Nagel, Holger

[["dc.bibliographiccitation.firstpage","351"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Diagnostic Cytopathology"],["dc.bibliographiccitation.lastpage","358"],["dc.bibliographiccitation.volume","22"],["dc.contributor.author","Papaparaskeva, K."],["dc.contributor.author","Nagel, H."],["dc.contributor.author","Droese, M."],["dc.date.accessioned","2018-11-07T10:46:54Z"],["dc.date.available","2018-11-07T10:46:54Z"],["dc.date.issued","2000"],["dc.description.abstract","The cytomorphologic features in fine-needle aspiration (FNA) biopsies from 91 histologically verified medullary carcinomas of the thyroid (MCT) were investigated. FNA was able to diagnose neoplasms with indications of surgical removal in 98.9% of cases and moreover, was accurate in specific tumor typing in 89% of cases. The most important cytologic criteria of MCT with FNA are: dispersed cell-pattern of polygonal or triangular cells, azurophilic cytoplasmic granules, and extremely eccentrically placed nuclei with coarse granular chromatin and amyloid. These and other cytologic features of MCT are discussed in detail. Fourteen cases of thyroid tumors originally diagnosed as MCT by cytology are illustrated to discuss the differential diagnosis of MCT and its potential pitfalls. If MCT is cytologically presumed but amyloid and azurophilic cytoplasmic granules are not demonstrated, the use of immunostaining is necessary for a correct tumor typing. The application of immunocytochemistry in MCT is discussed. Diagn. Cytopathol. 2000;22:351-358. (C) 2000 Wiley-Liss, Inc."],["dc.identifier.isi","000087331700005"],["dc.identifier.pmid","10820528"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/47847"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-liss"],["dc.relation.issn","8755-1039"],["dc.title","Cytologic diagnosis of medullary carcinoma of the thyroid gland"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","60"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Diagnostic Molecular Pathology"],["dc.bibliographiccitation.lastpage","65"],["dc.bibliographiccitation.volume","10"],["dc.contributor.author","Nagel, H."],["dc.contributor.author","Schlott, T."],["dc.contributor.author","Schulz, G. M."],["dc.contributor.author","Droese, M."],["dc.date.accessioned","2018-11-07T09:18:58Z"],["dc.date.available","2018-11-07T09:18:58Z"],["dc.date.issued","2001"],["dc.description.abstract","Diagnostic accuracy in effusion cytology based on morphologic examination is not always satisfactory. Therefore, various diagnostic adjuncts such as immunocytochemistry or deoxyribonucleic acid cytometry are employed in this diagnostic field. Recently, demonstration of telomerase activity has been proposed as a possible marker for malignancy. In this study a seminested reverse transcription-polymerase chain reaction (RT-PCR) strategy for expression analysis of the catalytic subunit of human telomerase (hEST2) was used in 58 serous effusions. RT-PCR results correlated with cytologic diagnoses in 14 of 17 malignant effusions. In eight effusions cytologically suspicious for malignancy, PCR results were in accordance with the clinical follow-up. However, hEST2 RT-PCR was also positive in six of 15 cytologically benign effusions that consisted predominantly of inflammatory and mesothelial cells. Using the telomeric repeat amplification protocol, it could be demonstrated that cultured, proliferating benign mesothelial cells may present a weak telomerase activity, as is known in other benign cells including activated lymphocytes. In conclusion, the simple and rapid method of hEST2 RT-PCR serves to support the cytologic diagnosis of malignancy, but false-positive PCR results resulting from activated lymphocytes and proliferating mesothelial cells must be considered."],["dc.identifier.doi","10.1097/00019606-200103000-00010"],["dc.identifier.isi","000167166200010"],["dc.identifier.pmid","11277397"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/28526"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Lippincott Williams & Wilkins"],["dc.publisher.place","Philadelphia"],["dc.relation.eventlocation","JENA, GERMANY"],["dc.relation.issn","1052-9551"],["dc.title","Gene expression analysis of the catalytic subunit of human telomerase (hEST2) in the differential diagnosis of serous effusions"],["dc.type","conference_paper"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","67"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Pathobiology"],["dc.bibliographiccitation.lastpage","76"],["dc.bibliographiccitation.volume","69"],["dc.contributor.author","Schlott, T."],["dc.contributor.author","Nagel, H."],["dc.contributor.author","Laskawi, Rainer"],["dc.contributor.author","Eiffert, Helmut"],["dc.contributor.author","Droese, M."],["dc.date.accessioned","2018-11-07T09:37:17Z"],["dc.date.available","2018-11-07T09:37:17Z"],["dc.date.issued","2001"],["dc.description.abstract","Introduction: Genetic alterations of oncogene MDM2 promote malignant transformation of several human tumors. In tumors of the salivary gland, however, the genetic status of MDM2 has not been evaluated so far. Methods and Results: Benign and malignant tumors of the salivary gland (6 pleomorphic adenomas, 3 Warthin's tumors, 1 adenocarcinoma, 1 basal cell adenocarcinoma, 1 mucoepidermoid carcinoma, 3 acinic cell carcinomas, 2 adenoid cystic carcinoma, 1 squamous cell carcinoma) were analyzed by fluorescence-based PCR techniques and immunochemistry for MDM2 gene amplification, MDM2 gene expression, MDM2 gene mutation, MDM2 RNA splicing and MDM2 accumulation. Data show that all samples contained nonamplified MDM2 genes with nonmutant zinc finger regions. However, in two benign and two malignant samples, novel MDM2 mRNA splicing variant types 1 and 2 were detected. Furthermore, three malignant tumors revealed significant nuclear MDM2 accumulation. Correlation between levels of MDM2 mRNA and MDM2 protein could not be detected in the specimens. Conclusion: The present study suggests that MDM2 gene mutation and gene amplification do not contribute to MDM2 accumulation detected in malignant tumors of the salivary gland. However, the role of novel MDM2 splicing variants in MDM2 expression and malignant transformation must be elucidated further. Copyright (C) 2001 S. Karger AG, Basel."],["dc.identifier.doi","10.1159/000048759"],["dc.identifier.isi","000173140900002"],["dc.identifier.pmid","11752900"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/32807"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Karger"],["dc.relation.issn","1015-2008"],["dc.title","Genetic analysis of the human oncoprotein MDM2 in benign and malignant tumors of the salivary gland"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]