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Featured researches published by Berthold Gerdes.


British Journal of Surgery | 2006

Negative stress-coping strategies among novices in surgery correlate with poor virtual laparoscopic performance†‡

Iyad Hassan; Peter Weyers; Katja Maschuw; B. Dick; Berthold Gerdes; M. Rothmund; A. Zielke

This study explored the impact of habitual stress‐coping strategies on the laparoscopic performance of novices in surgery using a virtual reality simulator.


Digestion | 1999

Analysis of β-Catenin Gene Mutations in Pancreatic Tumors

Berthold Gerdes; Annette Ramaswamy; Babette Simon; Torsten Pietsch; Daniel Bastian; Michael Kersting; Roland Moll; Detlef K. Bartsch

Background/Aim: Mutations of the adenomatous polyposis coli (APC) tumor suppressor gene have been described in a subset of pancreatic carcinomas. The APC gene modulates the β-catenin-Tcf pathway. The major player in this pathway is the β-catenin protein encoded by the β-catenin gene. A variety of different tumors, including colon, prostate, endometrial, and hepatocellular carcinomas, carry mutations in exon 3 of the β-catenin gene. The aim of this study was to determine the role of the β-catenin gene in the genesis of exocrine and endocrine tumors of the pancreas. Methods: 78 ductal pancreatic adenocarcinomas, 14 ductal pancreatic cancer cell lines, and 33 endocrine pancreatic tumors were evaluated for mutations in exon 3 of the β-catenin gene by single-strand conformation polymorphism analysis and direct DNA sequencing. In addition, 40 ductal pancreatic adenocarcinomas were analyzed for intracellular β-catenin accumulation by immunohistochemistry, indicating alterations of the β-catenin gene. Results: Neither the 111 exocrine and endocrine pancreatic tumors nor the 14 pancreatic cancer cell lines carried mutations in exon 3 of the β-catenin gene. Intracellular β-catenin accumulation was not identified in any of the 40 pancreatic adenocarcinomas. Conclusion: These data suggest that the β-catenin gene as the major player of the β-catenin-Tcf pathway does not play an important role in the genesis of pancreatic tumors.


Annals of Surgery | 2002

p16INK4a is a Prognostic Marker in Resected Ductal Pancreatic Cancer: An Analysis of p16INK4a, p53, MDM2, an Rb

Berthold Gerdes; Annette Ramaswamy; Andreas Ziegler; Sven Lang; Michael Kersting; Renate Baumann; Anja Wild; Roland Moll; M. Rothmund; Detlef K. Bartsch

ObjectiveTo identify the prognostic relevance of the G1/S cell cycle regulator genes p16INK4a, p53, MDM2, and Rb in patients with resected ductal pancreatic cancer (PC). Summary Background DataThe tumor suppressor genes p16INK4a, p53, and Rb are altered in PC in 27% to 95%, 40% to 70%, and 5%, respectively. The role of MDM2 is not clearly defined in PC. The prognostic value of these cell cycle regulators has not been clarified. MethodsSixty-two patients with PC with complete follow-up who underwent potentially curative resections were included in the study. An extreme group analysis was performed including the 20 patients with the shortest survival and the 20 patients with the longest survival. Protein expression of p16, p53, MDM2, and Rb was investigated, and mutation analysis of p16INK4a and p53 was performed. p16INK4a promoter hypermethylation was examined by methylation-specific polymerase chain reaction. ResultsSignificantly more tumors in the shortest-surviving patients had p16INK4a alterations compared with tumors of the longest-surviving patients. In contrast, the frequency of p53 alterations was not significantly higher in the shortest-surviving versus the longest-surviving groups. Stabilization of MDM2 and loss of Rb expression were identified in a minority of tumors, independent of survival length. ConclusionsThe presence of p16INK4a alterations in resected tumors of patients with PC is connected with a worse prognosis, indicating patients that might benefit from adjuvant therapy regimens. p53 alterations, MDM2 overexpression, and loss of Rb expression could not be identified as prognostic markers from this study, but a larger study with greater statistical power might show a different result with regard to p53.


International Journal of Cancer | 2004

Prevalence of familial pancreatic cancer in Germany

Detlef K. Bartsch; Ralf Kress; Mercedes Sina-Frey; Robert Grützmann; Berthold Gerdes; Christian Pilarsky; J. W. Heise; Klaus-Martin Schulte; Mario Colombo-Benkmann; Cristina Schleicher; Helmut Witzigmann; Olaf Pridöhl; Michael Ghadimi; Olaf Horstmann; Wolfgang von Bernstorff; Lisa Jochimsen; Jan Schmidt; Sven Eisold; Lope Estevez-Schwarz; Stephan A. Hahn; Karsten Schulmann; Wolfgang Böck; Thomas M. Gress; Nikolaus Zügel; Karl Breitschaft; Klaus Prenzel; Helmut Messmann; Esther Endlicher; Margarete Schneider; Andreas Ziegler

Based on several case‐control studies, it has been estimated that familial aggregation and genetic susceptibility play a role in up to 10% of patients with pancreatic cancer, although conclusive epidemiologic data are still lacking. Therefore, we evaluated the prevalence of familial pancreatic cancer and differences to its sporadic form in a prospective multicenter trial. A total of 479 consecutive patients with newly diagnosed, histologically confirmed adenocarcinoma of the pancreas were prospectively evaluated regarding medical and family history, treatment and pathology of the tumour. A family history for pancreatic cancer was confirmed whenever possible by reviewing the tumour specimens and medical reports. Statistical analysis was performed by calculating odds ratios, regression analysis with a logit‐model and the Kaplan‐Meier method. Twenty‐three of 479 (prevalence 4.8%, 95% CI 3.1–7.1) patients reported at least 1 first‐degree relative with pancreatic cancer. The familial aggregation could be confirmed by histology in 5 of 23 patients (1.1%, 95% CI 0.3–2.4), by medical records in 9 of 23 patients (1.9%, 95% CI 0.9–3.5) and by standardized interviews of first‐degree relatives in 17 of 23 patients (3.5%, 95% CI 2.1–5.6), respectively. There were no statistical significant differences between familial and sporadic pancreatic cancer cases regarding sex ratio, age of onset, presence of diabetes mellitus and pancreatitis, tumour histology and stage, prognosis after palliative or curative treatment as well as associated tumours in index patients and families, respectively. The prevalence of familial pancreatic cancer in Germany is at most 3.5% (range 1.1–3.5%) depending on the mode of confirmation of the pancreatic carcinoma in relatives. This prevalence is lower than so far postulated in the literature. There were no significant clinical differences between the familial and sporadic form of pancreatic cancer.


World Journal of Surgery | 2000

Management of nonfunctioning islet cell carcinomas.

Detlef K. Bartsch; Thomas Schilling; Annette Ramaswamy; Berthold Gerdes; I. Celik; Hans-Joachim Wagner; Babette Simon; M. Rothmund

Tumors arising from the pancreatic islet cells are rare and represent a heterogeneous group of benign or malignant lesions. Most tumors present with well characterized syndromes, whereas others appear to be nonfunctioning. The clinical features of 11 men and 7 women with nonfunctioning islet cell carcinomas operated on between 1983 and 1998 were reviewed. The median patient age was 53.5 years (range 26–74 years). The most frequent presenting symptoms were abdominal pain (13 patients), weight loss (7 patients), and obstructive jaundice (4 patients). Gut hormone profiles were normal in all patients. Abdominal sonography and computed tomography localized the tumor in 17 patients, and correct prediction of an endocrine tumor was achieved in 12 patients. Six of seven patients showed a hypervascular tumor upon angiograpy, and seven of eight patients preoperatively had positive somatostatin receptor scintigraphy. At operation, regional or distant metastases were present in 15 (83%) and 6 (33%) patients, respectively. Eleven patients underwent potentially curative resections, and the remaining seven patients were managed palliatively by resection (four patients) or bypass procedures (three patients). Three patients had up to three more resection for metastases. Eight patients received postoperative octreotide, interferon α therapy, or both. The overall cumulative 5- and 10-year survival rates were 65.4% and 49.1%, respectively. Of the 11 patients who underwent curative resection, 10 were alive after a median follow-up of 63 months (range 7–180 months), but only 5 are free from disease. Although surgical cure is rare in nonfunctioning islet cell carcinomas, significant long-term palliation can be achieved in a large proportion of patients with an aggressive surgical approach and, when indicated, additional medical therapy.


Digestion | 2000

Low Frequency of p16INK4a Alterations in Insulinomas

Detlef K. Bartsch; Michael Kersting; Anja Wild; Annette Ramaswamy; Berthold Gerdes; Marcus Schuermann; Babette Simon; M. Rothmund

Background/Aims: The molecular mechanisms contributing to the tumorigenesis of insulinomas are poorly understood. Disruption of the cell cycle due to inactivation of the p16INK4a tumor-suppressor gene was identified in a variety of human tumors, including gastrinomas and nonfunctioning endocrine pancreatic carcinomas. In this study the role of p16INK4a in the tumorigenesis of insulinomas was evaluated. Methods: Seventeen insulinomas (14 benign, 3 malignant) were analyzed for genetic alterations in the p16INK4a tumor-suppressor gene by SSCP, PCR-based deletion and methylation-specific assays. p16 expression was determined by immunohistochemistry. Results: One malignant insulinoma showed a homozygous deletion of p16INK4a and another two benign insulinomas revealed aberrant methylation of the p16INK4a promoter region. All three tumors lacked p16 expression according to immunohistochemistry. None of the insulinomas carried intragenic p16INK4a mutations. In total, 17% of insulinomas had p16INK4a alterations. Conclusions: The p16INK4a tumor-suppressor gene contributes to tumorigenesis in only a small subset of insulinomas.


Pancreas | 2003

Tumor-suppressing pathways in cystic pancreatic tumors.

Berthold Gerdes; Anja Wild; Judith Wittenberg; Peter J. Barth; Annette Ramaswamy; Michael Kersting; Jutta Lüttges; Günter Klöppel; Detlef K. Bartsch

Introduction and Aims Serous and mucinous cystic pancreatic tumors have different clinical behavior. We evaluated whether they also have genotypic differences by analyses of the tumor suppressor genes p16INK4a, p53, and DPC4. Methodology Seven serous cystadenomas (SCA) and seven malignant mucinous cystadenocarcinomas (MCC) were analyzed for alterations in the tumor suppressor genes p16INK4a, p53, and DPC4 by single-strand conformational variant analysis, direct sequencing, and immunohistochemical analysis. Methylation-specific polymerase chain reaction analysis was performed to identify p16INK4a promoter hypermethylation. Clinical data were compared with genetic data. Results None of the seven patients with SCAs but five of the seven patients with MCCs died of the tumor after a median follow-up of 44.5 months (range, 4–169 months). All seven MCCs had alterations in at least one tumor suppressor gene compared with none of the seven SCAs. Of the seven MCCs, three had inactivating p16INK4a promoter hypermethylation, five had p53 alterations, and three had DPC4 mutations. Conclusions The tumor suppressor genes p16INK4a, p53, and DPC4 appear to play an important role in the tumorigenesis of MCCs but not SCAs. These molecular data underscore the clinical and histologic differences of serous and mucinous cystic pancreatic tumors.


Pancreas | 2005

Alterations of the tissue inhibitor of metalloproteinase-3 (TIMP3) gene in pancreatic adenocarcinomas.

Fendrich; Slater Ep; Heinmöller E; Annette Ramaswamy; Celik I; Nowak O; Chaloupka B; Berthold Gerdes; Detlef K. Bartsch

Objectives: Tissue inhibitor of metalloproteinase-3 (TIMP3) antagonizes matrix metalloproteinase activity and can suppress tumor growth, angiogenesis, invasion, and metastases. In the present study, the involvement of TIMP3 in the tumorigenesis of 34 pancreatic adenocarcinomas was evaluated. Methods: Immunohistochemistry, methylation-specific PCR, and RNA expression analysis (RT-PCR) of TIMP3 were performed in 34 resected and microdissected primary pancreatic adenocarcinomas. Results: Immunohistochemistry showed loss or strongly reduced protein expression in 17 of 34 pancreatic adenocarcinomas (50%) that corresponded to loss of TIMP3-RNA-expression. Promoter hypermethylation was identified in 2 of 34 tumors (6%). It was tumor specific and corresponded to a loss of TIMP3 protein expression. TIMP3 alterations did not correlate with any clinical feature such as tumor size or survival. Conclusion: TIMP3 seems to play an important role in the tumorigenesis of primary pancreatic adenocarcinomas. In contrast to other tumors, hypermethylation seems not to be the key mechanism for the inactivation of TIMP3. Other methods of gene inactivation need to be identified.


Childs Nervous System | 2007

Spatial perception predicts laparoscopic skills on virtual reality laparoscopy simulator

Iyad Hassan; Berthold Gerdes; M. Koller; B. Dick; D. Hellwig; M. Rothmund; A. Zielke

ObjectsThis study evaluates the influence of visual-spatial perception on laparoscopic performance of novices with a virtual reality simulator (LapSim®).Materials and methodsTwenty-four novices completed standardized tests of visual-spatial perception (Lameris Toegepaste Natuurwetenschappelijk Onderzoek [TNO] Test® and Stumpf–Fay Cube Perspectives Test®) and laparoscopic skills were assessed objectively, while performing 1-h practice sessions on the LapSim®, comprising of coordination, cutting, and clip application tasks. Outcome variables included time to complete the tasks, economy of motion as well as total error scores, respectively.ResultsThe degree of visual-spatial perception correlated significantly with laparoscopic performance on the LapSim® scores. Participants with a high degree of spatial perception (Group A) performed the tasks faster than those (Group B) who had a low degree of spatial perception (p = 0.001). Individuals with a high degree of spatial perception also scored better for economy of motion (p = 0.021), tissue damage (p = 0.009), and total error (p = 0.007).ConclusionAmong novices, visual-spatial perception is associated with manual skills performed on a virtual reality simulator. This result may be important for educators to develop adequate training programs that can be individually adapted.


Pancreatology | 2001

Update of Familial Pancreatic Cancer in Germany

Detlef K. Bartsch; Mercedes Sina-Frey; Andreas Ziegler; Stephan A. Hahn; Elvira Przypadlo; Ralf Kress; Berthold Gerdes; Harald Rieder

Background/Aims: The prevalence of familial pancreatic cancer (FPC) and the characteristics of FPC have not yet been well investigated in the German population. Therefore, a German case collection for FPC was established in July 1999 to collect and evaluate data on FPC families. Methods: The prevalence of pancreatic cancer (PC) as well as other tumours and diseases was studied in families with at least 2 first-degree relatives with histologically confirmed PC, and in families of patients with PC and a first-degree relative with malignant melanoma. All participating family members were genetically counselled and evaluated by a standardised questionnaire. Results: In an 18-month period, 73 independent kindreds with potential FPC contacted the national case collection. So far, 20 kindreds have fulfilled the criteria for FPC and have undergone complete workups. Most families revealed an autosomal dominant pattern of inheritance. Twelve families revealed an isolated accumulation of PC. Importantly, in 8 of 20 (35%) families, additional tumour types such as melanoma, breast and prostate cancer occurred. Conclusion: The observed phenotypic heterogeneity indicates an association with predisposing tumour suppressor genes p16 and BRCA2 in up to 30% of FPC families. Mutation analysis of these candidate genes might lead to the identification of the predisposing gene defect in a proportion of FPC families.

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Andreas Ziegler

University of KwaZulu-Natal

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A. Zielke

University of Marburg

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Anja Wild

University of Marburg

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