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    Ada YONATH
    Professor of structural biology Nobel Prize in Chemistry 2009, Weizmann Institute of Science (Rehovot, Israel)

    Keynot lecture

    We initiated ribosomal crystallography about three decades ago, and determined the 3 A structures of functionally active conformations of the small and the large ribosomal subunits in 2000 and 2001. Further analysis revealed the mechanism of peptide bond formation and illuminated the fashion of the ribosomal involvement in cellular regulation. In addition, by investigating crystallographically the modes of binding of over a dozen antibiotics, we elucidated the structural basis for their action, as well as for their selectivity, and illuminated possible pathways for acquiring resistance by pathogenic bacteria.

  • Robert WEINBERG
    Massachusetts Institute of Technology (Cambridge, USA)


    Keynote lecture

    Research in the laboratory is focused on the molecular mechanisms that control carcinoma progression and metastasis. Our research is concentrated in three areas: (1) Understanding the collaborative impact of paracrine and systemic signaling on tumor growth and progression. (2) Identification of mechanisms through which paracrine and systemic signals can induce epithelial cells to enter into a mesenchymal/stem-cell state. (3) Ellucidating the complex molecular mechanisms that regulate carcinoma invasion and metastasis.

  • Thomas BRABLETZ
    Departement of experimental medicine
    (Friedrich-Alexander Universität, Germany)

    Thomas Brabletz is Professor for Molecular Oncology and Chairman of the Dept. of Experimental Medicine, University Erlangen, Germany. Focusing on malignant cancer progression, in particular mechanisms of invasion and metastasis, he aims to integrate basic and clinically relevant cancer research. He proposed a concept of transient rounds of EMT and MET, resulting in aberrant cellular plasticity and the generation of ‘Migrating cancer stem cells’ as driving force of metastasis. Currently his major interests are in uncovering underlying mechanisms, such as feedback loops between EMT-inducers, oncogenic pathways and microRNAs, as basis for novel therapeutic strategies to fight cancer metastasis.

  • Michele DE PALMA
    Swiss Institute for Experimental Cancer Research (Switzerland)

    Our laboratory investigates the interactions between genetically altered cancer cells and the ostensibly normal host tissues in which tumors arise, progress and develop to metastatic disease. We focus on the cross talk between malignant cells and the vascular system, immune cells, and secreted extracellular vesicles (exosomes), and the mechanisms whereby these heterotypic interactions regulate tumor progression in experimental cancer models. This is being studied primarily in transgenic mouse models of breast, lung and pancreatic neuronedocrine carcinogenesis, in which both malignant and host cells are genetically engineered to be visualized or depleted, or to modify their expression of coding or non-coding genes of interest. Furthermore, we examine how the interplay between the tumor and the host can be harnessed for improving tumor response to anti-cancer therapies.

  • Frederic DE SAUVAGE
    Genentech (San Francisco, USA)

    We are studying and targeting a number of important developmental signaling pathways such as Wnt, Hedgehog and Notch. These signaling pathways play critical roles during embryogenesis in pretty much every organ of the body where they modulate proliferation or differentiation of numerous cell types. It is however becoming increasingly clear that these pathways are involved in tumorigenesis when reactivated in adult tissues through mutations or overexpression of pathways components.

    This work has led to the development of vismodegib, a hedgehog pathway inhibitor, which targets Smoothened. Vismodegib was approved in 2012 by the FDA for the treatment of basal cell carcinoma (BCC), which has metastasized to other parts of the body, relapsed after surgery, or cannot be treated with surgery or radiation. We are also involved in a number of earlier stage initiatives using genetic mouse models of cancer to better predict drug efficacy, sequencing the genome of various tumor types to better understand how tumor develop and how to target them as well as cancer and functional genome projects to identify novel drug targets in various therapeutic areas. 

  • Michael F CLARKE
    Institute for Stem Cell Biology and Regenerative Biology, Standford University (USA)

    In addition to his clinical duties in the division of Oncology, Dr. Clarke maintains a laboratory focused on two areas of research: i) the control of self-renewal of normal stem cells and their malignant counterparts; and ii) the identification and characterization of cancer stem cells. A central issue in stem cell biology is to understand the mechanisms that regulate self-renewal of hematopoietic stem cells, which are required for hematopoiesis to persist for the lifetime of the animal. Until recently, the molecular mechanisms that regulate adult stem cell self-renewal were not known. His laboratory recently found that the proto-oncogene Bmi-1 regulates stem cell self-renewal via an epigenetic mechanism. By investigating the pathways upstream and downstream of Bmi1, the laboratory is actively investigating the molecular pathways that regulate self-renewal.

  • Isabelle JANOUEIX
    Insitut Curie (Paris, France)

    Neuroblastoma (NB) is an embryonal cancer of the sympathetic nervous system observed in early childhood and characterized by a broad spectrum of clinical behaviors, ranging from spontaneous regression to fatal outcome despite aggressive therapies. In order to improve the prognosis of this pediatric cancer and to identify new therapeutic targets, a better understanding of the mechanisms and genes implicated in oncogenesis is required.

    My research program aims at identifying the genes and mechanisms involved in NB development and/or progression and to characterize the genes linked to tumor predisposition. In 2008, we characterized somatic and germline gain-of-function mutations of the ALK (Anaplastic Lymphoma Kinase) gene, encoding a tyrosine kinase receptor, in sporadic and familial NB cases. Our data also provided a strong molecular rationale for ALK targeted therapy in NB. My project focuses on two main aspects: (1) characterization of the molecular mechanisms associated with ALK alterations in NB oncogenesis; (2) identification of other genes implicated in the neoplastic transformation.

  • Scott LOWE
    Memorial Sloan Kettering Cancer Center (New York, USA)

    Cancer arises through an evolutionary process in which normal cells acquire mutations that erode growth controls, leading to the expansion of aberrantly proliferating cells. Such mutations activate oncogenes or inactivate tumor suppressors, bestowing new capabilities to developing cancer cells. Our research is based on the premise that the path of cancer evolution dictates a tumor’s subsequent response to therapy and creates unique vulnerabilities that represent therapeutic opportunities.

    We use mouse models, RNA interference (RNAi), and cancer genomics to identify components of tumor suppressor gene networks and understand the molecular determinants of treatment response. We also use temporally regulatable RNAi technology to identify genes required for tumor maintenance and to explore the mechanisms involved in tumor regression, including both cell intrinsic and extrinsic mechanisms.

    Our goal is to gain a more comprehensive understanding of tumor suppressor networks and identify cancer maintenance genes that will be useful therapeutic targets relevant to specific cancer genotypes.

  • Martin McMAHON
    University of UTAH (Salt Lake City, USA)

    Mutational activation of RAS genes is detected in approximately 25 percent of human cancers. However, to date, activated RAS oncoproteins remain intractable pharmacological targets. Research in the McMahon Lab focuses on the importance of RAS effectors, such as the RAF family of protein kinases and phosphoinositide 3’ (PI3’)-kinases in the aberrant physiology of cancer cells.

    To do so, the lab employs genetically engineered mouse (GEM) models of human cancer, patient-derived xenografts (PDXs) and cultures of cancer cells in combination with various genetic or pharmacological to explore how signaling pathways contribute to cancer cell initiation, progression, and response to therapy.

    The McMahon lab’s translational cancer research program focuses on the mechanisms underlying the development of metastatic melanoma, lung, and thyroid cancer. Although these malignancies are derived from distinct cell types, they share a striking number of common genetic alterations especially activating mutations in KRAS, BRAF, PIK3CA, or CTNNB1 (b-catenin).

    In addition, many of these tumors display alterations in tumor suppressors such as CDKN2A, PTEN or TP53. To do this, Dr. McMahon’s laboratory works with cultured human cancer-derived cells and with genetically engineered mouse models of human cancer. Such model systems have demonstrated considerable value in the design and evaluation of new diagnostic, prognostic, and therapeutic tools to treat patients with cancer.

  • Max S. WICHA
    University of Michigan Comprehensive Cancer Center (USA)

    The Wicha laboratory is a leader in Cancer Stem Cell (CSC) biology. According to the ISI Citation Index, Dr. Wicha is among the most highly-cited investigators in the field of CSCs. His group was part of the team that first identified breast CSCs. Dr. Wicha’s laboratory identified a number of stem cell markers and developed in vitro and in vivo models to isolate and characterize these cells. These research models and resources have been widely adopted by other investigators. His laboratory subsequently elucidated a number of intrinsic and extrinsic pathways which regulate self-renewal and cell fate decisions in CSCs. Recently, the Wicha laboratory has focused on translating his pre-clinical research findings into the development of clinical trials designed to target breast CSCs.

  • Jane VISVADER
    Walter Heliza Hall institute (Parkville, Australia)

    Our laboratory is studying molecular regulators of normal breast development and cancer, with a particular interest in breast stem cells and the breast epithelial cell hierarchy.

    Through clonal cell-fate mapping studies using a stochastic multicolour cre-reporter combined with a novel 3D imaging strategy, we have recently provided evidence for the existence of bipotent MaSCs as well as distinct long-lived progenitor cells.

    Current efforts are directed towards further understanding the normal epithelial hierarchy and the cell subtypes that are most susceptible to becoming transformed in vivo, the so- called ‘cells of origin’. We are searching for markers that enable further purification of stem cells to enhance our understanding of the heterogeneity that lies within this pool, using a combination of transplantation and cell lineage tracing studies.

    We are also identifying transcriptional and epigenetic regulators that act along the hierarchy using gene-targeted models and CRISPR/CAS9 technology. Promoter-specific strains built in the laboratory enable us to interrogate potential cells of origin of cancer.

    The laboratory’s extensive bank of human breast cancer xenografts that are serving as important preclinical models for testing new therapeutic drug combinations in the treatment of breast cancer. We are currently developing potential chemoprevention strategies that may eventually benefit women at high risk of developing breast cancer.
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