Albert Roessner

Otto-von-Guericke-Universität Magdeburg, Magdeburg, Saxony-Anhalt, Germany

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Publications (590)1609.22 Total impact

  • [Show abstract] [Hide abstract]
    ABSTRACT: Tamoxifen is the standard endocrine therapy for patients with premenopausal, estrogen receptor positive (ER+) breast cancer. However, up to 30% of the carcinomas are resistant or develop resistance against this drug. Our current understanding of tamoxifen resistance indicates a contribution of membrane-bound estrogen receptors, such as the G-protein coupled estrogen receptor GPER or alternative splice products of the estrogen receptor α. In tamoxifen resistant breast cancer, the estrogen dependent growth is then replaced by signalling through growth factors such as the epidermal growth factor (EGF) or the insulin like growth factor 1(IGF-1). We here investigated the ER-positive breast cancer cell line MCF-7 as a model for aquired tamoxifen resistance. When these cells were exposed to 4-OH-tamoxifen, a tamoxifen-resistance phenotype developed within three months. We then analyzed transcriptomic changes by gene-array analysis during the time course of this adaptation and compared early to late changes in gene expression. Cluster analysis revealed that an early stress response lasting about one week was followed by a phase of establishing a stable gene expression pattern, characterized by an enhanced expression of NF-kB related genes and characteristic changes in mRNA abundance of genes involved in the organization of the extracellular matrix. We therefore propose that NF-kB plays a crucial role in the establishment of tamoxifen resistance.
    No preview · Conference Paper · Nov 2015
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    Full-text · Dataset · Sep 2015
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    ABSTRACT: Introduction It is postulated that focal IRE affords complete ablation of soft-tissue tumours while protecting the healthy peritumoral tissue. Therefore, IRE may be an interesting option for minimally invasive, kidney-tissue-sparing, non-thermal ablation of renal tumours. Aim With this current pilot study (“IRENE trial”), we present the first detailed histopathological data of IRE of human RCC followed by delayed tumour resection. The aim of this interim analysis of the first three patients was to investigate the ablation efficiency of percutaneous image-guided focal IRE in RCC, to assess whether a complete ablation of T1a RCC and tissue preservation with the NanoKnife system is possible and to decide whether the ablation parameters need to be altered. Methods Following resection 4 weeks after percutaneous IRE, the success of ablation and detailed histopathological description were used to check the ablation parameters. Results The IRE led to a high degree of damage to the renal tumours (1 central, 2 peripheral; size range 15–17 mm). The postulated homogeneous, isomorphic damage was only partly confirmed. We found a zonal structuring of the ablation zone, negative margins and, enclosed within the ablation zone, very small tumour residues of unclear malignancy. Conclusion According to these initial, preliminary study results of the first three renal cases, a new zonal distribution of IRE damage was described and the curative intended, renal saving focal ablation of localised RCC below <3 cm by percutaneous IRE by the NanoKnife system appears to be possible, but needs further, systematic evaluation for this treatment method and treatment protocol.
    Full-text · Article · Sep 2015 · CardioVascular and Interventional Radiology
  • T Wex · G Treiber · M Nilius · M Vieth · A Roessner · P Malfertheiner

    No preview · Article · Aug 2015 · Zeitschrift für Gastroenterologie
  • U Peitz · M Vieth · A Leodolter · S Kahl · A Roessner · P Malfertheiner

    No preview · Article · Aug 2015 · Zeitschrift für Gastroenterologie
  • Norbert Nass · Albert Roessner · Thomas Kalinski
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    ABSTRACT: Background: The dicarbonyls glyoxal and methylglyoxal are reactive alde- hydes with significant toxicity towards many cell types. Glyoxalase 1 is a major defence enzyme against dicarbonyl stress and upregulated in many cancer entities. We have recently shown that tamoxifen resistant mamma carcinoma cells derived from the estrogen receptor positive MCF-7 cell line exhibited increased sensitivity towards these aldehydes, which corre- lated with reduced amounts of free sulfhydryl groups in the tamoxifen re- sistant cell line. Here, we analysed whether glyoxalase 1 is responsible for aldehyde defence in these cells. Methods: Glyoxalase (GLO1) expression was determined by qRT-PCR and Western-Blotting. Reactive oxygen species (ROS) were determined by the ROS sensitive dye 2',7'-dichlorodihydrofluorescein diacetate (H2DCF- DA) and cell viability/proliferation was assessed by the resazurin assay. A specific glyoxalase 1 inhibitor and siRNA technique was applied to mod- ulate GLO1 activity. The inhibitors SB203580 and UO126 were used to study the importance of MAP-kinase activity and diphenylene-iodonium (DPI) was applied as specific inhibitor of NADPH-oxidases. Results: Aldehyde stress induced the production of reactive oxygen spe- cies by NADPH-oxidase in MCF-7 cells as well as in a tamoxifen resistant derivative (TamR). Inhibition of p38 MAPK caused reduced production of ROS. Inhibition of GLO1 resulted in higher sensitivity towards dicar- bonyl stress. GLO1-protein expression was not altered in the tamoxifen resistant cells, but the expression of the DJ-1 glyoxalase was significant- ly reduced. Also, mRNA-accumulation of several NF-kB subunits was al- tered in the TamR cell line, which correlates with the observation that TamR but not MCF-7 cells responded to aldehyde stress by phosphoryla- tion of IkBalpha and this further supports the proposal that NF-kB activ- ity contributes to tamoxifen resistance. Conclusions. Expression of glyoxalase 1 and DJ-1 might be useful as prog- nostic markers in ER-positive mamma carcinomas.
    No preview · Conference Paper · May 2015
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    ABSTRACT: Adenocarcinomas at the gastro-oesophageal junction (GOJ) are currently stratified by tumour location. This retrospective study examines the association of preneoplastic conditions and inflammation of the gastric mucosa with GOJ cancer at different locations and compares them with nonjunctional gastric cancers. A total of 520 patients with junctional and nonjunctional gastric cancer were assessed for the presence and degree of intestinal metaplasia, glandular atrophy and inflammation in the stomach. Histopathological data were complete for 428 patients (68.9% men, median age 67.7 years), including 172 patients with GOJ cancer (GOJ1: 1-5 cm proximal to the junction, GOJ2: 'true' junctional, GOJ3: 2-5 cm distal to the junction). Gastric inflammation and preneoplastic conditions were scored according to the updated Sydney classification and further stratified into respective operative link on gastritis assessment (OLGA) and operative link on gastritis assessment on intestinal metaplasia (OLGIM) stages. The prevalence and degree of gastric atrophy and intestinal metaplasia were significantly lower in GOJ1 than GOJ3 (P<0.01). Preneoplastic conditions in the stomach were similar in GOJ3 compared with nonjunctional gastric cancer. GOJ1 were almost exclusively (98.4%) of the intestinal type, whereas GOJ2 and GOJ3 were the diffuse type in 22.6 and 22.4% of the patients (P<0.001). Of all patients, only 8.5 and 12.7% presented with stage III/IV according to OLGA and OLGIM, respectively. However, data for OLGA and OLGIM staging were only available in 61.2 and 67.9% of patients, respectively. GOJ1 are less likely to be associated with gastric pathology compared with GOJ3 or nonjunctional gastric cancer. OLGA or OLGIM staging in patients with advanced gastro-oesophageal cancer seems to be of limited value.
    Full-text · Article · May 2015 · European journal of gastroenterology & hepatology
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    ABSTRACT: The lysosomal cysteine carboxypeptidase cathepsin X (CTSX), localized predominantly in immune cells, has been associated with the development and progression of cancer. To determine its specific role in colorectal carcinoma (CRC), we analyzed CTSX expression in non-malignant mucosa and carcinoma of 177 patients as well as in 111 adenomas and related it with clinicopathological parameters. Further, the role of CTSX in the adhesion and invasion of the colon carcinoma cell lines HT-29 and HCT116 was investigated in an in vitro culture cell system with fibroblasts and monocytes, reflecting the situation at the tumor invasion front. Epithelial CTSX expression significantly increased from normal mucosa to adenoma and carcinoma, with highest expression levels in high grade intraepithelial neoplasia and in early tumor stages. Loss of CTSX occurred with tumor progression, and correlated with advanced local invasion, lymph node and distal metastasis, lymphatic vessel and vein invasion, tumor cell budding and poorer overall survival of patients with CRC. The subcellular distribution of CTSX changed from vesicular paranuclear expression in the tumor center to submembranous expression in cells of the invasion front. Peritumoral macrophages showed highest expression of CTSX. In vitro assays identified CTSX as relevant factor for cell-cell adhesion and tumor cell anchorage to fibroblasts and basal membrane components, whereas inhibition of CTSX caused increased invasiveness of colon carcinoma cells in mono- and co-culture. In conclusion, CTSX is involved in early tumorigenesis and in the stabilization of tumor cell formation in CRC. The results suggest that loss of CTSX may be needed for tumor cell detachment, local invasion and tumor progression. In addition, CTSX in tumor-associated macrophages indicates a role for CTSX in the anti-tumor immune response.
    No preview · Article · Dec 2014 · Pathology - Research and Practice
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    ABSTRACT: Cathepsin X (CTSX, also called cathepsin Z/P) is a cysteine protease that still plays an unknown role in human cancer. It has been shown to bind cell surface heparin sulphate proteoglycans and integrins, indicating possible functions of CTSX in cellular adhesion, phagocytosis, and immune response. Our previous studies have shown an association between Helicobacter pylori (H. pylori) infection, a strong up-regulation of CTSX, and development of gastric cancer. In this study, yeast two-hybrid analysis revealed that RPLP0, a ribosomal protein P0, interacts with the human CTSX protein in gastric cancer. The CTSX/RPLP0 interaction was confirmed by co-immunoprecipitation assays. In addition, co-localization studies in cancer cell line N87 and gastric cancer tissue samples were performed. Laserscan microscopy revealed a shuttling of RPLP0 (and CTSX) from cytoplasm to the nucleus after CTSX knockdown. Down-regulation of RPLP0 resulted in G1 arrest of gastric cancer cells, whereas knockdown of CTSX led to G1 arrest and apoptosis after 48 h. Knockdown of both proteins caused increased apoptosis. RPLP0 deficiency could suppress cell growth and cell cycle progression by down-regulating CDK2. It was further demonstrated that RPLP0 affected p21 expression, but did not change the expression of Cyclin E. Down-regulation of both proteins at least through CDK2 suggests an anti-apoptotic effect on gastric cancer cells and opens up new possibilities for apoptotic immune modulation and gastric cancer therapy.
    No preview · Article · Sep 2014 · Pathology - Research and Practice
  • Norbert Nass · Albert Roessner · Thomas Kalinski
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    ABSTRACT: Objective Interleukin (IL)-1 signalling plays an important role in inflammatory and also malignant processes. IL-1 signals essentially via nuclear factor (NF)-κB, which controls the expression of genes involved in cell proliferation, invasion, angiogenesis and metastasis, among them vascular endothelial growth factor A (VEGF-A). As microenvironment-derived IL-1β is required for invasion and angiogenesis in malignant tumours, such as chondrosarcomas, we investigated whether the anti-inflammatory compound curcumin is able to interfere with IL-1-induced VEGF-a secretion. Methods Cell cultures of chondrosarcoma cell lines C3842 and SW1353 were treated with IL-1ß and curcumin and VEGF-A secretion was analysed by Western blotting. Gene expression was determined by qRT-PCR. The angiogenenic potential of cell culture supernatants was investigated by a 2-dimensional angiogenesis assay using human umbilical chord endothelial cells (HUVECs). Activation of the nuclear factor NF-κB was analysed by determination of IκBα phosphorylation on Western blots and immunofluorescence. Results IL-1 signalling and VEGF-A expression are blocked by curcumin in chondrosarcoma cells. We further show that curcumin blocks IL-1β-induced angiogenesis and NF-κB-related gene expression. Conclusions We propose that IL-1 blockade is an additionally treatment option in chondrosarcoma, either by curcumin, its derivatives or other IL-1 blocking agents.
    No preview · Conference Paper · Sep 2014
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    ABSTRACT: Recent studies have suggested that Helicobacter pylori (H. pylori) constitutes a risk for the development of colonic neoplasia. Hypergastrinemia can be induced by H. pylori infection and gastrin can act as putative promoter of colorectal carcinogenesis. Aim of the study was to assess whether H. pylori infection and/or increased serum gastrin levels are associated with the occurrence of colonic neoplasms. For this, we reviewed prospectively collected data of 377 patients with a minimum age of 50 years that underwent colonoscopy. H. pylori and CagA status were determined by serology. Serum gastrin levels were measured in fasting state by commercially available assay. In H. pylori infected patients (n=138; 36.6%), the overall prevalence of colonic neoplasms was more frequent compared to H. pylori negative patients (n=239; 63.4%) (OR=2.73, 95% CI: 1.76-4.24). H. pylori infection occurred more frequently in patients with hyperplastic polyps (OR= 2.66, 95% CI: 1.23-5.74) and adenomas presenting with low grade intraepithelial neoplasia (IEN) (OR= 1.85, 95% CI: 1.14-2.99). Attributable risk for adenomas with high grade IEN and colorectal adenocarcinoma (n=14) was not assessed due to the low number of cases. The expression of CagA was also associated with an increased risk for colonic neoplasms (OR= 2.25, 95% CI: 1.29-3.94). Hypergastrinemia did not increase the risk for any colonic neoplasms and there was no difference in basal serum gastrin levels between H. pylori positive and negative patients. In conclusion, H. pylori infection, including CagA expression is associated with an increased risk for the development of colonic neoplasm. © 2014 Wiley Periodicals, Inc.
    Preview · Article · Sep 2014 · International Journal of Cancer

  • No preview · Conference Paper · Sep 2014
  • F Popp · MC Popp · T Kalinski · A Roessner · H Lippert · C Bruns

    No preview · Article · Aug 2014 · Zeitschrift für Gastroenterologie

  • No preview · Article · Aug 2014 · Zeitschrift für Gastroenterologie
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    ABSTRACT: Tamoxifen is the standard adjuvant endocrine therapy for estrogen-receptor positive premenopausal breast cancer patients. However, tamoxifen resistance is frequently observed under therapy. A tamoxifen resistant cell line has been generated from the estrogen receptor positive mamma carcinoma cell line MCF-7 and was analyzed for putative differences in the aldehyde defence system and accumulation of advanced glycation end products (AGE). In comparison to wt MCF-7 cells, these tamoxifen resistant cells were more sensitive to the dicarbonyl compounds glyoxal and methylglyoxal and displayed increased caspase activity, p38-MAPK- and IκBα-phosphorylation. However, mRNA accumulation of the aldehyde- and AGE-defence enzymes glyoxalase-1 and -2 (GLO1, GLO2) as well as fructosamine-3-kinase (FN3K) was not significantly altered. Tamoxifen resistant cells contained less free sulfhydryl-groups (glutathione) suggesting that the increased sensitivity towards the dicarbonyls was due to a higher sensitivity towards reactive oxygen species which are associated with dicarbonyl stress. To further analyse, if these data are of more general importance, key experiments were replicated with tamoxifen resistant MCF-7 cell lines from two independent sources. These cell lines were also more sensitive to aldehydes, especially glyoxal, but were different in their cellular signalling responses to the aldehydes. In conclusion, glyoxalases and other aldehyde defence enzymes might represent a promising target for the therapy of tamoxifen resistant breast cancers.
    Full-text · Article · Jul 2014 · PLoS ONE
  • Norbert Nass · Albert Roessner · Thomas Kalinski
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    ABSTRACT: Aims. The alpha-oxo-aldehydes glyoxal and methylglyoxal are byproducts of fatty acid oxidation and glycolysis. Due to the high glycolytic activity caused by the Warburg effect, cancer cells produce significantly more aldehydes than other cells. These substances are highly reactive and modify amino groups on proteins, often resulting in loss of function. These modifications also result in stable accumulating products, the so called advanced glycation end products (AGEs). In this study we analysed the responses of the estrogen receptor positive mamma carcinoma cell line MCF-7 to glyoxal and methylglyoxal to evaluate if dialdehyde defence might be a target for breast cancer treatment. Methods. Cell vitality was determined by the resazurin assay. Activation of MAP-kinases and NF-κB was determined by Western blotting, using specific antibodies against the phosphorylated proteins. Oxidative stress was measured by loading the cells with the oxidation-sensitive fluorochrome dihydrofluorescein-diacetate. Mode of cell death was analysed by caspase activity assay and annexin-V flow cytometry. Results. Dialdehydes resulted in cell death in low millimolar concentrations. Cells exposed to the aldehydes responded by a rapid activation of MAP-kinase signalling especially p38-MAPK and production of reactive oxygen species as well as activation of caspase 3/7 activity, finally leading to cell death. Interestingly, a tamoxifen resistant derivative of MCF-7 showed an additional activation of the NF-κB transcription factor by methylglyoxal only and was altogether more sensitive to the aldehydes. Addition of the antioxidant N-acetyl cystein protected the cells, demonstrating that oxidative stress was a major cause of cell death. Conclusions. These data demonstrate that exogenous aldehyde stress is cytotoxic to mamma carcinoma cells by causing severe oxidative stress. Inhibition of aldehyde defence enzymes such as glyoxalases might therefore be a promising therapeutic option against breast cancer.
    No preview · Conference Paper · Jun 2014
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    Full-text · Dataset · Jun 2014
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    ABSTRACT: Interleukin (IL)-1 signaling plays an important role in inflammatory processes, but also in malignant processes. The essential downstream event in IL-1 signaling is the activation of nuclear factor (NF)-κB, which leads to the expression of several genes that are involved in cell proliferation, invasion, angiogenesis and metastasis, among them VEGF-A. As microenvironment-derived IL-1β is required for invasion and angiogenesis in malignant tumors, also in chondrosarcomas, we investigated IL-1β-induced signal transduction and VEGF-A expression in C3842 and SW1353 chondrosarcoma cells. We additionally performed in vitro angiogenesis assays and NF-κB-related gene expression analyses. Curcumin is a substance which inhibits IL-1 signaling very early by preventing the recruitment of IL-1 receptor associated kinase (IRAK) to the IL-1 receptor. We demonstrate that IL-1 signaling and VEGF-A expression are blocked by Curcumin in chondrosarcoma cells. We further show that Curcumin blocks IL-1β-induced angiogenesis and NF-κB-related gene expression. We suppose that IL-1 blockade is an additional treatment option in chondrosarcoma, either by Curcumin, its derivatives or other IL-1 blocking agents.
    Full-text · Article · Jun 2014 · PLoS ONE
  • T Ignatov · H Eggemann · S D Costa · A Roessner · T Kalinski · A Ignatov
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    ABSTRACT: The aim of the current study was to investigate the role of BRCA1 promoter methylation as predictive factor of response to platinum-taxane-based therapy in sporadic ovarian cancer. BRCA1 promoter methylation was analyzed in 42 sporadic epithelial ovarian cancers. The results were validated in a second cohort of 137 ovarian cancer patients. BRCA1 promoter methylation was observed in 35.7 % of patients in the first group and in 33.6 % in the second group. BRCA1 promoter methylation was associated with significant increase in median progression-free survival (PFS) of ovarian cancer patients receiving adjuvant platinum-taxane-based chemotherapy (P = 0.008). Multivariate analysis revealed that BRCA1 promoter methylation remains a favorable factor in regard to PFS (HR 0.52; 95 % CI 0.32-0.85, P = 0.009) after adjustment for other prognostic factors. Under the patients with recurrent disease, BRCA1 promoter methylation was associated with significant longer median PFS of 18.5 months in comparison with 12.8 months PFS for patients without BRCA1 promoter methylation. BRCA1 promoter methylation is predictive for better response to platinum-taxane-based therapy in EOC.
    No preview · Article · May 2014 · Journal of Cancer Research and Clinical Oncology
  • Albert Roessner · Angela Poehlmann
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    ABSTRACT: This chapter describes the continuing paramount importance of the histological diagnosis of Barrett's cancer and its prestages. It discusses the possible role of molecular predictors for estimation of the malignant potential of the prestages. The discussion includes a brief overview of the current experience with “biomarkers” for the diagnosis of Barrett's carcinogenesis, addressing the question of why their practical values have proven limited so far. The chapter also discusses the relationship between inflammation and Barrett's carcinogenesis, particularly for reflux esophagitis, including the role of genetic and epigenetic alterations in Barrett's carcinogenesis and the role of inflammation-associated reactive oxygen and nitrogen species (ROSs/RNSs).
    No preview · Chapter · Apr 2014

Publication Stats

10k Citations
1,609.22 Total Impact Points


  • 1994-2015
    • Otto-von-Guericke-Universität Magdeburg
      • • Institut für Pathologie
      • • Clinic for Gastroenterology, Hepatology and Infectiology
      • • Institute for Neuropathology
      Magdeburg, Saxony-Anhalt, Germany
    • St. Johannes Hopital Dortmund
      Dortmund, North Rhine-Westphalia, Germany
  • 1998-2010
    • University Hospital Magdeburg
      Magdeburg, Saxony-Anhalt, Germany
    • University of California, Irvine
      Irvine, California, United States
  • 1971-1996
    • University of Münster
      • • Gerhard-Domagk-Institute of Pathology
      • • Institute of Neuropathology
      • • Institute of Physical Chemistry
      • • Institute of Applied Physics
      Muenster, North Rhine-Westphalia, Germany
    • Fachhochschule Münster
      Muenster, North Rhine-Westphalia, Germany
  • 1993
    • Universitätsklinikum Münster
      Muenster, North Rhine-Westphalia, Germany
  • 1992
    • Kyoto University
      Kioto, Kyōto, Japan
  • 1989
    • Heinrich-Heine-Universität Düsseldorf
      Düsseldorf, North Rhine-Westphalia, Germany
  • 1987
    • University of Campinas
      Conceição de Campinas, São Paulo, Brazil
  • 1984
    • Pathologisches Institut Bremerhaven
      Bremerhaven, Bremen, Germany
  • 1975
    • Nagasaki University Hospital
      Nagasaki, Nagasaki, Japan
  • 1974
    • Johannes Gutenberg-Universität Mainz
      Mayence, Rheinland-Pfalz, Germany
  • 1972
    • University of Bonn - Medical Center
      Bonn, North Rhine-Westphalia, Germany