Bergmann, Fritz

[["dc.bibliographiccitation.firstpage","127"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","CANCER GENETICS AND CYTOGENETICS"],["dc.bibliographiccitation.lastpage","130"],["dc.bibliographiccitation.volume","120"],["dc.contributor.author","Gunawan, Bastian"],["dc.contributor.author","Weber, M."],["dc.contributor.author","Bergmann, F."],["dc.contributor.author","Wildberger, J."],["dc.contributor.author","Niethard, F. U."],["dc.contributor.author","Fuzesi, Laszlo"],["dc.date.accessioned","2018-11-07T10:39:27Z"],["dc.date.available","2018-11-07T10:39:27Z"],["dc.date.issued","2000"],["dc.description.abstract","We report cytogenetic findings in short-term cell cultures from five enchondromas and four chondrosarcomas. Clonal chromosome aberrations were found in one case of enchondroma, and in all cases of chondrosarcoma. The only enchondroma with nonrandom abnormalities had a reciprocal f(8;17)(q23;p13), and monosomies 9, 19, and/or 22. In contrast to the few karyotypic findings in one of five enchondromas, the four chondrosarcomas were commonly characterized by cytogenetic heterogeneity, with a tendency for increasing karyotypic complexity in higher grade tumors. Two cases, one grade III and one metastasizing grade II chondrosarcoma, revealed hypodiploid stem- and sidelines with loss of chromosomes 6, 10, 13, 14, and 22, as common chromosomal abnormalities, suggesting a distinct karyotypic pattern in a subset of biologically aggressive chondrosarcomas. (C) 2000 Elsevier Science me. All rights reserved."],["dc.identifier.doi","10.1016/S0165-4608(99)00254-X"],["dc.identifier.isi","000088925000006"],["dc.identifier.pmid","10942802"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/46050"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.relation.issn","0165-4608"],["dc.title","Clonal chromosome abnormalities in enchondromas and chondrosarcomas"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1011"],["dc.bibliographiccitation.issue","12"],["dc.bibliographiccitation.journal","ROFO-FORTSCHRITTE AUF DEM GEBIET DER RONTGENSTRAHLEN UND DER BILDGEBENDEN VERFAHREN"],["dc.bibliographiccitation.lastpage","1015"],["dc.bibliographiccitation.volume","172"],["dc.contributor.author","Mahnken, A. H."],["dc.contributor.author","Wildberger, J. E."],["dc.contributor.author","Bergmann, F."],["dc.contributor.author","Fuzesi, Laszlo"],["dc.contributor.author","Adam, Gerhard"],["dc.contributor.author","Gunther, R."],["dc.date.accessioned","2018-11-07T10:15:31Z"],["dc.date.available","2018-11-07T10:15:31Z"],["dc.date.issued","2000"],["dc.description.abstract","Objective: To analyze the CT appearance of papillary renal cell tumor (pRCT) under consideration of gross pathology. Material and Methods: Preoperative CT-scans of 10 patients suffering from pRCT were re-evaluated by two experienced radiologists. CT appearance was correlated to gross morphology. Results: On CT, 9/10 tumors were depicted as rounded, well circumscribed and sharply delineated masses. These tumors presented a hypodense central area correlating to necrosis in gross pathology. The central area of necrosis was surrounded by vital tumor tissue, presenting as a serpiginous, contrast-enhancing margin on CT. One tumor was polycyclic due to multiple tumor nodules, but sharply demarcated towards the surrounding renal tissue. Conclusions: pRCT presents a quite unique CT appearance similar to its gross pathology."],["dc.identifier.doi","10.1055/s-2000-9221"],["dc.identifier.isi","000166208200011"],["dc.identifier.pmid","11199428"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/40824"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Georg Thieme Verlag Kg"],["dc.relation.issn","1438-9029"],["dc.title","Papillary renal cell tumor: Comparison of CT and gross morphology"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","316"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Human Pathology"],["dc.bibliographiccitation.lastpage","321"],["dc.bibliographiccitation.volume","33"],["dc.contributor.author","Gunawan, Bastian"],["dc.contributor.author","Bergmann, F."],["dc.contributor.author","Hoer, J."],["dc.contributor.author","Langer, C."],["dc.contributor.author","Schumpelick, V."],["dc.contributor.author","Becker, H."],["dc.contributor.author","Fuzesi, Laszlo"],["dc.date.accessioned","2018-11-07T10:31:22Z"],["dc.date.available","2018-11-07T10:31:22Z"],["dc.date.issued","2002"],["dc.description.abstract","We report cytogenetic findings in 19 c-Kit-positive gastrointestinal stromal tumors (GISTs) that represent a heterogenous group of mesenchymal neoplasms with respect to site, histology, and biologic behavior. All of the GISTs (5 low-risk, 11 high-risk, 3 recurrences) displayed clonal chromosomal aberrations; 15 were hypo- to near-diploid, and 4 were near-triploid and hypotetraploid. The most common abnormalities were loss of chromosomes 14 and/or 22, demonstrated in 14 GISTs irrespective of site or predominant phenotype. Ten cases (2 low-risk, 5 high-risk, 3 recurrences) were characterized by loss of both chromosomes 14 and 22, 2 cases (1 low-risk, 1 high-risk), by loss of chromosome 14; and 2 high-risk cases, by loss of chromosome 22. Additional chromosomal aberrations occurred preferentially in high-risk and recurrent GISTs, including loss of 9p and 1p, in 8 cases each, loss of 15 in 6 cases, loss of 3p in 5 cases, loss of 13q and 10q in 4 cases each, loss of 19 in 3 cases, and complete or partial gains of chromosomes 5 and 4 in 2 cases each. More significantly, 5 of 6 patients with clinically aggressive GISTs, including 2 recurrences and 3 metastasing GISTs, were additionally characterized by loss of 9p; four of these had additional loss of chromosomes 1p and 15. The presented results herein indicate that loss of chromosome 14 and/or 22 is an early change in GIST tumorigenesis irrespective of site or differentiation, whereas malignant transformation and progression of GISTs appear to be associated with an increasing incidence of additional secondary aberrations. Copyright 2002, Elsevier Science (USA). All rights reserved."],["dc.identifier.doi","10.1053/hupa.2002.32216"],["dc.identifier.isi","000175340300008"],["dc.identifier.pmid","11979372"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/44092"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","W B Saunders Co"],["dc.relation.issn","0046-8177"],["dc.title","Biological and clinical significance of cytogenetic abnormalities in low-risk and high-risk gastrointestinal stromal tumors"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]