated by N-cadherin and neural cell adhesion molecule (N-CAM) was studied in the regulation of GH secretion. RT-PCR showed N-cadherin mRNA expression in eight of 12 of GH-secreting adenomas compared with one of seven of prolactin-cell adenomas. N-cadherin and N-CAM were similarly expressed in adenomas and in adult and fetal normal pituitary tissues. The effects of CAM homophilic binding on GH secretion from dispersed human fetal pituitary cultures were studied by manipulating CAM mediated cell-cell contact using either soluble N-cadherin-Fc or pituitary cells cocultured with NIH-3T3 cells stably expressing CAMs. CAM stimulation increased GH secretion from pituitary fetal cultures by 40-60% (P < 0.05) and also from cultured GH adenoma cells by 40-75% (P < 0.05). Disrupting N-cadherin homophilic binding by anti-N-cadherin antibody decreased fetal, but not tumorous GH secretion by 40% (P < 0.05). This study indicates that pituitary cell-cell contact mediated by homophilic interactions between adhesion molecules regulates human GH secretion.
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PMID:The cell adhesion molecules N-cadherin and neural cell adhesion molecule regulate human growth hormone: a novel mechanism for regulating pituitary hormone secretion. 1291 61

We report a case of an aldosterone producing adrenocortical adenoma with rhabdoid features in a 16-year-old girl. Grossly, the tumor measured 30 mm in diameter and weighed 24 g. Histologically, the tumor was composed of approximately equal parts of tumor cells with rhabdoid features arranged in a solid and trabecular pattern and cells characterized by compact eosinophilic cytoplasm, solid growth with focal necroses, and increased mitotic activity. The lipid-rich tumor cells with ample clear vacuolized cytoplasm represent a minor component. Immunohistochemically, all the tumor cells showed the same results and were positive for vimentin, synaptophysin, Melan A, and alpha-inhibin. Cytokeratin CAM 5.2 was positive only focally. Chromogranin A, actin, alpha-actin, S100 protein, EMA, and cytokeratin AE1/AE3 were negative. Rhabdoid features have been described in many tumors of variable histogenesis; however, to the best of our knowledge, the presence of rhabdoid phenotype has never been described in either adrenocortical adenoma or carcinoma.
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PMID:Adrenocortical adenoma with rhabdoid features. 1644 85

Familial isolated pituitary adenoma (FIPA) is a rare condition independent of Carney Complex or MEN1. An international multicenter study recently described 28 nonfunctioning pituitary adenomas in 26 families with only two homogeneous nonsecreting phenotype families consistent of silent GH and silent gonadotroph adenomas, respectively. We present the clinical, genetic, and morphological analysis of two silent pituitary adenomas occurring in a man and his daughter, and discuss the differential diagnosis associated with their histological, immunohistochemical, and ultrastructural features. The patients developed invasive nonsecreting macroadenomas manifesting only with compressive symptoms. Genetic analysis in the father showed no MEN-1 germ-line mutation. Tissue samples obtained after paraseptal trans-sphenoidal surgery were studied by immunohistochemistry for adenohypophyseal hormones, low molecular weight cytokeratins (CAM 5.2), proliferation markers, and anterior pituitary transcription factors (Pit-1 and SF-1) and by electron microscopy for secretory granules. The clinical, histological, and immunohistochemical features of the lesions posed a differential diagnosis between a null cell adenoma and a silent corticotroph adenoma (Type II); on the basis of immunohistochemical stains for cytokeratin and adenohypophysis cell lineage markers, tumor behavior and ultrastructural studies we concluded for the second. The reported cases represent an as yet undescribed example of homogeneous family with silent corticotroph adenomas (Type II). Our observations support the trend for more aggressive behavior in nonsecreting FIPAs as compared with sporadic adenomas.
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PMID:Silent familial isolated pituitary adenomas: histopathological and clinical case report. 1831 53


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