Meeting Program

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Friday, January 21
3:00 - 7:30 PM	Registration	Waterfront Foyer
7:30 - 8:30 PM	Keynote Address Registered attendees for this meeting can view Abstracts for this session starting on 12/21/2010	Waterfront Ballroom C
	Jean-Paul Thiery, Institute of Molecular and Cellular Biology, Singapore
Saturday, January 22
7:00 - 8:00 AM	Breakfast	Mackenzie Ballroom
8:00 - 11:00 AM	Epithelial Differentiation Plasticity Registered attendees for this meeting can view Abstracts for this session starting on 12/21/2010 NOTE: Epithelial cells have an inherent differentiation plasticity. Well-studied examples are the changes in epithelial phenotypes and organization in mammary gland epithelial cells during and following pregnancy and lactation, and the response of epithelial cells to injury, in which they transiently lose epithelial characteristics to then re-acquire them (as demonstrated in lung and skin epithelia). This session will also deal with how epithelial stem cells giving rise to differentiated epithelia.	Waterfront Ballroom C
	Yann Barrandon, Ecole Polytechnique Federale de Lausanne, Switzerland Epithelial Stem Cells
	* Mina J. Bissell, Lawrence Berkeley National Laboratory, USA The Wisdom of the Mammary Acini
	Jeffrey A. Whitsett, Cincinnati Children's Hospital Medical Center, USA Lung Alveolar Epithelium
	Keith E. Mostov, University of California, San Francisco, USA Epithelial Tubule Formation and Wound Healing
	Short Talk(s) to be Chosen from Abstracts,
9:20 - 9:40 AM	Coffee Break	Waterfront Foyer
11:00 AM- 1:00 PM	Poster Setup	Waterfront Ballroom AB
1:00 - 10:00 PM	Poster Viewing	Waterfront Ballroom AB
4:30 - 5:00 PM	Coffee Available	Waterfront Foyer
5:00 - 7:00 PM	Molecular Mechanisms: Signaling and Transcription I Registered attendees for this meeting can view Abstracts for this session starting on 12/21/2010 NOTE: This is the first of two sessions dealing primarily with the cell biology of loss of epithelial characteristics, EMT and associated motility and invasion. Wnt, TGF-beta family and Erk MAPK signaling are key signaling mechanisms. Furthermore, Snail, ZEB and bHLH family transcription factors play key roles in driving the changes in cell phenotype and behavior. The mechanisms and their functional interplay will be discussed.	Waterfront Ballroom C
	* M. Angela Nieto, CSIC-UMH, Spain Transcription Regulation of EMT
	Rik Derynck, University of California, San Francisco, USA TGF-beta-Induced non-Smad Signaling in EMT
	Gregory J. Goodall, Institute of Medical and Veterinary Science, Australia MicroRNAs in EMT
	Short Talk to be Chosen from Abstracts,
7:00 - 8:00 PM	Social Hour w/ Lite Bites	Waterfront Ballroom AB
7:30 - 10:00 PM	Poster Session 1 Registered attendees for this meeting can view Abstracts for this session starting on 12/21/2010	Waterfront Ballroom AB
Sunday, January 23
7:00 - 8:00 AM	Breakfast	Mackenzie Ballroom
8:00 - 11:00 AM	EMT in Early Development Registered attendees for this meeting can view Abstracts for this session starting on 12/21/2010 NOTE: Already in early development, epithelial differentiation plasticity is apparent. Embryonic stem cells are epithelial and undergo differentiation into non-epithelial niche cells. Additionally, one of the first differentiation events results in the generation of mesoderm from ectoderm. Neural crest is also a prominent example of how neuro-ectodermal cells give rise to a variety of cell types including different types of mesenchymal cells.	Waterfront Ballroom C
	Christopher M. Ward, University of Manchester, UK EMT of ES Cells
	David McClay, Duke University, Durham, USA Gastrulation in the Sea Urchin
	Raymond E. Keller, University of Virginia, Charlottesville, USA Several Patterns and Morphogenic Functions of EMT in Early Amphibian Development
	* Marianne Bronner-Fraser, California Institute of Technology, Pasadena, USA Gene Regulatory Interactions Mediating Neural Crest Emigration
	Short Talk(s) to be Chosen from Abstracts,
9:20 - 9:40 AM	Coffee Break	Waterfront Foyer
11:00 AM- 1:00 PM	Poster Setup	Waterfront Ballroom AB
1:00 - 10:00 PM	Poster Viewing	Waterfront Ballroom AB
4:30 - 5:00 PM	Coffee Available	Waterfront Foyer
5:00 - 7:00 PM	Molecular Mechanisms: Signaling and Transcription II Registered attendees for this meeting can view Abstracts for this session starting on 12/21/2010 NOTE: This is the second of two sessions primarily dealing with the cell biology of loss of epithelial characteristics, EMT and associated motility and invasion. Wnt, TGF-beta family and Erk MAPK signaling are key signaling mechanisms. Furthermore, Snail, ZEB and bHLH family transcription factors play key roles in driving the changes in cell phenotype and behavior. We will discuss these mechanisms and their functional interplay.	Waterfront Ballroom C
	* Amparo Cano Garcia, Instituto de Investigaciones Biomédicas, Spain Transcription Regulation of EMT
	Paolo M. Comoglio, University of Torino Medical School, Italy The Met Receptor: Genetic Control of Invasive Growth
	Aristidis Moustakas, Ludwig Institute for Cancer Research, Sweden Regulation of Epithelial to Mesenchymal Transition by Signaling Mediators under the Control of TGF-beta
	Short Talk to be Chosen from Abstracts,
7:00 - 8:00 PM	Social Hour w/ Lite Bites	Waterfront Ballroom AB
7:30 - 10:00 PM	Poster Session 2 Registered attendees for this meeting can view Abstracts for this session starting on 12/21/2010	Waterfront Ballroom AB
Monday, January 24
7:00 - 8:00 AM	Breakfast	Mackenzie Ballroom
8:00 - 11:00 AM	Epithelial Plasticity in Cancer Registered attendees for this meeting can view Abstracts for this session starting on 12/21/2010 NOTE: As epithelial cells become transformed and tumorigenic, they exhibit epithelial plasticity, giving rise to metaplasia, and eventually become invasive and undergo EMT. The role of EMT in invasion and metastasis will be discussed. This session will also discuss the role of EMT in the acquisition of a cancer stem cell phenotype.	Waterfront Ballroom C
	Robert A. Weinberg, Whitehead Institute for Biomedical Research, Cambridge, USA EMT and Cancer Stem Cells
	John Condeelis, Albert Einstein College of Medicine, Bronx, USA Molecular Mechanisms of EMT that also Contribute to Metastasis in Breast Tumors
	Shoukat Dedhar, British Columbia Cancer Agency, Canada Integrin Signaling, Invasion and Metastasis
	* Zena Werb, University of California, San Francisco, USA EMT in Mammary Carcinogenesis
	Short Talk(s) to be Chosen from Abstracts,
9:20 - 9:40 AM	Coffee Break	Waterfront Foyer
11:00 AM- 1:00 PM	Poster Setup	Waterfront Ballroom AB
1:00 - 10:00 PM	Poster Viewing	Waterfront Ballroom AB
4:30 - 5:00 PM	Coffee Available	Waterfront Foyer
5:00 - 7:00 PM	EMT in Tissue Differentiation Registered attendees for this meeting can view Abstracts for this session starting on 12/21/2010 NOTE: This session is a continuation of session 3, but focusing on other and perhaps later aspects of development, in particular in organ systems. Endothelial to mesenchymal differentiation will be discussed, in addition to developmental EMT in heart, pancreas and lung.	Waterfront Ballroom C
	* Raymond Runyan, University of Arizona, Tucson, USA EMT in Heart Valve Formation
	Peter Ten Dijke, Leiden University Medical Center, The Netherlands Endothelial to Mesenchymal Differentiation
	Speaker to be Announced,
	Short Talk to be Chosen from Abstracts,
7:00 - 8:00 PM	Social Hour w/ Lite Bites	Waterfront Ballroom AB
7:30 - 10:00 PM	Poster Session 3 Registered attendees for this meeting can view Abstracts for this session starting on 12/21/2010	Waterfront Ballroom AB
Tuesday, January 25
7:00 - 8:00 AM	Breakfast	Mackenzie Ballroom
8:00 - 11:00 AM	EMT in Fibrosis Registered attendees for this meeting can view Abstracts for this session starting on 12/21/2010 NOTE: The roles of epithelial plasticity and EMT in tissue fibrosis, with particular emphasis on lung, liver and kidney fibrosis, will be discussed. This session will incorporate information on possible therapeutic approaches.	Waterfront Ballroom C
	* Anna Mae Diehl, Duke University Medical Center, Durham, USA Hedgehog and Hepato-Biliary Fibrosis
	Harold A. Chapman, University of California, San Francisco, USA EMT in Lung Fibrosis
	Raghu Kalluri, Harvard Medical School/BIDMC, Boston, USA Cardiac and Liver Fibrosis
	Volker H. Haase, Vanderbilt University Medical Center, Nashville, USA Hypoxia and Kidney and Liver Fibrosis
	Short Talk(s) to be Chosen from Abstracts,
9:20 - 9:40 AM	Coffee Break	Waterfront Foyer
4:30 - 5:00 PM	Coffee Available	Waterfront Foyer
5:00 - 7:00 PM	EMT in Cancer Invasion and Metastasis Registered attendees for this meeting can view Abstracts for this session starting on 12/21/2010 NOTE: This session is a continuation of session 5. The role of epithelial plasticity in cancer dissemination and metastasis will be discussed, as will information on possible therapeutic approaches.	Waterfront Ballroom C
	* Kohei Miyazono, University of Tokyo, Japan TGF-beta, EMT and TGF-beta Signaling Inhibitors in Cancer Progression
	Rik Thompson, St. Vincent's Institute of Medical Research, Australia EMT and MET in Cancer Progression
	David M. Epstein, OSI Pharmaceuticals, Inc., New York, USA Therapeutic Inhibition of EMT
7:00 - 8:00 PM	Social Hour w/ Lite Bites	Waterfront Ballroom AB
8:00 - 11:00 PM	Entertainment	Waterfront Ballroom AB
Wednesday, January 26
	Departure
*=Session Chair     †=Speaker invited, not yet responded.

Epithelial-to-mesenchymal transition (EMT) is a basic cellular process in which epithelial cells lose epithelial properties, e.g. their polarized organization and cell-cell junctions, undergo changes in cytoskeleton and cell shape, acquire mesenchymal characteristics and become migratory and invasive. EMT was first recognized as distinct cell differentiation process in the late 70’s, and has received increasing attention, as it not only occurs in normal development but is also an integral component of various pathological conditions. An increasing understanding of the signaling and transcription processes that mediate EMT is starting to provide a framework of the underlying molecular mechanisms. During development, EMT occurs as early as gastrulation, when ectodermal cells give rise to mesoderm. In addition, embryonic stem cells in culture are epithelial in nature and, during colony formation, rapidly give rise to niche cells that lack epithelial characteristic and appear mesenchymal. EMT is reiterated at different stages and in different developmental contexts. Notably, neural crest cells delaminate and migrate to give rise to various mesenchymal cell populations. In addition, EMT occurs at distinct sites and stages in organogenesis, e.g. in the heart and pancreas. Conversely, mesenchymal to epithelial transition (MET) also occurs and may account for the reversal of cells that have undergone EMT back to the epithelial phenotype, illustrating the potential of EMT to be a transient and reversible process. Finally, it has become increasingly apparent that endothelial cells, similarly to epithelial cells, can lose endothelial characteristics and acquire mesenchymal properties. EMT has also been recognized as an important component of pathological conditions, and contributes to cancer progression, specifically invasion and metastasis of cancers, and fibrosis. While the contributions of EMT to cancer progression and fibrosis are debated, epithelial cells have been shown to undergo EMT in vivo under pathological conditions. In addition, in response to injury, epithelial cells reversibly lose epithelial characteristics and become migratory, illustrating the plasticity of the epithelial cells in wound healing. Studies on EMT have greatly benefited from the discovery that some growth and differentiation factors, most notably FGFs and HGF that act through receptor tyrosine kinases, and members of the TGF-beta family can induce EMT both in cell culture and in vivo, and from the establishment of cell culture models. These studies have provided great impetus to the dissection of signaling pathways that drive or contribute to EMT. Further, the identification of distinct families of transcription factors, whose expression is activated during EMT, allows a rapidly increasing insight into the transcription programs that drive EMT. Importantly, the signaling mechanisms and transcription programs that characterize EMT during development appear to be largely recapitulated during EMT processes under pathological conditions. Although EMT has been well documented during development, there is debate about its role and contribution in pathological conditions. The transient and reversible nature of EMT in cancer progression may contribute to some aspects of this debate, as cells that have undergone EMT may revert to their epithelial differentiation state and are therefore not easily identified. Another aspect of the debate centers around the acquisition of mesenchymal properties, especially since mesenchymal characteristics are ill-defined. Furthermore, in many cases epithelial cells lose epithelial characteristics and become migratory, but do not acquire mesenchymal marker expression. These observations suggest that a spectrum of epithelial plasticity changes can occur, resulting in downregulation of epithelial differentiation and integrity to different extents, and in changes that may or may not qualify as EMT. By considering EMT as the most striking manifestation of epithelial plasticity, much of the debate on the relative contribution of EMT to disease may be moot since different degrees of epithelial plasticity are observed. For example, while EMT has been implicated in cancer invasion, increased migration and invasion of cells with epithelial characteristics has also been documented as a basis for cancer invasion and progression. As another example, the changes in epithelial differentiation and organization of mammary epithelial cells during and following pregnancy and lactation also illustrate the inherent plasticity of epithelial cells that does not need to result in EMT. Further, during epithelial wound healing, different degrees of epithelial plasticity are observed. For example, striking plasticity is displayed by the airway respiratory epithelium following injury, where rapid conversion to a squamous phenotype protects the airway surface integrity, followed by reacquisition of multiple epithelial phenotypes during recovery. Finally, the realization that EMT provides a basis for cell invasion, leading to metastasis of carcinomas or fibrosis in different organs has also stimulated interest to find therapeutic modalities to inhibit EMT that consequently may interfere with or prevent the progression of metastases or fibrosis. In cancer, these considerations are energized by recent pre-clinical and clinical evidence that VEGF inhibitors as single agents promote invasion and metastasis, adversely affecting survival, and by preclinical results indicating that TGF-beta signaling inhibitors prevent or interfere with invasion and metastasis. Already, several recent clinical trials with antibodies and small molecules target signaling pathways known to drive EMT. Purpose of the Proposed Conference: We propose a conference roster to highlight the progress in our understanding of EMT against the background of the inherent plasticity of the epithelial cells. Following a keynote address, we propose a first session that will set the stage for subsequent sessions on EMT. This first session will discuss current insights into the differentiation of epithelial cells from stem cells, the maintenance of epithelial integrity and the inherent plasticity of epithelial cells. Against this background, the next seven sessions will discuss progress in our understanding of (1) the molecular mechanisms underlying epithelial plasticity and EMT (2 sessions), (2) the roles of EMT in normal development (2 sessions), (3) the roles of EMT in cancer (2 sessions) and fibrosis (1 session), including progress toward therapies based on inhibition of EMT. We appreciate that these divisions are artificial, since e.g. mechanistic studies are often validated in the context of development, cancer or fibrosis. Nevertheless, as artificial as these three subdivisions may be, we aim to give about equal weight to the cell biology of EMT, its developmental roles and its roles in pathology. The overall subject matter of the different aspects of the proposed conference is highlighted in the Background section above and in the discussion of the individual sessions further below, to which we refer. The purpose of this conference will be to bring together scientists who work on disparate aspects of epithelial plasticity and EMT. We expect to see an integration of cell and molecular biologists, developmental biologists, cancer biologists and organ/tissue biologists. Many of these scientists may be basic scientists, yet we also expect a substantial participation by scientists with translational interest and clinician-scientists, and significant interest from pharmaceutical and biotechnology industry.