Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: HUMANGGP:012675 (S100)
 6,012 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Fifty-three breast lesions, which had been fixed in formalin and embedded in paraffin, were immunohistochemically analyzed with monoclonal antibodies to cytokeratin subtypes 1, 5, 10, 14 (34BE12), muscle-specific actins (HHF35) and antiserum to S100 protein, all of which have been used as markers for myoepithelial cells. With these antibodies, a continuous myoepithelial cell layer could generally be seen around the benign ducts and acini. In in situ carcinomas, such a layer could still be observed, though it was usually discontinuous and sometimes absent. In infiltrating carcinomas, no myoepithelial cell layer could be observed. In intraductal hyperplasias, scattered HHF35, 34BE12 and S100-positive cells could be seen amongst the proliferating intraductal cells. In in situ and infiltrating carcinomas, however, such cells could also be observed. This was seen especially with antibodies 34BE12 and S100, and to a lesser extent also with HHF35. Morphologically these cells seemed to belong to the malignant cell population. Although myoepithelial cell preservation is an important morphological parameter in the histological evaluation of breast lesions, the results suggest that the myoepithelial cell markers 34BE12, HHF35 and S100 cannot be used in the differential diagnosis between benign and malignant breast lesions in a straightforward manner. This is because in situ carcinomas have a more or less preserved myoepithelial cell layer, and because many infiltrating and in situ carcinomas contain a subpopulation of neoplastic cells expressing these markers, possibly signifying myoepithelial cell differentiation.
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PMID:Immunohistochemical evaluation of the cytoarchitecture of benign and malignant breast lesions. 128 Jan 48

This study on the different types of epithelial hyperplasia in fibrocystic disease was inspired by the observation of myoepithelial (basocellular) hyperplasia identified by strong expression of S100 protein and a weak reaction with antibodies against cytokeratin (KL1) in cells forming solid and acinar buds. The cells do not contain immunohistochemically detectable actin or desmin. Glandular transformation and proliferation give rise to basocellular circumductal adenosis. Normal breast tissue, 51 cases of fibrocystic disease with mild, florid and atypical hyperplasias, 7 fibroadenomas and 20 cases of carcinoma in situ were studied and a semiquantitative analysis revealed basal buds and adenosis in less than 40% of cases of mild hyperplasia and up to 73% in florid hyperplasia. Epitheliosis is characterized by a heterogeneous cell pattern with cells positive for S100 protein in 30-60%, but in small ducts up to 100% with an immediate connection to the basal cell layer were positive. Carcinoma in situ contained very rare tumour cells positive for S100 protein. The cells expressing S100 protein in terminal ducts, in adenosis and epitheliosis showed only some of the characteristics of myoepithelial cells, since they lack immunoreactivity with antibodies against actin. These basal clear cells are interpreted as transitional or indeterminate cells with features of myoepithelial precursor cells, but with the ability to develop basocellular nodular and glandular hyperplasia in the ductulo-lobular units in cases of adenosis and juvenile fibroadenoma.
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PMID:Histopathology of myoepithelial (basocellular) hyperplasias in adenosis and epitheliosis of the breast demonstrated by the reactivity of cytokeratins and S100 protein. An analysis of heterogenic cell proliferations in 90 cases of benign and malignant breast diseases. 128 Aug 83

Hepatocellular carcinoma (HCC) may uncommonly present with distant metastasis in the absence of a documented neoplasm in the liver. The authors herein describe the case of a 60-year-old man with cirrhosis who developed unilateral enlargement of the breast and a subareolar mass. This problem was clinically thought to represent gynecomastia, but a mammary fine-needle aspiration biopsy demonstrated a malignant epithelial neoplasm composed of large granular amphophilic cells. Bile pigment was visualized in the tumor on aspirate smears and cell block preparations; immunostains showed reactivity for cytokeratin and alpha-fetoprotein, but there was no positivity for epithelial membrane antigen, gross cystic disease fluid protein-15, vimentin, estrogen receptors, progesterone receptors, or S100 protein. These results indicated a diagnosis of metastatic HCC, which was subsequently confirmed by computed tomography of the abdomen.
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PMID:Metastatic hepatocellular carcinoma of the breast, simulating gynecomastia: diagnosis by fine-needle aspiration biopsy. 133 27

All definite cases of oncogenic osteomalacia have, until now, been classified as mesenchymal tumours. We report here a case of oncogenic osteomalacia caused by a spinal tumour. Microscopically, it resembled the mixed connective tissue variant of previously described phosphaturic tumours. Immunohistochemical studies, however, showed the tumour cells to be positive for low molecular weight cytokeratin (CAM 5.2), S100 protein, PGP 9.5, and synaptophysin. Electron microscopy demonstrated neurosecretory granules. The histopathological findings strongly suggest that this is a neuroendocrine tumour.
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PMID:A neuroendocrine cause of oncogenic osteomalacia. 137 90

We have established a cell line (KU-SN) from a peripheral neuroectodermal tumor originating in the left scapula of a 4-year-old girl. The original tumor was immunoreactive with antibodies for neurofilament proteins, neuron-specific enolase, vimentin, S100 protein, and beta 2-microglobulin. Dense core granules, 50-150 nm in diameter, were identified by electron microscopy. The cell line was established from tumor cells in metastatic lung fluid. KU-SN cells were immunoreactive with the antibodies for neurofilament proteins, vimentin, neuron-specific enolase, S100 protein, glial fibrillary acidic protein, cytokeratin, and carcinoembryonic antigen. Besides these neuronal features, KU-SN cells express type 2 collagen and insulin-like growth factor 1 receptor. The addition of insulin-like growth factor 1 (100 ng/ml) increased the growth rate of KU-SN cells 2.1-fold over control. Some cells were positive for Alcian blue and alkaline phosphatase staining. Cytogenetic analysis of KU-SN cells disclosed a reciprocal chromosomal translocation [t(11,22)]. Northern blot analysis of KU-SN cells demonstrated amplified expression of the c-myc gene but not the N-myc gene. When tumor cells were transplanted into nude mice, cartilage was formed. The cartilage was immunoreactive with the antibody for HLA-ABC, indicating that it was derived from the tumor cells, not from mouse tissue. Chondrocytic differentiation was not observed in xenografts of Ewing's sarcoma cell lines SK-ES or RD-ES or the peripheral neuroectodermal tumor cell line SK-N-MC. These results indicate that KU-SN cells represent primitive neural crest cells having the potential for chondrocytic differentiation.
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PMID:Chondrocytic differentiation of peripheral neuroectodermal tumor cell line in nude mouse xenograft. 137 22

Cytogenetic studies of pediatric tumors have revealed a number of reproducible karyotypic abnormalities, including del(p13) found in aniridia-Wilms' tumor association, t(8;14) in Burkitt's lymphoma, and t(11;22) in Ewing's sarcoma. To date, no consistent cytogenetic abnormality has been reported in association with hepatoblastoma. We report the case of a 7-month-old male infant with the undifferentiated small cell variant of hepatoblastoma. Immunohistochemistry revealed reactivity with antibodies to cytokeratin and vimentin throughout the tumor. Alpha-fetoprotein, neuron-specific enolase, and S100 stains were negative. Chromosomal analysis of metaphase cells from a culture of tumor tissue revealed a translocation of most of the long arm of chromosome 22 to the distal long arm of chromosome 10.
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PMID:Undifferentiated small cell hepatoblastoma with a unique chromosomal translocation: a case report. 138 17

We analyzed 46 gastrointestinal stromal tumors (GISTs) using a panel of antibodies to determine the frequency of smooth muscle differentiation and the relationship of immunophenotype to histopathologic features and clinical behavior. Thirty-six GISTs were classified as benign or malignant based exclusively on clinical behavior; a 2-year minimum follow-up was required for benign lesions. GISTs were immunopositive in the following categories: vimentin 45 of 46, desmin nine of 45, muscle-specific actin (MSA) 36 of 46, alpha-smooth muscle actin (SMA) 34 of 46, chicken gizzard actin-7 zero of 38, cytokeratin two of 46, S100 protein six of 46, glial fibrillary acidic protein (GFAP) zero of 46, synaptophysin zero of 46, and chromogranin one of 46. At least one muscle marker was positive in 39 of 46 tumors. Five GISTs were MSA positive/SMA negative, and three were MSA negative/SMA positive. All desmin-positive cases reacted with MSA or SMA. Eight GISTs were positive for vimentin, MSA, SMA, and desmin, whereas seven were vimentin positive only. Compared with the latter, the former tended to be smaller, less often necrotic, and clinically benign (p less than 0.05 for each). All vimentin-positive only GISTs were malignant. Immunohistochemical features did not correlate with tumor site, cellularity, nuclear pleomorphism, or mitotic rate. Benign GISTs were less cellular than were malignant GISTs (p less than 0.05), but they did not differ statistically in degree of nuclear pleomorphism, necrosis, mitotic rate, or size. We conclude that (a) 85% of GISTs react with at least one muscle antibody; (b) immunohistochemical features are unrelated to anatomic site; (c) SMA is, in effect, as sensitive as MSA, whereas desmin is less sensitive; and (d) simultaneous vimentin, MSA, SMA, and desmin positivity correlates with a benign outcome.
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PMID:Muscle differentiation and clinicopathologic features of gastrointestinal stromal tumors. 141 3

A primary extraspinal medulloepithelioma with lung metastases is reported. The tumour was located in the presacral area. Microscopically, it showed typical features of medulloepithelioma with focal ependymal differentiation. Medulloepitheliomas are malignant tumours of primitive neuro-epithelium usually involving the cerebral hemispheres. This report demonstrates their possible extraspinal presacral occurrence. By immunohistochemistry, neuron-specific-enolase, S100 protein, vimentin, cytokeratin and glial fibrillary acidic protein were found in some tumour cells. Electron microscopy demonstrated poorly differentiated cells forming stratified epithelium resting on a basal lamina and short junctional complexes at the apical pole. Ultrastructural evidence of ependymal differentiation was observed. Presacral medulloepithelioma may arise from undifferentiated embryonic cells forming the presacral remnants of the neurenteric canal.
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PMID:Ectopic intrapelvic medulloepithelioma: case report. 152 92

We report a case of leiomyomatosis that involved the small intestine and colon. On gross examination, the bowel wall was irregularly thickened at various levels. Histologically, the lesions were characterized by multifocal, diffuse tumor masses that were present in the muscular layers. These masses consisted of proliferating smooth-muscle cells that often surrounded prominent blood vessels. Cytologic atypia was not observed, and the mitotic count was low, illustrating the benign nature of the tumors. Findings from immunohistochemical analysis of the lesions were essentially negative; vimentin, cytokeratin, actin, desmin, and S100 stains showed no reactivity in the tumor cells, despite positive internal controls. By reviewing the literature, we found several reports on related lesions that occurred in the gastrointestinal tract; diffuse leiomyomatosis of the esophagus and the colon have been reported. We did not find any report on the small intestinal variant of the disease; therefore, it seemed useful to term this new localization as leiomyomatosis of the small intestine and colon.
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PMID:Combined leiomyomatosis of the small intestine and colon. 841 66

We wished to assess the antigenic expression of primary lung tumors diagnosed as either carcinosarcoma or sarcoma in order to determine whether this information would be useful in distinguishing the two. We therefore immunohistochemically analyzed six pulmonary carcinosarcomas and five primary lung sarcomas for the presence of carcinoembryonic antigen (CEA), S100 protein, cytokeratin and vimentin using commercially available monoclonal and polyclonal antibodies on formalin fixed tissues. Six of six carcinosarcomas stained positively for cytokeratin while none of the sarcomas stained. In three carcinosarcomas both the carcinomatous and sarcomatous areas were positive while in three only the carcinomatous areas were positive. CEA staining was present in five carcinosarcomas and absent in all the sarcomas. CEA positivity was strong and not confined to those tumors with obvious gland formation. Staining for S100 protein was positive in two carcinosarcomas but only in those areas showing chondroid differentiation. Immunohistochemical staining for vimentin using two different monoclonal antibodies gave inconsistent results. We conclude that in differentiating between a carcinosarcoma and a sarcoma of the lung, immunohistochemical staining for both cytokeratin and CEA are useful with cytokeratin marginally preferable. The data indicate that carcinosarcoma of the lung, like that of the upper aerodigestive tract, expresses antigens suggesting both epithelial and mesenchymal differentiation.
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PMID:An immunohistological comparison of primary lung carcinosarcoma and sarcoma. 169 5


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