Cancer Research in Switzerland - Krebsliga Schweiz

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102 this study we will examine the therapeutic potential of let7 microRNA precursors and other microRNAs in the development of cancer. Project coordinator Prof. Dr. Jonathan Hall Institut für pharmazeutische Wissenschaften ETH Zürich HCI H 437 WolfgangPauliStrasse 10 CH8093 Zürich Phone +41 (0)44 633 74 35 Fax +41 (0)44 633 13 69 jonathan.hall@pharma.ethz.ch Hemmings Brian A. | Dissecting translation reveals therapeutic prospects for malignant gliomas (KFS 02714082010) Duration: 01.03.2011 – 01.03.2014 Glioblastoma multiforme (GBM) is the most common and aggressive brain tumour entity, with a median survival of approximately one year. The proposed study aims to uncover novel molecular mechanisms regulating gene expression at the translation level triggered by deregulated signalling pathways. Further, therapeutic perspectives of the results obtained will be validated in the GBM animal models. Understanding of the novel molecular mechanisms that regulate selective translation will not only explain principles underlying rapid signalling responses controlling translation and its phenotypical consequences but will also allow proposal and development of molecular strategies for therapeutic interference for malignant brain tumours. Project coordinator Dr. Brian A. Hemmings Friedrich Miescher Institut für biomedizinische Forschung (FMI) Maulbeerstrasse 66 CH4058 Basel Phone +41 (0)61 697 48 72 brian.hemmings@fmi.ch Hottiger Michael O. | Multiplex analysis of the ionizing radiation induced signaling network at the single cell level (KLS 02396022009) Duration: 01.05.2009 – 01.05.2012 Every cell is exposed to genotoxic stresses such as radiation or chemicals that can cause harmful and deleterious mutations in the genome. Cells have evolved an intricate regulatory protein network to detect and repair DNA damage with the aim to maintain genomic stability and thus prevent tumourigenesis. Until now, technical and practical limitations prohibited comprehensive deciphering of this regulatory network. The goal of this study is to measure, with reverse protein micro arrays, simultaneously changes and modifications of hundreds of proteins in human cells (fibroblasts) upon exposure to genotoxic stress. Thereby, we will define key players of the genotoxic signalling network and predict functional interaction between different signalling components, which will be experimentally probed further for their function and connections. The results of this project will provide a comprehensive picture of a cell’s response to genotoxic stress and the opportunity to improve our possibilities to detect and treat tumours. Project coordinator Prof. Dr. Michael O. Hottiger Institut für Veterinärbiochemie und Molekularbiologie Universität Zürich Winterthurerstrasse 190 CH8057 Zürich Phone +41 (0)44 635 54 74 hottiger@vetbio.uzh.ch Huard Betrand | APRIL blockade for the treatment of multiple myeloma (KFS02464082009) Duration: 01.05.2010 – 01.05.2013 Multiple myeloma (MM) is a tumour arising after transformation of antibodyproducing plasma cells residing in the bone marrow (BM). There are about 450 new MM cases yearly in Switzerland. MM develops in BM and induces severe bone lesions. Nowadays a high response rate (95 %) in MM patients is achieved by the introduction of new chemotherapeutic drugs and their combination. Unfortunately, MM remains an incurable disease, due to uncontrolled relapse events, even when heavy treatment such as BM transplantation is performed. Current treatments are not highly specific to MM cells. However, the exclusive MM growth in BM revealed that BM must contain MM specific growth factor(s). Identifying them will lead to new targets for MM treatment. In the laboratory, we have recently observed that the BM is constitutively rich in a molecule called a proliferationinducing ligand (APRIL). The physiological function of APRIL is to support longterm survival of plasma cells in BM, by this means maintaining our immune antibody memory. All these observation render APRIL a good candidate for a key MM growth factor. Aim of the study To test whether antibodymediated APRIL blockade induces MM regression. Methods One major problem in MM research is the lack of an appropriate animal model. In collaboration with a Norwegian group, we created a mouse model highly relevant to the human pathology. The cell that we isolated, called MOPC315BM, develops actively in BM after intravenous injection and leads to paralysis and death. In addition, we generated the first blocking antibody against mouse APRIL. In this research project, we plan to test whether APRIL blockade impairs MOPC315BM development.
Patients’ perspectives In the case that we observe an inhibition of MOPC315BM development by APRIL blockade, we will be able to quickly generate a similar antibody reacting with human APRIL. This antibody could be tested in MM patients. This will lead to a highly specific treatment targeting a growth factor used by MM cells. Project coordinator Dr Bertrand Huard Département de pathologie et immunologie Faculté de médecine Université de Genève 1, rue MichelServet CH1211 Genève 4 Phone +41 (0)22 379 58 11 Fax +41 (0)22 379 57 46 bertrand.huard@unige.ch Hübscher Ulrich | Regulation of base excision repair by human DNA polymerase l through posttranslational modifications: Degradation versus stabilization (KLS 02339022009) Duration: 01.04.2009 – 01.04.2011 The maintenance of genetic stability is of crucial importance for any form of life. The genetic material, the DNA itself, is highly reactive and is constantly attacked by endogenous factors and is also easily altered by intracellular processes such as oxidation. The base guanine as 8oxo G is recognized as one of the most important oxidative DNA lesions because of its prevalence in DNA and its mutagenic potential in aging, tumourigenesis and neurodegenerative diseases. We identified that DNA polymerase l can correctly incorporate C opposite 8oxoG and identified the initial steps of how this protein is regulated in the cell. In particular it is stabilized during cell cycle progression, enabling proper repair of damaged DNA. With this project we would like to understand the molecular mechanisms of DNA polymerase l regulation during the cell cycle and thus investigate the role of the two posttranslation modifications phosphorylation and ubiquitination. Project coordinator Prof. Dr. Ulrich Hübscher Institut für Veterinärbiochemie und Molekular biologie Universität Zürich Winterthurerstrasse 190 CH8057 Zürich Phone +41 (0)44 635 54 72 Fax +41 (0)44 635 68 40/5904 hubscher@vetbio.uzh.ch Huelsken Joerg | Stemness control in cancer stem cells (KFS 02667082010) Duration: 01.01.2011 – 01.01.2014 As the cellular target for initiation of cancerogenesis, we and other laboratories recently identified normal, tissuespecific stem cells. These stem cells usually drive the continuous replenishment of tissues. Similarly, also tumours contain a small population of cancer stem cells that are responsible for formation and maintenance of the cancer. We were able to show that the Wnt signalling pathway controls essential stem cell properties, such as their apparent unlimited proliferation potential in normal and cancer tissues (Malanchi et al., Nature 2008). We now want to understand in more detail how Wnt signalling controls this process and will study the components of the epigenetic control of stem cell identity and mechanisms of their regulation. Our results will aid understanding of the fundamental processes that control tumour maintenance and will allow development of better targeted approaches for the elimination of such cancer stem cells. Project coordinator Prof. Dr Joerg Huelsken UPHUE Institut suisse de recherche expérimentale sur le cancer (ISREC) Faculté des sciences de la vie EPF de Lausanne (EPFL) SV 2823 (Bâtiment SV) Station 19 CH1015 Lausanne Phone +41 (0)21 693 07 52 Fax +41 (0)21 693 07 70 joerg.huelsken@epfl.ch Hynes Nancy | Reciprocal cross-talk between lowdensity lipoprotein receptor-related protein 1 and receptor tyrosine kinases: Implications for modulating in vitro and in vivo properties of breast tumor cells (KFS 02528022010) Duration: 01.08.2010 – 01.08.2012 Lowdensity lipoprotein receptorrelated protein 1 (LRP1) is a 600 kDa transmembrane protein that binds more than 40 distinct ligands, many of which are involved in regulation of extracellular protease activity. LRP1 is also crossregulated by various receptor tyrosine kinases (RTK). Ligand binding to LRP1 stimulates intracellular signalling pathways by unknown mechanisms. We have shown that binding of the serpin protease nexin1 (PN1) to LRP1 in mammary cancer cell lines stimulates the ERK pathway, regulates MMP9 expression and, in vivo, is responsible for the metastatic spread of a breast cancer model to the lungs. Based on this, the goals are: 1) in vitro experiments analyzing crosstalk between LRP1 and RTKs; 2) in vivo studies on metastatic breast tumour models, targeting PN1 alone or in combination with RTK inhibitors. Project coordinator Prof. Dr. Nancy Hynes Friedrich Miescher Institut für biomedizinische Forschung (FMI) Maulbeerstrasse 66 CH4058 Basel Phone +41 (0)61 697 81 07 Fax +41 (0)61 697 39 76 nancy.hynes@fmi.ch 103
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Cancer Research in Switzerland A pu
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Cancer Research in Switzerland
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Basic biomedical research 55 Cancer
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policy work and was in charge of de
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The main focus of the research fund
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gramme research funding decreased b
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Table 2 Distribution of funds for i
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Funding patient-centred research Pa
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value was not clearly discernible.
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New organization of the Foundation
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The board of the Foundation Cancer
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The president of the Scientific Com
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Prof. Martin Pruschy, PhD Departmen
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Swartz wants to find out how tumour
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The scientific and medical research
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3. The original order/sequence of t
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As a federation, the Cancer League
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List of funded research projects, i
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Zippelius Alfred | 2009: CHF 100,00
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Kridel Robert | 2010: CHF 100,000.-
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Thurgau Cancer League Biotechnologi
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Weller Michael | 2010: CHF 65,828.-
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manageable funding of individual pr
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enhances breast cancer cell motilit
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Rüegg Curzio et al. | Tumor-mediat
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International Clinical Cancer Resea
Page 53 and 54: in PHIV were shown for Hodgkin’s
Page 55: Zucca Emanuele et al. | Internation
Page 58 and 59: 56 “hierarchical structure” of
Page 60 and 61: 58 the attempt should be made to st
Page 62 and 63: 60 Gönczy Pierre | KLS 0202402
Page 64 and 65: 62 Romero Pedro | OCS 020110220
Page 66 and 67: 64 Beermann Friedrich | In vivo scr
Page 68 and 69: 66 Christofori Gerhard | Podoplanin
Page 70 and 71: 68 Frei Christian | The function of
Page 72 and 73: 70 cell, this novel mechanism serve
Page 74 and 75: 72 Results The induction of viral p
Page 76 and 77: 74 Hübscher Ulrich | Repair of oxi
Page 78 and 79: 76 Methods and experimental approac
Page 80 and 81: 78 of cMyc and/or NMyc and demo
Page 82 and 83: 80 In summary, this work improves o
Page 84 and 85: 82 Pruschy Martin | Microtubule int
Page 86 and 87: 84 Renner Christoph | Selective inh
Page 88 and 89: 86 Goal Here we build on these obse
Page 90 and 91: 88 by TDG prevents efficient downst
Page 92 and 93: 90 To address these questions, we a
Page 94 and 95: 92 Translational relevance The resu
Page 96 and 97: 94 Grünberg Jürgen | KFS 025460
Page 98 and 99: 96 Tschan Mario P. | KFS 0248608
Page 100 and 101: 98 Boyman Onur | Preclinical testin
Page 102 and 103: 100 Constam Daniel | Role of activi
Page 106 and 107: 104 Janscak Pavel | Study of the ro
Page 108 and 109: 106 Müller Anne | The molecular pa
Page 110 and 111: 108 Radtke Freddy | The role of Not
Page 112 and 113: 110 Schär Primo | DNA repair, epig
Page 114 and 115: 112 In this project we will investi
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Page 118 and 119: 116 and Research). Other financial
Page 120 and 121: 118 be totally unaffordable for aca
Page 122 and 123: 120 Clinical research List of compl
Page 124 and 125: 122 Hunger Robert E. | OCS 02262-08
Page 126 and 127: 124 Clinical research Presentation
Page 128 and 129: 126 Benhattar Jean | Identification
Page 130 and 131: 128 Bertoni Francesco | Genome-wide
Page 132 and 133: 130 Interpretation ESA treatment in
Page 134 and 135: 132 Our results could pave the way
Page 136 and 137: 134 new drugs that specifically tar
Page 138 and 139: 136 slides in two different concent
Page 140 and 141: 138 Conclusions A strong network of
Page 142 and 143: 140 tions introduced to ARE motifs
Page 144 and 145: 142 Müller Beatrice U. | The maste
Page 146 and 147: 144 A novel method was developed fo
Page 148 and 149: 146 (SAKK 35-98) the Swiss Group fo
Page 150 and 151: 148 Timmermann Beate | Prospective
Page 152 and 153: 150 recurrence of the disease, we a
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152 Zucca Emanuele | A prospective
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154 Heinimann Karl | KFS 02489-08-2
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156 Riggi Nicolò | BIL KFS 02717-0
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158 activity at the single cell lev
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160 Our research projects aim at un
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162 Körner Meike | In vitro evalua
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164 Nadal David | Is endemic Burkit
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166 (> 50.000/patient). For their a
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168 Zeller Rolf | Functional analys
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170
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172 area of health services researc
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174 The financing of palliative car
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176 National Strategy for Palliativ
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178 Psychosocial research List of c
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180 Within the patient group, level
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182 Further, the results suggest th
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184 It is in this context that the
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186 Recommendation Female spouses o
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188 Psychosocial research Presentat
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190 rates communication skills rema
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Epidemiological research Epidemiolo
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data from cancer registries. In the
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The importance of cancer registries
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Ess Silvia | Patterns of care and s
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Epidemiological research List of ap
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Impact This work will serve as the
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Thürlimann Beat | Management of br
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