Cancer Research in Switzerland - Krebsliga Schweiz

More documents

Recommendations

Info

98 Boyman Onur | Preclinical testing of interleukin-2- antibody complexes for tumor immunotherapy (KFS 02672082010) Duration: 01.02.2011 – 01.02.2014 Despite the use of improved treatment options, most patients with metastatic tumours die within a few years. This is also the case for metastatic malignant melanoma, a deadly skin tumour. Apart from chemotherapeutic regimens, the use of interleukin 2 (IL2) immunotherapy in the treatment of metastatic melanoma has shown promising results. IL2 belongs to the family of cytokines that are produced by the body’s defence system (immune system) and is able to activate cytotoxic T lymphocytes (also called CD8 + T cells). Activated CD8 + T cells are able to attack and kill tumour cells. For these properties, IL2 was used at high doses in metastatic melanoma, and it led to a longterm survival of about 13 % of patients for over twenty years, which is considerable, given the survival rate of below 5 % within five years in untreated patients. However, IL2 immunotherapy can lead to serious side effects, such as lung oedema or liver damage, which is the reason why this treatment is not used more frequently. Recently, we showed in an animal model that IL2/anti IL2 antibody complexes are more efficient against malignant melanoma and show fewer (or no) side effects. Based on these promising results in a mouse model of melanoma, we will examine the effects of human IL2/anti IL2 antibody complexes on the activation of human CD8 + T cells against melanoma cells. To this end, we will use humanized mice, which carry human immune cells, including CD8 + T cells. Testing of IL2/antiIL2 antibody complexes on human T cells using humanized mice is a crucial step towards being able to proceed to clinical studies. Project coordinator Prof. Dr. Onur Boyman Dermatologische Klinik UniversitätsSpital Zürich Gloriastrasse 31 CH8091 Zürich Phone +41 (0)44 255 25 60 onur.boyman@usz.ch Brisken Cathrin | Mechanisms of action of progesterone in the human breast (KFS 02462082009) Duration: 01.02.2010 – 01.02.2013 The mechanisms by which the pregnancy hormone progesterone acts on the human breast and contributes to breast carcinogenesis are poorly understood, because we lack adequate models to study them. Our work in the mouse model revealed that progesterone acts on a subset of cells in the milk ducts and induces them to secrete a protein called RANKL that in turn acts on neighbouring cells and makes them proliferate. We are developing a novel approach using fresh tissue from reduction mammoplasties to preserve the microenvironment and essential interactions between the cells to identify the mediators of progesterone in the human breast. New drugs that interfere with progesterone or RANKL signalling are already in clinical trials for different purposes, and many inhibitors of specific signalling pathways have been developed. The insights gained will be instrumental to determine whether progesterone indeed has cancerpromoting effects in the human breast. As a consequence, drugs blocking progesterone receptor (PgR) signalling and/ or its mediators may be useful as novel therapeutic and preventive strategies in the management of breast cancer. Project coordinator Prof. Dr Cathrin Brisken Institut suisse de recherche expérimentale sur le cancer (ISREC) NCCR Molecular Oncology Faculté des sciences de la vie EPF de Lausanne (EPFL) SV2.832 Station 19 CH1015 Lausanne Phone +41 (0)21 693 07 81 Fax +41 (0)21 693 07 40 cathrin.brisken@epfl.ch Brown Steven A. | The mechanism of cancer and circadian clock interactions and its usefulness in the design of therapeutic strategies (KFS 2642082010) Duration: 01.01.2011 – 01.01.2014 The circadian clock and the cell cycle are cell autonomous processes. The interaction between them is complex; the clock gates the cell cycle but ticks on even if the cell cycle is halted. Perturbations of the clock and the cell cycle can lead to cancer. In our project, we want to elucidate how the clock interacts with the cell cycle and then use this knowledge to improve the timing and thereby the efficiency of radiotherapeutic treatment regimes in models of brain tumours. Tumour clocks and/or clocks in the tissue surrounding the tumour could play a major role in tumour growth and prognosis for the patient. Thus, our goal is to understand the interaction of the various clocks with the cell cycle that determines tumour growth, and with this knowledge determine an optimal timing of treatment. We propose first to analyze circadian clock function in multiple different tumour cell lines to understand how the circadian clock is affected by oncogenic transformation. We will then test synthetically engineered clockcontaining and clockless tumours for growth in mice with or without circadian clocks to understand the contributions of clocks in the tumour and in the organism to tumour growth. Finally, we will treat these clockcontaining and clockless tumours radiotherapeutically to assess the contribution of clock function in both tumour and host to treatment outcome. Our results – especially the results of the therapeutic models – could lead to an improved efficacy of existing patient treatments by modifying already existing treatment regimes. Project coordinator Prof. Dr. Steven A. Brown Institut für Pharmakologie und Toxikologie Medizinische Fakultät Universität Zürich Winterthurerstrasse 190 CH8057 Zürich Phone +41 (0)44 635 59 99 Fax +41 (0)44 635 57 07 steven.brown@pharma.unizh.ch
Christofori Gerhard | The functional role of the transcription factors Dlx2 and Lhx2 in epithelial- mesenchymal transition (EMT) and in malignant tumor progression (KLS 02535022010) Duration: 01.09.2010 – 01.09.2013 The actual cause of death of most patients with cancer is due to metastasis. Malignant cancer cells leave their primary tumours, invade blood vessels and disseminate throughout the body to seed metastasis in distant organs. In this project, we investigated the functional contribution of the transcription factors Lhx2 and Dlx2 to metastasis. We found that both factors regulate genes that are critically required for cancer cell migration and metastasis formation. Lhx2 appears to directly regulate genes stimulating cell migration and invasion, whereas Dlx2 modulates the expression of genes required for cell survival during the metastatic process. Currently, we are identifying the genes that are regulated by Lhx2 and Dlx2 and investigating their functional contribution to cancer metastasis. The elucidation of the regulatory circuits underlying the metastatic process is a prerequisite for the development of innovative therapy to prevent cancer metastasis and thus patients’ death. Project coordinator Prof. Dr. Gerhard Christofori Institut für Biochemie und Genetik Departement Biomedizin Universität Basel Mattenstrasse 28 CH4058 Basel Phone +41 (0)61 267 35 62 Fax +41 (0)61 267 35 66 gerhard.christofori@unibas.ch
Page 1 and 2:
Cancer Research in Switzerland A pu
Page 3 and 4:
Cancer Research in Switzerland
Page 5 and 6:
Basic biomedical research 55 Cancer
Page 7 and 8:
policy work and was in charge of de
Page 9 and 10:
The main focus of the research fund
Page 11 and 12:
gramme research funding decreased b
Page 13 and 14:
Table 2 Distribution of funds for i
Page 15 and 16:
Funding patient-centred research Pa
Page 17 and 18:
value was not clearly discernible.
Page 19 and 20:
New organization of the Foundation
Page 21 and 22:
The board of the Foundation Cancer
Page 23 and 24:
The president of the Scientific Com
Page 25 and 26:
Prof. Martin Pruschy, PhD Departmen
Page 27 and 28:
Swartz wants to find out how tumour
Page 29 and 30:
The scientific and medical research
Page 31 and 32:
3. The original order/sequence of t
Page 33 and 34:
As a federation, the Cancer League
Page 35 and 36:
List of funded research projects, i
Page 37 and 38:
Zippelius Alfred | 2009: CHF 100,00
Page 39 and 40:
Kridel Robert | 2010: CHF 100,000.-
Page 41 and 42:
Thurgau Cancer League Biotechnologi
Page 43 and 44:
Weller Michael | 2010: CHF 65,828.-
Page 45 and 46:
manageable funding of individual pr
Page 47 and 48:
enhances breast cancer cell motilit
Page 49 and 50: Rüegg Curzio et al. | Tumor-mediat
Page 51 and 52: 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 102 and 103: 100 Constam Daniel | Role of activi
Page 104 and 105: 102 this study we will examine the
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
Page 116 and 117: 114
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
Page 154 and 155:
152 Zucca Emanuele | A prospective
Page 156 and 157:
154 Heinimann Karl | KFS 02489-08-2
Page 158 and 159:
156 Riggi Nicolò | BIL KFS 02717-0
Page 160 and 161:
158 activity at the single cell lev
Page 162 and 163:
160 Our research projects aim at un
Page 164 and 165:
162 Körner Meike | In vitro evalua
Page 166 and 167:
164 Nadal David | Is endemic Burkit
Page 168 and 169:
166 (> 50.000/patient). For their a
Page 170 and 171:
168 Zeller Rolf | Functional analys
Page 172 and 173:
170
Page 174 and 175:
172 area of health services researc
Page 176 and 177:
174 The financing of palliative car
Page 178 and 179:
176 National Strategy for Palliativ
Page 180 and 181:
178 Psychosocial research List of c
Page 182 and 183:
180 Within the patient group, level
Page 184 and 185:
182 Further, the results suggest th
Page 186 and 187:
184 It is in this context that the
Page 188 and 189:
186 Recommendation Female spouses o
Page 190 and 191:
188 Psychosocial research Presentat
Page 192 and 193:
190 rates communication skills rema
Page 195 and 196:
Epidemiological research Epidemiolo
Page 197 and 198:
data from cancer registries. In the
Page 199 and 200:
The importance of cancer registries
Page 201 and 202:
Ess Silvia | Patterns of care and s
Page 203 and 204:
Epidemiological research List of ap
Page 205 and 206:
Impact This work will serve as the
Page 207 and 208:
Thürlimann Beat | Management of br
show all

Cancer Research in Switzerland - Krebsliga Schweiz

You also want an ePaper? Increase the reach of your titles

Delete template?

Save as template?