Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0017638 (glioma)
 30,880 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

During the last several decades, immunohistochemical studies of tumors, along with other approaches, have suggested that the clinical and biological progression results, at least in part, from the sequential appearance within the neoplasm of cellular subpopulations whose new characteristics reflect specific somatic genetic changes. However, CNS may provide a different microenvironment for activation and proliferation than other tissues. The tissue-specific distribution of intermediate filament proteins, in particular the keratins, permits their use as marker in histopathology, but several important exceptions are recognized. In this connection, it is of interest that, according to the other reports, glial tumors may be positive for different anti-keratin antibodies. However, the gliomas did not show an immunoreaction in any of the cases when HEA-125 and Ber-EP4 were applied. The great number of multihormonal pituitary adenomas and possible change of the immunohistochemically detectable hormone status in cases of recurrent tumors have particularly re-emphasized the need for new thinking about patterns of classification. The diagnosis of malignant melanoma has been considerably facilitated recently by the introduction of immunohistological labelling with antibodies selective against melanoma antigen (HMB-45). Our results confirmed the necessity of cautious interpretation of HMB-45 immunoreactivity because a HMB-45 expression can be observed in several non-melanotic tumors.
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PMID:[Changes of microenvironment and tumor cell heterogeneity--consequences for bioptic diagnosis]. 137 17

Gliosarcomas are mixed tumors with malignant glial and mesenchymal elements. The number of GFAP-positive tumor cells decreases with the increase of sarcomatous components, until whole areas may be GFAP negative. These distinct differentiations may, however, lead to false interpretations in small tissue samples. In this connection, it is of interest that, according to other reports, glial tumors may be positive for different anti-keratin antibodies and this prompted us to undertake a systematic investigation of the immunoreactivity of gliosarcomas using a panel of well-characterized monoclonal antibodies against cytokeratins (KL1, AE 1/3, Lu-5, CK-19, CK MNF 116 and Ma-903). These cases were further studied with the anti-epithelial non-cytokeratin antibodies EMA, HEA 125, Ber-EP4, CEA as well as the melanoma-antibody HMB-45, Leu-M1, GFAP and vimentin. As screening study we examined 20 cerebral metastatic carcinomas, 21 malignant gliomas (including 6 gliosarcomas) and 3 metastatic melanomas with the monoclonal antibodies KL1 and HMB-45. All cerebral metastatic carcinomas and 4/6 gliosarcomas were positive for KL1, whereas all melanomas, 2 metastatic carcinomas and 3 gliosarcomas showed an immunostaining with HMB-45. All gliosarcomas were positive with at least one of the tested anti-cytokeratin antibodies. The gliosarcomas did not show an immunoreaction in any of the cases when CEA, HEA 125, Ber-EP4, EMA or Leu M1 were applied. In our opinion, the monoclonal antibodies HEA 125 and Ber-EP4 could obviously be helpful in differentiating gliosarcomas from metastatic carcinomas.
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PMID:Epithelial and melanoma antigens in gliosarcoma. An immunohistochemical study. 159 90

Immunohistochemical analysis of intermediate filament (IF) proteins was performed on frozen sections of 16 childhood glial tumors using a library of 10 antigen-specific IF protein directed monoclonal antibodies (MoABs) and a four-step biotin-streptavidin-alkaline phosphatase conjugated antigen detection immunocytochemical technique. Human glial fibrillary acidic protein (GFAP) and vimentin were expressed in all brain tumors. High molecular weight (200 kDa) neurofilament (NF-H) protein was expressed in 15 out of 16 tumors; medium molecular weight (160 kDa) neurofilament (NF-M) in seven out of 16 tumors; and low molecular weight (68 kDa) neurofilament (NF-L) in five out of 16. Positive acidic keratin reactivity was found in five out of 16 tumors using MoAB AE1. Expression of a keratin pair was detected with MoAB AE2 in five out of 16 tumors. A second keratin pair in 14 out of 16 glial tumors was demonstrated with MoAB AE3. Immunostaining with AE5 defined the expression of another basic keratin (64 kDa) in nine out of 16 glial tumors. Finally, in 14 out of 16 astrocytomas an individual 51 kDa acidic keratin (detected with MoAB AE8) was expressed. Glial tumor cells contain cell lineage specific and nonspecific IF proteins in the following IF pattern: AE3+, AE8+, GFAP+, vimentin+, and NF-H+. The heterogenous composition of these cytoskeletal IF proteins in childhood glial tumors may reflect a direct stage dependent correlation with their neoplastic transformation.
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PMID:Co-expression of four intermediate filament subclasses in childhood glial neoplasms. 172 88

Three new human medulloblastoma (MB) cell lines (D384 Med, D425 Med, and D458 Med) and their transplantable xenografts were examined for antigenic expression with antibodies against neuroectodermal antigens, cytoskeletal proteins, neuroendocrine markers, glioma-associated antigens, tenascin, human lymphocyte antigen molecules, epidermal growth factor receptor, and T-cell antigen by indirect immunofluorescence, avidin-biotin complex peroxidase immunohistochemistry, and immunoblot methods. We found that each of the three cell lines expressed vimentin; low-, middle-, and high-molecular-weight neurofilament proteins; and the synaptic vesicle membrane glycoprotein synaptophysin. Each of the cell lines also reacted with antibodies against neural cell adhesion molecules, but none of them were positive for antibodies against glial fibrillary acidic protein, keratin, microtubule-associated protein tau and microtubule-associated protein 2, human lymphocyte antigen-DR, epidermal growth factor receptor, and T-cell antigen. Immunoreactivities with anti-tenascin and anti-glioma-associated antibodies were variable in these cell lines. Anti-human lymphocyte antigen-A,B and anti-beta 2-microglobulin antibodies reacted with xenografts of D384 Med and D425 Med and were weakly positive for a small population of D384 Med cultured cells. In summary, the detection of neurofilament proteins and synaptophysin and the absence of glial fibrillary acidic protein provide strong evidence for a neuronal phenotype of D384 Med, D425 Med, and D458 Med.
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PMID:Differentiation characteristics of newly established medulloblastoma cell lines (D384 Med, D425 Med, and D458 Med) and their transplantable xenografts. 190 13

The cytoskeleton (CSK) of eukaryotic cells is composed of a complex interconnected network of filaments which is important in a wide variety of cellular functions including changes in cell shape, cell motility, mitosis, anchorage-dependent growth, and the localization of cellular organelles such as mitochondria, polyribosomes, and secretory granules. The various proteins comprising the cytoskeleton include actin in microfilaments, tubulin in microtubules, and the heterogeneous group of intermediate filament proteins that are associated with different cell types (keratin in epithelial cells, vimentin in fibroblasts, desmin in muscle cells, glial filament protein in glial cells, and the neurofilament protein subunits in neural tissue). Many other proteins in glial cells, and the neurofilament protein subunits in neural tissue). Many other proteins are closely associated with the cytoskeleton and influence its organization. In neoplastic cells, the expression of these different CSK proteins, especially the intermediate filament proteins, reflects their morphologic and functional differentiation. The carcinomas contain keratin; identification of individual keratin components may allow further sub-classification of carcinomas which is consistent with their tissue of origin. The sarcomas of muscle origin contain desmin. Vimentin is found primarily with cells of mesenchymal origin, but may coexist with other intermediate filament proteins in other tumors. One example is the coexistence of keratin and vimentin in tumors, such as mesotheliomas, which are derived from epithelial cells of embryonic origin. Glial fibrillary acidic protein is the most specific marker for glial tumors. Tumors of neural origin are characterized by the presence of neurofilament subunits. Therefore, analysis of CSK composition would be useful in diagnosis of clinical specimens and aid in studies of lineage relationships of neoplasms. Although no consistent differences in cytoskeletal structure between neoplastic and normal cells have been identified so far, the presence of more subtle biochemical alterations in the cytoskeletal structure of neoplastic cells that contributes to malignant behavior has not been ruled out. Since the cytoskeletal network plays an important role in cell shape and cell locomotion, which in turn are thought to be involved in growth control, invasion, and metastasis, further work is directed at identifying the various alterations in cytoskeletal architecture that may influence the malignant behavior of neoplastic cells.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Cytoskeleton-associated proteins: their role as cellular integrators in the neoplastic process. 241 18

Six cases are reported (four gliosarcomas and two glioblastomas) in which the epithelial-like areas of glial anaplasia showed focal squamous cell differentiation, characterized by the development of epithelial whorls, keratin pearls and immunopositivity for cytokeratin. The expression of glial fibrillary acidic protein and the development of squamous metaplasia usually were mutually exclusive. Autopsy findings in two patients and clinical work-up in five failed to disclose a primary extraneural malignancy. It is suggested that squamous differentiation may represent an extreme form of epithelial metaplasia in a malignant glioma. This possibility should be kept in mind in the diagnostic evaluation of such cases, especially in view of the current emphasis on the immunomorphologic demonstration of intermediate filament tumor markers.
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PMID:Patterns of epithelial metaplasia in malignant gliomas. II. Squamous differentiation of epithelial-like formations in gliosarcomas and glioblastomas. 333 69

Keratin intermediate filaments (Ifs) are specific for epithelial cell differentiation. This study demonstrates the presence of keratin in two recently established human glioblastoma cell lines 8-MG-BA and 42-MG-BA. Immunofluorescence staining was performed on cells within passage 230 to 235 using monoclonal pan-cytokeratin antibodies. The cells were analyzed during several DIV at different cell density. Keratin-positive stained cells reached 5 to 7% in 8-MG-BA and less than 0.1% in 42-MG-BA cell line. The presence of keratin-positive cells was independent on cell density and days in vitro. Keratin-positive cells appeared unevenly distributed in both cell lines. They were observed as single or areas of keratin-positive cells. The morphological features of keratin-positive and keratin-negative cells were similar. The results are discussed with respect to previous studies on glial fibrillary acidic protein (GFAP) and vimentin to show the heterogeneity of IFs expression in glioma cell lines.
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PMID:Heterogeneity of keratin intermediate filaments expression in human glioma cell lines. 1073 69

The morphologic distinction of ependymomas with epithelial cytology from metastatic carcinoma may pose a significant problem in differential diagnosis. The known presence of keratin in glioma cells further complicates the issue. Using the labeled streptavidin-biotin method with automated staining, we studied epithelial and glial marker expression in 52 ependymomas of varying type and grade, including 20 epithelial-appearing, 14 glial-appearing, eight mixed pattern, and 10 myxopapillary tumors; 38 were low grade and 14 anaplastic. All tumors were immunoreactive for glial fibrillary acidic protein (GFAP), and S-100 protein. Diffuse staining for GFAP was noted in glial-appearing ependymomas featuring perivascular pseudorosettes. Diffuse immunostaining for S-100 protein was seen in cellular lesions exhibiting epithelial-like features. Staining was more diffuse for GFAP than S-100 protein in anaplastic ependymomas. Keratin (AE1/AE3) reactivity was seen in 98% of cases, the pattern being similar to that of GFAP. The frequency of staining for other keratins varied: wide-spectrum keratin (35%), cytokeratin (CK)7 (20%), CAM 5.2 (19%), CK903 (14%), and CK20 (8%); as a rule, it was scant and limited to occasional cells and processes. epithelial membrane antigen (EMA) staining was seen in 36% of all cases and in 67% of epithelial-appearing tumors wherein it often high-lighted microlumina. Aside from AE1/AE3 staining and very infrequent wide-spectrum keratin and EMA reactivity, expression of epithelial markers was not seen in anaplastic ependymomas. No carcinoembryonic antigen (CEA) positivity was noted in any case. Collagen IV reactivity was limited to tumor cell-stroma interfaces. Although variable, S-100 protein and GFAP staining is seen in all ependymomas, particularly in true and perivascular pseudorosettes. Widespread reactivity for keratin AE1/AE3 corresponds closely to the pattern of GFAP staining. Significant staining for other keratins or for CEA is inconsistent with a diagnosis of ependymoma. EMA reactivity is largely limited to luminal staining of rosettes and tubules.
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PMID:The immunophenotype of ependymomas. 1093 45

The present case involved a 70-year-old woman who was diagnosed with a right cerebral hemorrhage. Excisional surgery of the hematoma was performed. Grossly, a whitish, solid tumor (1 x 1 x 0.8 cm in size) was recognized in the hematoma. Histologically, the tumor was composed of large, polygonal cells and small undifferentiated cells in a jumbled architectural arrangement with a cartilage component. The large, polygonal cell component was conspicuous and somewhat rhabdoid in appearance and appeared to be an astrocytic tumor showing glial differentiation. The small, undifferentiated cell component resembled tumor cells of a primitive neuroectodermal tumor (PNET). Clinical follow-up of the patient for 2 months after the first operation revealed recurrence with rapid growth. A second operation was performed, but the patient died 8 months after the first operation (2 months after the second). Immunohistochemically, the tumor cells suggesting glial differentiation were positive for glial fibrillary acidic protein (GFAP), S-100, neuron-specific enolase (NSE), and vimentin. PNET-like components in the primary tumor were positive for NSE, GFAP, and S-100, and weakly positive for vimentin and synaptophysin. Each tumor cell was negative for epithelial membrane antigen (EMA), keratin, desmin, actin, myoglobin, neurofilament (NF), and MIC2 protein. The recurrent tumor revealed predominantly PNET-like components; however, only a few tumor cells were positive for GFAP. This appearance suggested that this brain tumor might originate from a common multipotential stem cell. Considering its histopathological and immunohistochemical characteristics, the primary tumor was finally regarded as an undifferentiated glioma with dedifferentiation of the glial component in the recurrent tumor.
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PMID:A case of undifferentiated glioma in a 70-year-old woman. 1151 75

Antibodies recognizing tissue-specific antigens are widely used to identify the histological origin of tumors. Here we tested the fidelity of selected tissue markers on all 167 solid tumor-derived continuous cell lines in the DSMZ cell lines bank. Most lines had an intermediate filament content consistent with the tumor type from which they were derived. Thus, 93% of all carcinoma cell lines expressed keratin filaments. With certain antibodies, some subclassification was possible. For example, the CK7 keratin 7 antibody can differentiate between colon and pancreas-derived carcinoma cell lines. Cell lines derived from non-carcinomas, in general, did not express keratin but were vimentin-positive. Four of 10 glioma/astrocytoma cell lines expressed GFAP, five of six neuroblastoma cell lines expressed neurofilaments, and the TE-671 rhabdomyosarcoma cell line expressed desmin. When other tissue markers were tested, 12/16 melanoma-derived cell lines expressed HMB-45, while PSA, CA125, and thyroglobulin were less useful. These results demonstrate that cell lines retain some but not all markers typical of the original tumor type and identify certain markers useful in characterizing the histological origin of cell lines. Our data question the identity of some cell lines submitted to the bank in the past. The immunoprofiles of 167 solid tumor-derived and 131 hematopoetic cell lines can be found at www.dsmz.de.
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PMID:Immunocytochemical analysis of cell lines derived from solid tumors. 1166 90


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