Axel Ullrich

Summary

Country: Germany

Publications

  1. ncbi request reprint Molecular targets in cancer therapy and their impact on cancer management
    Axel Ullrich
    Department of Molecular Biology, Max Planck Institut fur Biochemie, Am Klopferspitz 18a, D 82152 Martinsried, Germany
    Oncology 63:1-5. 2002
  2. ncbi request reprint Targeting polo-like kinase 1 for cancer therapy
    Klaus Strebhardt
    Department of Obstetrics and Gynecology, School of Medicine, J W Goethe University, Theodore Stern Kai 7, 60590 Frankfurt, Germany
    Nat Rev Cancer 6:321-30. 2006
  3. ncbi request reprint Smart drugs: tyrosine kinase inhibitors in cancer therapy
    Laura K Shawver
    SUGEN, Inc, 230 East Grand Avenue, South San Francisco, CA 94080, USA
    Cancer Cell 1:117-23. 2002
  4. ncbi request reprint EGFR signaling leads to downregulation of PTP-LAR via TACE-mediated proteolytic processing
    Jens E Ruhe
    Department of Molecular Biology, Max Planck Institute for Biochemistry, Am Klopferspitz 18a, D 82152 Martinsried, Germany
    Cell Signal 18:1515-27. 2006
  5. doi request reprint UV-induced EGFR signal transactivation is dependent on proligand shedding by activated metalloproteases in skin cancer cell lines
    Bhuminder Singh
    Department of Molecular Biology, Max Planck Institute of Biochemistry, Martinsried, Germany
    Int J Cancer 124:531-9. 2009
  6. pmc Bosutinib inhibits migration and invasion via ACK1 in KRAS mutant non-small cell lung cancer
    Daniel S W Tan
    Singapore OncoGenome Laboratory, Institute of Medical Biology, Agency of Science Technology and Research, Singapore, Singapore
    Mol Cancer 13:13. 2014
  7. pmc Regulation of Akt(ser473) phosphorylation by choline kinase in breast carcinoma cells
    Boon Tin Chua
    Singapore OncoGenome Project, Institute of Medical Biology, A STAR, 8A Biomedical Grove, 06 06 Immunos, Singapore
    Mol Cancer 8:131. 2009
  8. ncbi request reprint Distinct ADAM metalloproteinases regulate G protein-coupled receptor-induced cell proliferation and survival
    Beatrix Schäfer
    Department of Molecular Biology, Max Planck Institute of Biochemistry, Martinsried D 82152, Germany
    J Biol Chem 279:47929-38. 2004
  9. ncbi request reprint GPCR-induced migration of breast carcinoma cells depends on both EGFR signal transactivation and EGFR-independent pathways
    Stefan Hart
    Department of Molecular Biology, Max Planck Institute of Biochemistry, Am Klopferspitz 18a, D 82152 Martinsried, Germany
    Biol Chem 386:845-55. 2005
  10. pmc Furin-, ADAM 10-, and gamma-secretase-mediated cleavage of a receptor tyrosine phosphatase and regulation of beta-catenin's transcriptional activity
    Lars Anders
    Department of Molecular Biology, Max Planck Institute of Biochemistry, Martinsried, Germany
    Mol Cell Biol 26:3917-34. 2006

Collaborators

Detail Information

Publications75

  1. ncbi request reprint Molecular targets in cancer therapy and their impact on cancer management
    Axel Ullrich
    Department of Molecular Biology, Max Planck Institut fur Biochemie, Am Klopferspitz 18a, D 82152 Martinsried, Germany
    Oncology 63:1-5. 2002
  2. ncbi request reprint Targeting polo-like kinase 1 for cancer therapy
    Klaus Strebhardt
    Department of Obstetrics and Gynecology, School of Medicine, J W Goethe University, Theodore Stern Kai 7, 60590 Frankfurt, Germany
    Nat Rev Cancer 6:321-30. 2006
    ..We address the structural features of the kinase domain and the unique polo-box domain of PLK1 that are most suited for drug development and discuss our current understanding of the therapeutic potential of PLK1...
  3. ncbi request reprint Smart drugs: tyrosine kinase inhibitors in cancer therapy
    Laura K Shawver
    SUGEN, Inc, 230 East Grand Avenue, South San Francisco, CA 94080, USA
    Cancer Cell 1:117-23. 2002
    ..An extension of the initial successes in molecular oncology will occur more quickly and successfully through an appreciation of lessons learned with the first group of agents in their progress through clinical development...
  4. ncbi request reprint EGFR signaling leads to downregulation of PTP-LAR via TACE-mediated proteolytic processing
    Jens E Ruhe
    Department of Molecular Biology, Max Planck Institute for Biochemistry, Am Klopferspitz 18a, D 82152 Martinsried, Germany
    Cell Signal 18:1515-27. 2006
    ....
  5. doi request reprint UV-induced EGFR signal transactivation is dependent on proligand shedding by activated metalloproteases in skin cancer cell lines
    Bhuminder Singh
    Department of Molecular Biology, Max Planck Institute of Biochemistry, Martinsried, Germany
    Int J Cancer 124:531-9. 2009
    ..Together, our data provide novel insights into the mechanism of UV-induced EGFR activation, suggesting broad relevance of the UV-ADAM-proligand-EGFR-Erk/Akt pathway and its significance in skin cancer...
  6. pmc Bosutinib inhibits migration and invasion via ACK1 in KRAS mutant non-small cell lung cancer
    Daniel S W Tan
    Singapore OncoGenome Laboratory, Institute of Medical Biology, Agency of Science Technology and Research, Singapore, Singapore
    Mol Cancer 13:13. 2014
    ..In conclusion, inhibition of ACK1 with bosutinib attenuates migration and invasion in the context of KRAS mutant NSCLC and may fulfil a therapeutic niche through combinatorial treatment approaches. ..
  7. pmc Regulation of Akt(ser473) phosphorylation by choline kinase in breast carcinoma cells
    Boon Tin Chua
    Singapore OncoGenome Project, Institute of Medical Biology, A STAR, 8A Biomedical Grove, 06 06 Immunos, Singapore
    Mol Cancer 8:131. 2009
    ..Here, we transfected the MDA-MB 468 breast cell line with the human kinome siRNA library and measured Akt activation using an antibody specific for phosphoserine 473 of Akt...
  8. ncbi request reprint Distinct ADAM metalloproteinases regulate G protein-coupled receptor-induced cell proliferation and survival
    Beatrix Schäfer
    Department of Molecular Biology, Max Planck Institute of Biochemistry, Martinsried D 82152, Germany
    J Biol Chem 279:47929-38. 2004
    ..Thus, ADAM15 and -17 function as effectors of GPCR-mediated signaling and define critical characteristics of cancer cells...
  9. ncbi request reprint GPCR-induced migration of breast carcinoma cells depends on both EGFR signal transactivation and EGFR-independent pathways
    Stefan Hart
    Department of Molecular Biology, Max Planck Institute of Biochemistry, Am Klopferspitz 18a, D 82152 Martinsried, Germany
    Biol Chem 386:845-55. 2005
    ..We conclude that GPCR-induced chemotaxis of breast cancer cells is mediated by EGFR-dependent and -independent signalling pathways, with both parallel pathways having to act in concert to achieve a complete migratory response...
  10. pmc Furin-, ADAM 10-, and gamma-secretase-mediated cleavage of a receptor tyrosine phosphatase and regulation of beta-catenin's transcriptional activity
    Lars Anders
    Department of Molecular Biology, Max Planck Institute of Biochemistry, Martinsried, Germany
    Mol Cell Biol 26:3917-34. 2006
    ..Our results identify intramembrane proteolysis as a regulatory switch in RPTPkappa signaling and implicate PIC in the activation of beta-catenin-mediated transcription...
  11. ncbi request reprint Reactive oxygen species mediate Met receptor transactivation by G protein-coupled receptors and the epidermal growth factor receptor in human carcinoma cells
    Oliver M Fischer
    Department of Molecular Biology, Max Planck Institute of Biochemistry, Am Klopferspitz 18a, D 82152 Martinsried, Germany
    J Biol Chem 279:28970-8. 2004
    ....
  12. ncbi request reprint Cannabinoids induce cancer cell proliferation via tumor necrosis factor alpha-converting enzyme (TACE/ADAM17)-mediated transactivation of the epidermal growth factor receptor
    Stefan Hart
    Department of Molecular Biology, Max Planck Institute of Biochemistry, Am Klopferspitz 18a, D 82152 Martinsried, Germany
    Cancer Res 64:1943-50. 2004
    ....
  13. pmc Oxidative and osmotic stress signaling in tumor cells is mediated by ADAM proteases and heparin-binding epidermal growth factor
    Oliver M Fischer
    Department of Molecular Biology, Max Planck Institute of Biochemistry, D 82152 Martinsried, Germany
    Mol Cell Biol 24:5172-83. 2004
    ....
  14. pmc Structural basis for Gas6-Axl signalling
    Takako Sasaki
    Max Planck Institut fur Biochemie, Martinsried, Germany
    EMBO J 25:80-7. 2006
    ..Specificity at the major contact is suggested to result from the segregation of charged and apolar residues to opposite faces of the newly formed beta-sheet...
  15. pmc TACE cleavage of proamphiregulin regulates GPCR-induced proliferation and motility of cancer cells
    Andreas Gschwind
    Department of Molecular Biology, Max Planck Institute of Biochemistry, Am Klopferspitz 18a, D 82152 Martinsried, Germany
    EMBO J 22:2411-21. 2003
    ..Thus, TACE can function as an effector of GPCR-mediated signalling and represents a key element of the cellular receptor cross-talk network...
  16. doi request reprint A single nucleotide change in the mouse genome accelerates breast cancer progression
    Nina Seitzer
    Department of Molecular Biology, Max Planck Institute of Biochemistry, 85152 Martinsried, Germany
    Cancer Res 70:802-12. 2010
    ..Our findings definitively identify the FGFR4 Arg388 allele as a functional prognostic marker for breast cancer progression...
  17. doi request reprint AXL is a potential target for therapeutic intervention in breast cancer progression
    Yi Xiang Zhang
    Max Planck Institute of Biochemistry, Martinsried, Germany
    Cancer Res 68:1905-15. 2008
    ....
  18. doi request reprint Mitogen-inducible gene-6 is a negative regulator of epidermal growth factor receptor signaling in hepatocytes and human hepatocellular carcinoma
    Markus Reschke
    Max Planck Institute of Biochemistry, Department of Molecular Biology, Martinsried, Germany
    Hepatology 51:1383-90. 2010
    ..Moreover, mig-6 is down-regulated in human hepatocellular carcinoma and this correlates with increased EGFR expression...
  19. ncbi request reprint FGFR4 GLY388 isotype suppresses motility of MDA-MB-231 breast cancer cells by EDG-2 gene repression
    Christiane Regina Stadler
    Department of Molecular Biology, Max Planck Institute of Biochemistry, Am Klopferspitz 18a, D 82152 Martinsried, Germany
    Cell Signal 18:783-94. 2006
    ..Therefore, the positive effect of FGFR4 R388 on disease progression appears to result from a loss of the tumour suppressor activity displayed by FGFR4 G388 rather than the acquisition or enhancement of oncogenic potential...
  20. doi request reprint Negative regulation of the EGFR-MAPK cascade by actin-MAL-mediated Mig6/Errfi-1 induction
    Arnaud Descot
    Department of Molecular Biology, Max Planck Institute of Biochemistry, Martinsried, Germany
    Mol Cell 35:291-304. 2009
    ..Our results show the existence of negatively acting transcriptional networks between pro- and antiproliferative signaling pathways toward SRF...
  21. ncbi request reprint Beyond Herceptin and Gleevec
    Oliver M Fischer
    Max Planck Institute of Biochemistry, Department of Molecular Biology, Am Klopferspitz 18a, D 82152 Martinsried, Germany
    Curr Opin Chem Biol 7:490-5. 2003
    ....
  22. ncbi request reprint Negative regulation of HER2 signaling by the PEST-type protein-tyrosine phosphatase BDP1
    Miriam Gensler
    Department of Molecular Biology, Max Planck Institute of Biochemistry, Am Klopferspitz 18a, D 82152 Martinsried, Germany
    J Biol Chem 279:12110-6. 2004
    ....
  23. doi request reprint HER3 is a determinant for poor prognosis in melanoma
    Markus Reschke
    Department of Molecular Biology, Max Planck Institute of Biochemistry, Munich, Germany
    Clin Cancer Res 14:5188-97. 2008
    ..However, the relevance of HER3 with regard to its prognostic significance and function in primary melanoma and metastases remains largely elusive...
  24. ncbi request reprint Identification of MMP-15 as an anti-apoptotic factor in cancer cells
    Reimar Abraham
    Department of Molecular Biology, Max Planck Institute for Biochemistry, 82152 Martinsried, Germany
    J Biol Chem 280:34123-32. 2005
    ..Our findings therefore strongly suggest that cancer characteristics such as metastatic potential, which are thought to evolve late in cancer progression, could be manifested early on by selection for an anti-apoptotic phenotype...
  25. pmc Monocytes/macrophages support mammary tumor invasivity by co-secreting lineage-specific EGFR ligands and a STAT3 activator
    Philip Vlaicu
    Department of Molecular Biology, Max Planck Institute of Biochemistry, Martinsried 82152, Germany
    BMC Cancer 13:197. 2013
    ..We sought to analyze which EGFR- and STAT3-activating factors are secreted by monocytes/macrophages exposed to tumor cell-secreted factors...
  26. ncbi request reprint Anti-HER-3 MAbs inhibit HER-3-mediated signaling in breast cancer cell lines resistant to anti-HER-2 antibodies
    Edward Htun van der Horst
    Department of Molecular Biology, Max Planck Institute for Biochemistry, Martinsried, Munich, Germany
    Int J Cancer 115:519-27. 2005
    ..Our data reinforce the notion that HER3 could be a key target in cancer drug design and show the great potential of anti-HER3 antibodies for the therapy of breast cancer and other malignancies characterized by overexpression of HER3...
  27. ncbi request reprint Protein tyrosine kinase Syk modulates EGFR signalling in human mammary epithelial cells
    Anja Ruschel
    Department of Molecular Biology, Max Planck Institute of Biochemistry, Am Klopferspitz 18, D 82152 Martinsried, Germany
    Cell Signal 16:1249-61. 2004
    ..Our findings demonstrate that Syk acts a negative control element of EGFR signalling...
  28. doi request reprint Toward the prognostic significance and therapeutic potential of HER3 receptor tyrosine kinase in human colon cancer
    Abdelhamid Beji
    Department of Molecular Biology, Max Planck Institute of Biochemistry, Martinsried, Munich, Germany
    Clin Cancer Res 18:956-68. 2012
    ..We have previously shown that in melanoma HER3 is frequently overexpressed and is associated with poor prognosis. However, the importance of HER3 in colon cancer and its putative prognostic significance is still unknown...
  29. doi request reprint Resistance to chemotherapy is associated with fibroblast growth factor receptor 4 up-regulation
    Andreas Roidl
    Department of Molecular Biology, Max Planck Institute of Biochemistry, Martinsried, Germany
    Clin Cancer Res 15:2058-66. 2009
    ..To investigate the underlying mechanisms, we developed an experimental approach that is based on the genetic plasticity of cancer cells and the selection for cell survival on treatment with chemotherapeutic agents...
  30. ncbi request reprint The unique C-terminal tail of the mitogen-activated protein kinase ERK5 regulates its activation and nuclear shuttling
    Marcus Buschbeck
    Max Planck Institute of Biochemistry, Department of Molecular Biology, D 82152 Martinsried, Germany
    J Biol Chem 280:2659-67. 2005
    ..Taken together, these results indicate that ERK5 signaling is directed by the presence of its unique C-terminal tail, which might be the key to understanding the key role of ERK5 in MAPK signaling...
  31. ncbi request reprint EGFR and FGFR signaling through FRS2 is subject to negative feedback control by ERK1/2
    Yingjie Wu
    Department of Molecular Biology, Max Planck Institute of Biochemistry, D 82152 Martinsried, Germany
    Biol Chem 384:1215-26. 2003
    ..Our findings support a broader role of FRS2 in EGFR-controlled signaling pathways in A-431 cells and provide insight into a molecular mechanism for ligand-stimulated feedback regulation with FRS2 as a central regulatory switch point...
  32. ncbi request reprint Tyrosine phosphorylation of PYK2 mediates heregulin-induced glioma invasion: novel heregulin/HER3-stimulated signaling pathway in glioma
    Edward Htun van der Horst
    Department of Molecular Biology, Max Planck Institute for Biochemistry, Munich, Germany
    Int J Cancer 113:689-98. 2005
    ..These results suggest a novel Heregulin/HER3-stimulated signaling pathway in glioblastoma-derived cell lines that involves phosphorylation of PYK2 and mediates invasiveness of glioma cells...
  33. ncbi request reprint Involvement of the FGFR4 Arg388 allele in head and neck squamous cell carcinoma
    Sylvia Streit
    Department of Molecular Biology, Max Planck Institute for Biochemistry, Martinsried, Germany
    Int J Cancer 111:213-7. 2004
    ....
  34. doi request reprint PRKX, TTBK2 and RSK4 expression causes Sunitinib resistance in kidney carcinoma- and melanoma-cell lines
    Claus Bender
    Department of Molecular Biology, Max Planck Institute, Martinsried, Germany
    Int J Cancer 131:E45-55. 2012
    ..Hence, we propose that PRKX, TTBK2 and RSK4 are potential resistance markers in Sunitinib therapy and might therefore represent targets for the development of novel strategies to overcome resistance...
  35. pmc Investigation of protein-tyrosine phosphatase 1B function by quantitative proteomics
    Philipp Mertins
    Department of Molecular Biology, Max Planck Institute of Biochemistry, Am Klopferspitz 18, 82152 Martinsried, Germany
    Mol Cell Proteomics 7:1763-77. 2008
    ..Importantly the MS-based strategies described here are entirely generic and can be used to address the poorly understood aspects of cellular PTP function...
  36. pmc PTK 7 is a transforming gene and prognostic marker for breast cancer and nodal metastasis involvement
    Silvia Gartner
    Department of Molecular Biology, Max Planck Institute of Biochemistry, Martinsried, Germany
    PLoS ONE 9:e84472. 2014
    ..PTK7 is highly expressed in TNBC cell lines. It represents a novel prognostic marker for BC patients and has potential therapeutic significance. ..
  37. doi request reprint Inhibition of doxorubicin-induced HER3-PI3K-AKT signalling enhances apoptosis of ovarian cancer cells
    Martin Bezler
    Max Planck Institute of Biochemistry, Department of Molecular Biology, Martinsried, Germany
    Mol Oncol 6:516-29. 2012
    ..Based on these results, we postulate that activation of the HER3-PI3K-AKT cascade represents a major mechanism of chemoresistance in ovarian cancer...
  38. ncbi request reprint Nuclear translocation of the tumor marker pyruvate kinase M2 induces programmed cell death
    Attila Stetak
    Department of Molecular Biology, Max Planck Institute for Biochemistry, Martinsried, Germany
    Cancer Res 67:1602-8. 2007
    ..These results show that the tumor marker PKM2 plays a general role in caspase-independent cell death of tumor cells and thereby defines this glycolytic enzyme as a novel target for cancer therapy development...
  39. ncbi request reprint Endothelin-1 inhibits adipogenesis: role of phosphorylation of Akt and ERK1/2
    Indranil Bhattacharya
    Department of Molecular Biology, Max Planck Institute for Biochemistry, Am Klopferspitz 18, D 82152 Martinsried, Germany
    FEBS Lett 580:5765-71. 2006
    ..We suggest that treatment with ET-1 and EGF together induce a more potent anti-adipogenic response, involving increased Erk1/2 phosphorylation and biphasic attenuation of Akt phosphorylation...
  40. ncbi request reprint Identification of a transcriptionally active hVH-5 pseudogene on 10q22.2
    Ingemarie R Berger
    Department of Molecular Biology, Max Planck Institute of Biochemistry, Am Klopferspitz 18a, D 82152 Martinsried, Germany
    Cancer Genet Cytogenet 159:155-9. 2005
    ..In respect to the normal hVH-5 gene, the pseudogene contains several point mutations and a frame shift due to the deletion of 2 bases that would lead to the truncation of the putative psihVH-5 product...
  41. ncbi request reprint PTP-PEST phosphatase variations in human cancer
    Sylvia Streit
    Department of Molecular Biology, Max Planck Institute of Biochemistry, Am Klopferspitz 18a, D 82152 Martinsried, Germany
    Cancer Genet Cytogenet 170:48-53. 2006
    ..These data demonstrate the existence of PTP-PEST variants that might be meaningful for human cancer and underscore the need for further characterizing PTP-PEST and its signaling pathways in context of this disease...
  42. ncbi request reprint Multiple G-protein-coupled receptor signals converge on the epidermal growth factor receptor to promote migration and invasion
    Beatrix Schäfer
    Department of Molecular Biology, Max Planck Institute of Biochemistry, Martinsried D 82152, Germany
    Oncogene 23:991-9. 2004
    ....
  43. pmc Abl-kinase-sensitive levels of ERK5 and its intrinsic basal activity contribute to leukaemia cell survival
    Marcus Buschbeck
    Department of Molecular Biology, Max Planck Institute of Biochemistry, Am Klopferspitz 18a, 82152 Martinsried, Germany
    EMBO Rep 6:63-9. 2005
    ..These results suggest that the ability to regulate the cellular abundance of ERK5 contributes to the oncogenic potential of Abl kinases...
  44. ncbi request reprint Lysophosphatidic acid-induced squamous cell carcinoma cell proliferation and motility involves epidermal growth factor receptor signal transactivation
    Andreas Gschwind
    Department of Molecular Biology, Max Planck Institute of Biochemistry, D 82152 Martinsried, Germany
    Cancer Res 62:6329-36. 2002
    ..Our findings suggest that highly abundant GPCR ligands such as LPA may function as tumor promoters and determinants of HNSCC progression...
  45. pmc Erk2 but not Erk1 regulates crosstalk between Met and EGFR in squamous cell carcinoma cell lines
    Simone Gusenbauer
    Department of Molecular Biology, Max Planck Institute of Biochemistry, Am Klopferspitz 18, D 82152, Martinsried, Germany
    Mol Cancer 14:54. 2015
    ..In the present work we describe the pathway responsible for the amphiregulin induction...
  46. ncbi request reprint Crystal structure of a C-terminal fragment of growth arrest-specific protein Gas6. Receptor tyrosine kinase activation by laminin G-like domains
    Takako Sasaki
    Max Planck Institut fur Biochemie, D 82152 Martinsried, Germany
    J Biol Chem 277:44164-70. 2002
    ..Mutagenesis of some residues in this patch reduces Gas6-LG binding to the extracellular domain of Axl as well as Axl activation in glioblastoma cells, identifying a component of the receptor-binding site of Gas6...
  47. pmc Metformin and salinomycin as the best combination for the eradication of NSCLC monolayer cells and their alveospheres (cancer stem cells) irrespective of EGFR, KRAS, EML4/ALK and LKB1 status
    Zhiguang Xiao
    Department of Molecular Biology, Max Planck Institute of Biochemistry, Am Klopferspitz, Martinsried, Germany
    Oncotarget 5:12877-90. 2014
    ..In conclusion, METF in combination with SAL could be a promising treatment option for patients with advanced NSCLC irrespective of their EGFR, KRAS, EML4/ALK and LKB1 status. ..
  48. doi request reprint Erk2 but not Erk1 regulates crosstalk between Met and EGFR in squamous cell carcinoma cell lines
    Simone Gusenbauer
    Department of Molecular Biology, Max Planck Institute of Biochemistry, Am Klopferspitz 18, D 82152, Martinsried, Germany
    Mol Cancer 14:319. 2015
    ..In the present work we describe the pathway responsible for the amphiregulin induction...
  49. ncbi request reprint Cancer progression and tumor cell motility are associated with the FGFR4 Arg(388) allele
    Johannes Bange
    Department of Molecular Biology, Max Planck Institute of Biochemistry, Am Klopferspitz 18a, D 82152 Martinsried, Germany
    Cancer Res 62:840-7. 2002
    ..Our results support the conclusion that the FGFR4 Arg(388) allele represents a determinant that is innocuous in healthy individuals but predisposes cancer patients for significantly accelerated disease progression...
  50. ncbi request reprint Receptor tyrosine kinases as targets for anticancer drugs
    Esther Zwick
    Dept of Molecular Biology, Max Planck Institut of Biochemistry, Am Klopferspitz 18a, 82152, Martinsried, Germany
    Trends Mol Med 8:17-23. 2002
    ..Strategies towards the prevention and interception of RTK signaling include monoclonal antibodies, small-molecule inhibitors, immunotoxins and antisense oligonucleotides...
  51. ncbi request reprint FGFR4 Arg388 allele is associated with resistance to adjuvant therapy in primary breast cancer
    Christoph Thussbas
    Department of Obstetrics and Gynecology, Institute of Pathology, and Institute for Medical Statistics and Epidemiology, Technical University of Munich, Munich, Germany
    J Clin Oncol 24:3747-55. 2006
    ..5 months)...
  52. ncbi request reprint Active antimetastatic immunotherapy in Lewis lung carcinoma with self EGFR extracellular domain protein in VSSP adjuvant
    Belinda Sánchez Ramírez
    Vaccine Department, Center of Molecular Immunology, Havana, Cuba
    Int J Cancer 119:2190-9. 2006
    ..These results further encouraged the development of the Her1-ECD/VSSP vaccine project for patients with EGFR+ tumors...
  53. ncbi request reprint Mutual regulation of protein-tyrosine phosphatase 20 and protein-tyrosine kinase Tec activities by tyrosine phosphorylation and dephosphorylation
    Naohito Aoki
    Department of Applied Molecular Biosciences, Graduate School of Bioagricultural Sciences, Nagoya University, Japan
    J Biol Chem 279:10765-75. 2004
    ..Taken together, PTP20 appears to play a negative role in Tec-mediated signaling, and Tec-PTP20 interaction might represent a negative feedback mechanism...
  54. ncbi request reprint Effect of tumor-associated mutant E-cadherin variants with defects in exons 8 or 9 on matrix metalloproteinase 3
    Margit Fuchs
    Technische Universitat Munchen, Klinikum rechts der Isar, Institut für allgemeine Pathologie und pathologische Anatomie, Munchen, Germany
    J Cell Physiol 202:805-13. 2005
    ..Both observations may be highly relevant for tumor progression since they concern degradation of the extracellular matrix and tumor cell spread...
  55. ncbi request reprint Pancreatic cancer growth is inhibited by blockade of VEGF-RII
    Peter Buchler
    Department of Surgery, UCLA School of Medicine, University of California Los Angeles, 10833 Le Conte, Los Angeles, CA 90095 6904, USA
    Surgery 134:772-82. 2003
    ..Therefore antiangiogenic therapy targeting endothelial cells may represent a promising therapeutic option. The aim of the study was to evaluate antiangiogenic therapy as a potential therapeutic option in pancreatic cancer...
  56. ncbi request reprint Dissecting the epidermal growth factor receptor signal transactivation pathway
    Oliver M Fischer
    Pfizer Global Research and Development, Sandwich Laboratories, Kent, UK
    Methods Mol Biol 327:85-97. 2006
    ..Here we describe methods to investigate GPCR-stimulated EGFR signal transactivation allowing the identification of both the EGF-like ligands and the metalloproteinases involved...
  57. ncbi request reprint Characterization of a conserved structural determinant controlling protein kinase sensitivity to selective inhibitors
    Stephanie Blencke
    Axxima Pharmaceuticals AG, Max Lebsche Platz 32, 81377 Munich, Germany
    Chem Biol 11:691-701. 2004
    ..Our data establish a conserved structural determinant of protein kinase sensitivity relevant for both signal transduction research and drug development...
  58. pmc Mitochondrial AKAP121 binds and targets protein tyrosine phosphatase D1, a novel positive regulator of src signaling
    Luca Cardone
    Dipartimento di Biologia e Patologia Molecolare e Cellulare, Via S Pansini, 5, 80131 Naples, Italy
    Mol Cell Biol 24:4613-26. 2004
    ..This represents the first example of physical and functional interaction between AKAPs and a protein tyrosine phosphatase...
  59. ncbi request reprint Combined inhibition of VEGF and PDGF signaling enforces tumor vessel regression by interfering with pericyte-mediated endothelial cell survival mechanisms
    Ralf Erber
    Department of Neurosurgery, Medical Faculty of the University of Heidelberg, Mannheim, Germany
    FASEB J 18:338-40. 2004
    ....
  60. ncbi request reprint The Protein-tyrosine-phosphatase SHP2 is phosphorylated on serine residues 576 and 591 by protein kinase C isoforms alpha, beta 1, beta 2, and eta
    Volker Strack
    Medical Clinic, Department IV, Eberhard Karls University Tubingen, Otfried Muller Strasse 10, D 72076 Tubingen, Germany
    Biochemistry 41:603-8. 2002
    ..However, no change of phosphatase activity by TPA treatment was detected in an in vitro assay. In summary, SHP2 is phosphorylated on serine residues 576 and 591 by PKC isoforms alpha, beta 1, beta 2, and eta...
  61. ncbi request reprint Lysophosphatidic acid-regulated mitogenic ERK signaling in androgen-insensitive prostate cancer PC-3 cells
    Pao F Kue
    Department of Surgery Urology, Duke University Medical Center, Durham, NC 27710, USA
    Int J Cancer 102:572-9. 2002
    ..Together, our data show that LPA and EGF cooperate to induce mitogenic signaling in prostate cancer cells in an MMP-regulated activation of the ERK pathway...
  62. ncbi request reprint Peptide-mediated inhibition of neutrophil transmigration by blocking CD47 interactions with signal regulatory protein alpha
    Yuan Liu
    Department of Pathology and Laboratory Medicine, Emory University, Atlanta, GA 30322, USA
    J Immunol 172:2578-85. 2004
    ..Such peptide reagents may be useful for studies on experimental models of inflammation and provide a template for the design of anti-inflammatory agents...
  63. ncbi request reprint Combined inhibition of vascular endothelial growth factor and platelet-derived growth factor signaling: effects on the angiogenesis, microcirculation, and growth of orthotopic malignant gliomas
    Mohammad Reza Farhadi
    Department of Neurosurgery, University Hospital, Faculty of Clinical Medicine, University of Heidelberg, Mannheim, Germany
    J Neurosurg 102:363-70. 2005
    ....
  64. ncbi request reprint A critical role for ras-mediated, epidermal growth factor receptor-dependent angiogenesis in mouse skin carcinogenesis
    M Llanos Casanova
    Project on Cell and Molecular Biology and Gene Therapy, Centro de Investigaciones Energeticas, Medioambientales y Tecnologicas, 28040 Madrid, Spain
    Cancer Res 62:3402-7. 2002
    ..It is tempting to speculate that EGFR family members may function as angiogenic regulators in other epithelial tumors such as those of the colon, breast, and prostate, reinforcing their value as targets for therapeutic intervention...
  65. pmc Tyrosine phosphorylated Par3 regulates epithelial tight junction assembly promoted by EGFR signaling
    Yiguo Wang
    Key Laboratory of Proteomics and Laboratory of Molecular Cell Biology, Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai, China
    EMBO J 25:5058-70. 2006
    ..Collectively, these data suggest a novel, phosphotyrosine-dependent fine-tuning mechanism of Par3 in epithelial TJ assembly controlled by the EGF receptor-SFK signaling pathway...
  66. ncbi request reprint Mig6 is a negative regulator of EGF receptor-mediated skin morphogenesis and tumor formation
    Ingvar Ferby
    Department of Molecular Neurobiology, Max Planck Institute of Neurobiology, Klopferspitz 18, 82152 Martinsried, Germany
    Nat Med 12:568-73. 2006
    ..These results indicate that Mig6 is a specific negative regulator of Egfr signaling in skin morphogenesis and is a novel tumor suppressor of Egfr-dependent carcinogenesis...
  67. ncbi request reprint Genetic alterations in the tyrosine kinase transcriptome of human cancer cell lines
    Jens E Ruhe
    Institute of Medical Biology, Singapore, Singapore
    Cancer Res 67:11368-76. 2007
    ..Our data therefore provide extensive system information for the design and interpretation of cell line-based cancer research, and may stimulate further investigations into broader clinical applications of current cancer therapeutics...
  68. pmc Estrogen transactivates EGFR via the sphingosine 1-phosphate receptor Edg-3: the role of sphingosine kinase-1
    Olga Sukocheva
    Signal Transduction Laboratory, Division of Human Immunology, Hanson Institute, Institute of Medical and Veterinary Science, Adelaide SA 5000, Australia
    J Cell Biol 173:301-10. 2006
    ..They also suggest a new signal transduction model across three individual ligand-receptor systems, i.e., "criss-cross" transactivation...
  69. pmc Dominant-negative inhibition of the Axl receptor tyrosine kinase suppresses brain tumor cell growth and invasion and prolongs survival
    Peter Vajkoczy
    Department of Neurosurgery, Medical Faculty of the University of Heidelberg, D 68167 Mannheim, Germany
    Proc Natl Acad Sci U S A 103:5799-804. 2006
    ..Our findings implicate Axl in gliomagenesis and validate it as a promising target for the development of approaches toward a therapy of these highly aggressive but, as yet, therapy-refractory, tumors...
  70. doi request reprint Paul Ehrlich's magic bullet concept: 100 years of progress
    Klaus Strebhardt
    Klaus Strebhardt is at the Department of Obstetrics and Gynaecology, School of Medicine, J W Goethe University, Theodour Stern Kai 7, 60590 Frankfurt, Germany
    Nat Rev Cancer 8:473-80. 2008
    ..His postulate of creating 'magic bullets' for use in the fight against human diseases inspired generations of scientists to devise powerful molecular cancer therapeutics...
  71. ncbi request reprint The adaptor function of SHP-2 downstream of the prolactin receptor is required for the recruitment of p29, a substrate of SHP-2
    Parham Minoo
    Division of Hematology, Department of Medicine, Molecular Oncology Group, H5 81, Royal Victoria Hospital, McGill University, 687 Pine Avenue West, Montreal, Quebec, Canada H3A 1A1
    Cell Signal 15:319-26. 2003
    ..Together, our results indicate that SHP-2 may function as an adaptor molecule downstream of the PRLR and highlight a new recruitment mechanism of SHP-2 substrates...
  72. pmc EphB4 controls blood vascular morphogenesis during postnatal angiogenesis
    Ralf Erber
    Department of Neurosurgery, Faculty for Clinical Medicine of the University of Heidelberg, University Hospital Mannheim, Mannheim, Germany
    EMBO J 25:628-41. 2006
    ..This implies that both neoplastic and non-neoplastic vascularization is driven not only by a vascular initiation program but also by a vascular patterning program mediated by guidance molecules...
  73. ncbi request reprint Mutation of threonine 766 in the epidermal growth factor receptor reveals a hotspot for resistance formation against selective tyrosine kinase inhibitors
    Stephanie Blencke
    Axxima Pharmaceuticals AG, Max Lebsche Platz 32, 81377 Munchen, Germany
    J Biol Chem 278:15435-40. 2003
    ..Our data identify Thr-766 of the EGFR as a structural determinant that bears the potential to become a relevant feature in resistance formation during cancer therapy with EGFR-specific 4-anilinoquinazoline inhibitors...
  74. doi request reprint SHPS-1/SIRP1alpha contributes to interleukin-6 signalling
    Radoslaw M Sobota
    Department of Biochemistry, RWTH Aachen University, Pauwelsstrasse 30, D 52074 Aachen, Germany
    Cell Signal 20:1385-91. 2008
    ..Our observations will help to understand the tight balance of MAPK- and STAT3-activation in response to IL-6 which was found to be misbalanced in many autoimmune diseases, inflammatory proliferative diseases and cancer...