Thomas Seufferlein

Ruhr-Universität Bochum, Bochum, North Rhine-Westphalia, Germany

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Publications (238)835.67 Total impact

  • [Show abstract] [Hide abstract]
    ABSTRACT: The kinase PRKD2 is a crucial regulator of tumor cell-endothelial cell communication in gastrointestinal tumors and glioblastomas, but its mechanistic contributions to malignant development are not understood. Here we report that the oncogenic chaperone HSP90 binds to and stabilizes PRKD2 in human cancer cells. Pharmacologic inhibition of HSP90 with structurally divergent small molecules currently in clinical development triggered proteasome-dependent degradation of PRKD2, augmenting apoptosis in human cancer cells of various tissue origins. Conversely, ectopic expression of PRKD2 protected cancer cells from the apoptotic effects of HSP90 abrogation, restoring blood vessel formation in two preclinical models of solid tumors. Mechanistic studies revealed that PRKD2 is essential for hypoxia-induced accumulation of HIF-1α and activation of NF-κB in tumor cells. Notably, ectopic expression PRKD2 was able to partially restore HIF-1α and secreted VEGF-A levels in hypoxic cancer cells treated with HSP90 inhibitors. Taken together, our findings indicate that signals from hypoxia and HSP90 pathways are interconnected and funneled by PRKD2 into the NF-κB/ VEGF-A signaling axis to promote tumor angiogenesis and tumor growth.
    Cancer research. 10/2014;
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    ABSTRACT: Pancreatic adenocarcinomas are associated with a poor survival prognosis. Besides curative surgical resection, only limited therapies with modest impact are available. New evidence suggests that the mammalian target of rapamycin pathway may be involved in the pathogenesis of neuroendocrine tumors, and breast and renal cell cancer. The phase I study described here was therefore designed to determine the maximum tolerated dose (MTD) and dose-limiting toxicity (DLT) of escalating doses of the mammalian target of rapamycin inhibitor everolimus in combination with gemcitabine in patients with advanced pancreatic cancer. Eligible patients had histologically confirmed locally advanced and/or metastatic pancreatic carcinoma and were administered 5 mg everolimus every second day (cohort 1, 2, 3) or 5 mg daily (cohort 4, 5) in combination with escalating low-dose gemcitabine. It was found that if two patients showed DLTs, MTD was reached and gemcitabine dose escalation was stopped at this level. Twenty-seven patients were enrolled in the study (cohort 1: n=3; cohort 2: n=4; cohort 3: n=6; cohort 4: n=7; cohort 5: n=7) and received a maximum 600 mg gemcitabine/week. In cohort 5, two of the six patients experienced DLTs (grade 3 liver toxicity lasting for>7 days). MTD was measured as 400 mg/m/week gemcitabine plus 5 mg/day everolimus. The MTD of a low-dose gemcitabine treatment in combination with everolimus was determined and no new safety concerns were identified in patients with advanced pancreatic cancer.
    Anti-cancer drugs. 07/2014;
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    ABSTRACT: Background Gemcitabine plus a platinum-based agent (eg, cisplatin or oxaliplatin) is the standard of care for advanced biliary cancers. We investigated the addition of cetuximab to chemotherapy in patients with advanced biliary cancers. Methods In this non-comparative, open-label, randomised phase 2 trial, we recruited patients with locally advanced (non-resectable) or metastatic cholangiocarcinoma, gallbladder carcinoma, or ampullary carcinoma and a WHO performance status of 0 or 1 from 18 hospitals across France and Germany. Eligible patients were randomly assigned (1:1) centrally with a minimisation procedure to first-line treatment with gemcitabine (1000 mg/m2) and oxaliplatin (100 mg/m2) with or without cetuximab (500 mg/m2), repeated every 2 weeks until disease progression or unacceptable toxicity. Randomisation was stratified by centre, primary site of disease, disease stage, and previous treatment with curative intent or adjuvant therapy. Investigators who assessed treatment response were not masked to group assignment. The primary endpoint was the proportion of patients who were progression-free at 4 months, analysed by intention to treat. This study is registered with, number NCT00552149. Findings Between Oct 10, 2007, and Dec 18, 2009, 76 patients were assigned to chemotherapy plus cetuximab and 74 to chemotherapy alone. 48 (63%; 95% CI 52–74) patients assigned to chemotherapy plus cetuximab and 40 (54%; 43–65) assigned to chemotherapy alone were progression-free at 4 months. Median progression-free survival was 6·1 months (95% CI 5·1–7·6) in the chemotherapy plus cetuximab group and 5·5 months (3·7–6·6) in the chemotherapy alone group. Median overall survival was 11·0 months (9·1–13·7) in the chemotherapy plus cetuximab group and 12·4 months (8·6–16·0) in the chemotherapy alone group. The most common grade 3–4 adverse events were peripheral neuropathy (in 18 [24%] of 76 patients who received chemotherapy plus cetuximab vs ten [15%] of 68 who received chemotherapy alone), neutropenia (17 [22%] vs 11 [16%]), and increased aminotransferase concentrations (17 [22%] vs ten [15%]). 70 serious adverse events were reported in 39 (51%) of 76 patients who received chemotherapy plus cetuximab (34 events in 19 [25%] patients were treatment-related), whereas 41 serious adverse events were reported in 25 (35%) of 71 patients who received chemotherapy alone (20 events in 12 [17%] patients were treatment-related). One patient died of atypical pneumonia related to treatment in the chemotherapy alone group. Interpretation The addition of cetuximab to gemcitabine and oxaliplatin did not seem to enhance the activity of chemotherapy in patients with advanced biliary cancer, although it was well tolerated. Gemcitabine and platinum-based combination should remain the standard treatment option. Funding Institut National du Cancer, Merck Serono.
    The Lancet Oncology 07/2014; · 25.12 Impact Factor
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    ABSTRACT: Ductal adenocarcinoma of the pancreas is the fourth most common cause of death from cancer in men and women in Germany: about 15 000 persons die of this disease each year.
    Deutsches Ärzteblatt international. 05/2014; 111(22):396-402.
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    ABSTRACT: Epidermal growth factor receptor inhibitor (EGFRI) induced skin toxicity has a prognostic value suggesting skin toxicity can be a useful surrogate marker for successful epidermal growth factor receptor (EGFR) inhibition, improved response and survival. But the pathophysiology of EGFRI induced skin toxicity remains elusive. However the involvement of immunological mechanisms has been speculated. This study investigates the possible underlying mechanism of EGFR inhibition associated cytokine production in keratinocytes as well as in patients after treatment with epidermal growth factor receptor inhibitors (EGFRIs).
    European journal of cancer (Oxford, England: 1990) 05/2014; · 4.12 Impact Factor
  • Christoph Wille, Thomas Seufferlein, Tim Eiseler
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    ABSTRACT: Highly invasive pancreatic tumors are often recognized in late stages due to a lack of clear symptoms and pose major challenges for treatment and disease management. Broad-band Protein Kinase D (PKD) inhibitors have recently been proposed as additional treatment option for this disease. PKDs are implicated in the control of cancer cell motility, angiogenesis, proliferation and metastasis. In particular, PKD2 expression is elevated in pancreatic cancer, whereas PKD1 expression is comparably lower. In our recent study we report that both kinases control PDAC cell invasive properties in an isoform-specific, but opposing manner. PKD1 selectively mediates anti-migratory/anti-invasive features by preferential regulation of the actin-regulatory Cofilin-phosphatase Slingshot1L (SSH1L). PKD2, on the other hand enhances invasion and angiogenesis of PDAC cells in 3D-ECM cultures and chorioallantois tumor models by stimulating expression and secretion of matrix-metalloproteinase 7 and 9 (MMP7/9). MMP9 also enhances PKD2-mediated tumor angiogenesis releasing extracellular matrix-bound VEGF-A. We thus suggest high PKD2 expression and loss of PKD1 may be beneficial for tumor cells to enhance their matrix-invading abilities. In our recent study we demonstrate for the first time PKD1 and 2 isoform-selective effects on pancreatic cancer cell invasion, in-vitro and in-vivo, defining isoform-specific regulation of PKDs as a major future issue.
    Bioarchitecture. 05/2014; 4(3).
  • T Seufferlein, A Kleger, S Nitschmann
    Der Internist 03/2014; · 0.33 Impact Factor
  • A Kleger, L Perkhofer, T Seufferlein
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    ABSTRACT: Pancreatic ductal adenocarcinoma (PDAC) is one of the leading causes of cancer death in the Western world. Owing to a lack of specific symptoms and no accessible precursor lesions, primary diagnosis is commonly delayed, resulting in only 15%-20% of patients with potentially curable disease. The standard of care in advanced pancreatic cancer has improved. Apart from gemcitabine (plus erlotinib), FOLFIRINOX and the combination of gemcitabine plus nab-paclitaxel are novel and promising therapeutic options for patients with metastatic PDAC. A better molecular understanding of pancreatic cancer has led to the identification of a variety of potential molecular therapeutic targets. Many targeted therapies are currently under clinical evaluation in combination with standard therapies for PDAC. This review highlights the current status of targeted therapies and their potential benefit for the treatment of advanced PDAC.
    Annals of Oncology 03/2014; · 7.38 Impact Factor
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    ABSTRACT: In order to improve the quality of treatment for cancer patients the German Cancer Society (Deutsche Krebsgesellschaft) implemented a certification system for oncological care institutions. The certified colorectal cancer centers present the structures, processes and results of their network in the framework of an auditing procedure. The current benchmarking report by the certified centers reflects the centers' reference results over a period of 3 years. The figures included in the benchmarking report reflect the areas of interdisciplinary collaboration, guideline-compliant treatment, and expertise of the main treatment partners. High percentages were shown for indicators reflecting pretreatment and postoperative case presentations in multidisciplinary team meetings (91.8 % or 98.1 %), psycho-oncologic care (54.8 %) as well as social service counseling (77.1 %). Good quality of the TME rectal specimen and adequate lymph-node retrieval (12 lymph nodes at least) was achieved by 93 % or 96.6 % of the centers. Adjuvant chemotherapy (colon, Union for International Cancer Control [UICC] stage III) or neoadjuvant radiotherapy or chemoradiotherapy (rectum, UICC stages II and III) received 73.7 % or 80 % of relevant patients. Quotas of anastomotic leakage in the colon or rectum were 4.4 % or 7.6 %, whereas postoperative mortality amounted to 2.6 %. The present analysis of the results, together with the centers' statements and the auditors' reports, shows that most of the targets for indicator figures are being better met over the course of time. In addition, however, there is a clear potential for improvement and the centers are verifiably addressing this. A transparent presentation of the quality of care and reflection on and discussion of the results among the treatment partners in the certified network and with the auditors during the certification process may contribute to constant quality improvement in oncological care.
    International Journal of Colorectal Disease 03/2014; · 2.24 Impact Factor
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    ABSTRACT: Pluripotent stem cells possess a remarkable unlimited self-renewal capacity and offer unparalleled in vitro differentiation potential. This provides a unique model system not only to study early human development but also gives renewed hope in terms of developing cell therapies and regenerative medicine. S. Yamanaka, a medical doctor and researcher, reported the possibility of reprogramming somatic cells to so-called induced pluripotent stem cells via the ectopic expression of four transcription factors, namely Oct4, Sox2, Klf4 and c-Myc. This Nobel Prize winning work has since revolutionized stem cell research and paved the way for countless new avenues within regenerative medicine. This includes disease modeling in a patient-specific context with the ultimate aim of individually tailored pharmaceutical therapy. Additionally, genetic correction studies have rapidly increased in basic science and thus there is hope that these can be effectively and efficiently translated into clinical applications. Addressing the medical community this review gives a broad general overview about the state of the research field and possible clinical applications of pluripotent stem cells.
    Der Internist 02/2014; · 0.33 Impact Factor
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    ABSTRACT: Background and AimsThe rs738409 variant (I148M) of the patatin-like phospholipase domain-containing protein 3 (PNPLA3) gene is associated with several liver malfunctions. Its impact on end-stage liver disease has not been addressed yet. Methods The I148M polymorphism was genotyped in a well-characterised cohort of 421 Caucasian patients and retrospectively analysed from the time of enrolment at Eurotransplant. ResultsThe G allele of the I148M variant was significantly overrepresented in patients with alcoholic liver disease (ALD, p < 0.001) and associated with hepatocellular carcinoma (HCC) development (OR = 2.399; 95% CI: 1.292–4.455; p = .008) while not affecting the other liver disease entities. Time until hydropic decompensation (p = .04) and hepatic encephalopathy (p = .043) was significantly impaired for ALD patients carrying either one or two mutated G alleles. Actuarial survival free of liver transplantation was further reduced for ALD carriers of the I148M variant (CC = 30.7 months ±7.9, 95% CI: 15.1–46.2 vs. CG/GG: 17.1 months ±3.3, 95%CI: 3.3-10.6; p = .012) compared to wild-type patients. Cox multivariate analysis identified the PNPLA3 I148M genotype as an independent predictor actuarial survival free of liver transplantation (OR = 1.77; 95% CI: 1.27-2.47; p = .001). Conclusions In end-stage liver disease patients, we identified ALD to be predominantly affected by the PNPLA3 I148M variant resulting in an increased risk of HCC and reduced transplantation free survival. Genetic testing of the I148M genotype in ALD patients awaiting liver transplantation might be beneficial for these patients.
    Journal of Gastroenterology and Hepatology 02/2014; · 3.33 Impact Factor
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    ABSTRACT: For almost 15 years there has been stagnation in the systemic treatment of patients with pancreatic ductal adenocarcinoma (PDAC). Recently, several developments seem to indicate clinically relevant improvements in the treatment of patients with metastatic disease. One of these developments is the introduction of nanoparticle albumin-bound paclitaxel (nab-paclitaxel) into the firstline treatment of metastatic disease. In this review, underlying preclinical and clinical data are discussed, with a special focus on mechanisms of action, the potential interaction with albumin and calcium-binding matricellular glycoproteins, such as the secreted protein acidic and rich in cysteine (SPARC), as well as the clinical outcome associated with the use of nab-paclitaxel. © 2014 S. Karger GmbH, Freiburg.
    Oncology research and treatment. 01/2014; 37(3):128-34.
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    ABSTRACT: Aim Epidermal growth factor receptor inhibitor (EGFRI) induced skin toxicity has a prognostic value suggesting skin toxicity can be a useful surrogate marker for successful epidermal growth factor receptor (EGFR) inhibition, improved response and survival. But the pathophysiology of EGFRI induced skin toxicity remains elusive. However the involvement of immunological mechanisms has been speculated. This study investigates the possible underlying mechanism of EGFR inhibition associated cytokine production in keratinocytes as well as in patients after treatment with epidermal growth factor receptor inhibitors (EGFRIs). Methods Normal human epidermal keratinocytes (NHEK) were incubated for 2 and 24 h with different concentrations of EGFRI (erlotinib) for Western blot analysis and cytokine expression analysis, respectively. Inhibition of EGFR, extracellular-signal-regulated kinase 1/2 (Erk 1/2) and c-Jun was examined by Western blot analysis. Cytokine concentrations were measured by enzyme-linked immunosorbent assay (ELISA) in the NHEK cell supernatant and also in the serum of 186 cancer patients who are followed up for EGFRI induced skin rash. Results A significant inhibitory effect of EGFRI was seen on EGFR (Y845), Erk 1/2 and c-Jun in a dose dependent manner. Further downstream, increased CC-chemokine ligand 2 (CCL2), CC-chemokine ligand 5 (CCL5) and decreased interleukin-8 (IL-8) or CXCL8 expression was observed in keratinocytes. In EGFRI treated patients, low levels of serum CXCL8 corresponding to stronger EGFR inhibition were associated with a higher grade of skin toxicity (p = 0.0016) and a prolonged overall survival (p = 0.018). Conclusions The results obtained in this study indicate that EGFRI can regulate cytokines by modulating EGFR signalling pathway in keratinocytes. Moreover, serum levels of CXCL8 in EGFRI treated patients may be important for individual EGFRI induced skin toxicity and patient’s survival.
    European Journal of Cancer. 01/2014;
  • T. Seufferlein, A. Kleger, S. Nitschmann
    Der Internist 01/2014; 55(4). · 0.33 Impact Factor
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    ABSTRACT: Pluripotente Stammzellen besitzen ein unbegrenztes Selbsterneuerungs- und Differenzierungspotenzial zur Gewinnung sämtlicher Zellarten des menschlichen Organismus. Damit stellen sie ein einzigartiges Modell für die Beantwortung entwicklungsbiologischer Fragestellungen wie auch für die Zelltherapie und regenerative Medizin dar. Dem Arzt und Stammzellforscher S. Yamanaka gelang erstmals die Reprogrammierung somatischer Zellen zu sog. induzierten pluripotenten Stammzellen durch die ektope Expression der Transkriptionsfaktoren Oct4 (,,Octamer-binding transcription factor 4“), Sox2 (,,sex determining region Y – box 2“), Klf4 (,,Kruppel-like factor 4“) und c-Myc (,,v-myc myelocytomatosis viral oncogene homolog“). Damit revolutionierte er die Möglichkeiten in der regenerativen Medizin. Insbesondere eröffneten sich durch die Anwendung dieser Techniken im patienten- bzw. krankheitsspezifischen Kontext neue Möglichkeiten zur Modellierung von Krankheiten und zur individualisierten Testung von Medikamenten. Zudem rückt das sog. therapeutische Klonen einen ganzen Schritt näher. Die vorliegende Übersichtsarbeit soll daher dem klinisch tätigen Arzt einen Überblick über den Stand der Forschung und die klinische Anwendung pluripotenter Stammzellen geben.
    Der Internist 01/2014; 55(4). · 0.33 Impact Factor
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    S. Wesselmann, T. Seufferlein
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    ABSTRACT: Die Erkenntnis der letzten Jahre, dass bei Patienten mit kolorektalem Karzinom (KRK) und isolierten Lebermetastasen bei erfolgreicher Metastasenresektion Aussicht auf Langzeitüberleben, ja sogar Heilung der Tumorerkrankung besteht, hat weltweit die Therapie dieser Patientengruppe deutlich verändert und zu einer massiven Zunahme von Lebermetastasenresektionen geführt. Die Lebermetastasenresektion hat dementsprechend auch Eingang in die interdisziplinäre deutsche S3-Leitlinie, aber auch in internationale Guidelines zur Therapie des KRK gefunden. Die Behandlung kolorektaler Lebermetastasen setzt ein interdisziplinär abgestimmtes Vorgehen erfahrener Diagnostiker und Therapeuten voraus. In den zertifizierten Darmkrebszentren der Deutschen Krebsgesellschaft sind die interdisziplinäre Abstimmung der Behandlungsabläufe im Rahmen der Tumorkonferenzen und der Nachweis einer entsprechenden Expertise der Behandlungspartner Voraussetzung für die Zertifizierung. Die Umsetzung der Anforderungen und der dazugehörigen Kennzahlen für Tumorkonferenzen und für die primäre und sekundäre Lebermetastasenresektion ist Teil der Audits, in denen die Ergebnisse dargestellt und diskutiert werden. Das Zertifizierungssystem der Darmkrebszenten fordert und fördert damit die personellen und strukturellen Voraussetzungen, die im Sinne der Patienten eine optimale und leitliniengerechte Behandlung kolorektaler Lebermetastasen ermöglichen. Tatsächlich spiegeln die primären und sekundären Resektionsraten in den Zentren die gelebte Interdisziplinarität wider. Die Analyse der Auditberichte zeigt die enge Zusammenarbeit der Kooperationspartner in den zertifizierten Netzwerken, die auch externe Kooperationen mit hochspezialisierten Kliniken bei besonderen Befundkonstellationen einschließt. Die Jahresauswertung der Ergebnisse der zertifizierten Zentren macht weiteres Verbesserungspotenzial bei der interdisziplinären Zusammenarbeit deutlich.
    Der Chirurg 01/2014; 85(1). · 0.52 Impact Factor
  • Thomas J Ettrich, Thomas Seufferlein
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    ABSTRACT: Regorafenib (BAY 73-4506, Stivarga(®)) is an oral diphenylurea multikinase inhibitor that targets angiogenic (VEGFR1-3, TIE2), stromal (PDGFR-β, FGFR), and oncogenic receptor tyrosine kinases (KIT, RET, and RAF). Regorafenib is the first small-molecule multikinase inhibitor to achieve survival benefits in metastatic colorectal cancer that has progressed after all standard therapies. Consequently, regorafenib was FDA approved for this indication. In addition, regorafenib treatment resulted in a significant improvement in progression-free survival (PFS) compared with placebo in patients with metastatic gastrointestinal stromal tumors (GIST) after progression on standard treatments and is also an FDA approved indication. Currently, regorafenib is examined in several clinical trials (mostly phase II) in different tumor entities, including renal cell carcinoma (RCC), hepatocellular carcinoma (HCC), and soft tissue sarcoma (STS).
    Recent results in cancer research. Fortschritte der Krebsforschung. Progrès dans les recherches sur le cancer 01/2014; 201:185-96.
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    S Wesselmann, T Seufferlein
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    ABSTRACT: Successful resection of liver metastases increases overall survival and can even be a curative approach in patients with colorectal cancer (CRC) and isolated liver metastases. Resection of liver metastases has clearly changed the therapy of this group of patients and has become a standard procedure that is being used increasingly more. Accordingly, liver metastasis resection has been included in the German evidence-based guidelines and also in international guidelines on the treatment of CRC. The treatment of colorectal liver metastases requires a multidisciplinary team of experts in the disease, including experienced radiologists, medical oncologists, radiotherapists, pathologists and surgeons. The interdisciplinary approach to the treatment in specialized tumor boards staffed by qualified experts is a prerequisite for successful certification as a colorectal cancer center by the German Cancer Society. Regular audits ensure that these requirements and that defined quality indicators regarding the tumor board and primary and secondary liver metastasis resection, are fulfilled. The certification system of the colorectal cancer centers requires and promotes conditions that allow an optimal and guideline-oriented treatment of colorectal liver metastases both at the level of personnel and infrastructure of a given center. The high primary and secondary resection rates in these centers testify that the multidisciplinary teams are effective. A detailed analysis of the audit reports reveals the close collaboration of all partners within the certified networks. These networks also comprise external cooperation with highly specialized hospitals if and when necessary. However, the annual report of the certificated colorectal cancer centers also demonstrates areas for further improvements in multidisciplinary cooperation.
    Der Chirurg 12/2013; · 0.52 Impact Factor
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    ABSTRACT: Pancreatic cancer cell invasion, metastasis and angiogenesis are major challenges for the development of novel therapeutic strategies. Protein Kinase D (PKD) isoforms are involved in controlling tumor cell motility, angiogenesis and metastasis. In particular PKD2 expression is up-regulated in pancreatic cancer, whereas PKD1 expression is lower. We here report that both kinases control pancreatic cancer cell invasive properties in an isoform-specific manner. PKD2 enhances invasion in 3D-ECM cultures by stimulating expression and secretion of matrix-metalloproteinase 7 and 9 (MMP7/9), whereby MMP7 is likely to act upstream of MMP9. Knockdown of MMP7/9 blocks PKD2-mediated invasion in 3D-ECM assays and in-vivo utilizing tumors growing on chorioallantois membranes (CAM). Furthermore, MMP9 enhances PKD2-mediated tumor angiogenesis by releasing extracellular matrix-bound VEGF-A, thereby increasing its bio-availability and angiogenesis. Interestingly, specific knockdown of PKD1 in PKD2-expressing pancreatic cancer cells further enhanced the invasive properties in 3D-ECM systems by generating a high-motility phenotype. Loss of PKD1 thus may be beneficial for tumor cells to enhance their matrix-invading abilities. In conclusion, we define for the first time PKD1 and -2 isoform-selective effects on pancreatic cancer cell invasion and angiogenesis, in-vitro and in-vivo, addressing PKD isoform-specificity as a major factor for future therapeutic strategies.
    Molecular biology of the cell 12/2013; · 5.98 Impact Factor
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    Zeitschrift für Gastroenterologie 12/2013; 51(12):1395-440. · 1.41 Impact Factor

Publication Stats

4k Citations
835.67 Total Impact Points


  • 2006–2014
    • Ruhr-Universität Bochum
      Bochum, North Rhine-Westphalia, Germany
    • Catholic University of Louvain
      Walloon Region, Belgium
  • 1999–2014
    • Universität Ulm
      • • Clinic of Internal Medicine I
      • • Institute of General Medicine
      • • Department of Internal Medicine
      • • Clinic of Radiation Oncology
      Ulm, Baden-Württemberg, Germany
  • 2013
    • Deutsche Krebsgesellschaft e.V.
      Berlín, Berlin, Germany
  • 2009–2013
    • Universitätsklinikum Halle (Saale)
      Halle-on-the-Saale, Saxony-Anhalt, Germany
  • 2009–2012
    • Martin Luther University of Halle-Wittenberg
      • Poliklinik für Innere Medizin I (Gastroenterologie, Pneumologie)
      Halle, Saxony-Anhalt, Germany
  • 2011
    • Max Planck Institute for Intelligent Systems, Stuttgart
      Stuttgart, Baden-Württemberg, Germany
    • Universität Heidelberg
      • Institute of Physical Chemistry
      Heidelberg, Baden-Wuerttemberg, Germany
  • 2010
    • Max Planck Institute for Solid State Research
      Stuttgart, Baden-Württemberg, Germany
  • 2008
    • Universitäts- und Rehabilitationskliniken Ulm
      Ulm, Baden-Württemberg, Germany
  • 2002–2008
    • KU Leuven
      • Faculty of Medicine
      Leuven, VLG, Belgium
  • 2007
    • Otto-von-Guericke-Universität Magdeburg
      Magdeburg, Saxony-Anhalt, Germany
  • 2005
    • Massachusetts Institute of Technology
      • Department of Materials Science and Engineering
      Cambridge, MA, United States
    • Prosper-Hospital Recklinghausen
      Recklinghausen, North Rhine-Westphalia, Germany
  • 2003
    • Klinikum Augsburg
      • II. Department of Internal Medicine
      Augsberg, Bavaria, Germany