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This meeting took place in 2011



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Epithelial Plasticity and Epithelial to Mesenchymal Transition (A8)


Organizer(s) Rik Derynck, Harold A. Chapman and Raymond Runyan
January 21—26, 2011
Fairmont Waterfront • Vancouver, British Columbia Canada
Abstract Deadline: Sep 21, 2010
Late Abstract Deadline: Oct 25, 2010
Scholarship Deadline: Sep 21, 2010
Early Registration Deadline: Nov 22, 2010

Supported by the Directors’ Fund

Summary of Meeting:
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.

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Conference Program    Print  |   View meeting in 12 hr (am/pm) time


FRIDAY, JANUARY 21

15:00—19:30
Registration

Waterfront Foyer
18:15—19:15
Refreshments

Waterfront Foyer
19:15—20:30
Welcome and Keynote Address
Meeting has ended...abstracts no longer viewable online.

Waterfront Ballroom C
Jean-Paul Thiery, Institute of Molecular and Cellular Biology, Singapore
EMT in the Progression of Carcinoma


SATURDAY, JANUARY 22

07:00—08:00
Breakfast

Mackenzie Ballroom
08:00—11:15
Epithelial Differentiation Plasticity
Meeting has ended...abstracts no longer viewable online.
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, École Polytechnique Fédérale de Lausanne, Switzerland
Deciphering Epithelial Stem Cell Potency

* Zena Werb, University of California, San Francisco, USA
Epithelial to Mesenchymal Transition in Mammary Tumorigenesis

Jeffrey A. Whitsett, Cincinnati Children's Hospital Medical Center, USA
Respiratory Epithelial Cells: Differentiation and Plasticity

Keith E. Mostov, University of California, San Francisco, USA
Epithelial Recovery from Injury and Homeostasis

Andras Kapus, Keenan Research Centre, St. Michael's Hospital, Canada
Short Talk: How does beta-catenin Regulate Epithelial-Myofibroblast Transition?

Jing Yang, University of California, San Diego, USA
Short Talk: Twist1-Induced Invadopodia Formation Promotes Tumor Metastasis

09:20—09:40
Coffee Break

Waterfront Foyer
11:15—13:00
Poster Setup

Waterfront Ballroom AB
13:00—22:00
Poster Viewing

Waterfront Ballroom AB
11:15
On Own for Lunch and Recreation

16:30—17:00
Coffee Available

Waterfront Foyer
17:00—19:15
Molecular Mechanisms: Signaling and Transcription I
Meeting has ended...abstracts no longer viewable online.
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
Rik Derynck, University of California, San Francisco, USA
TGF-beta-Induced Non-Smad Signaling in Epithelial-Mesenchymal Transition (EMT)

* M. Angela Nieto, Instituto de Neurociencias de Alicante, CSIC-UMH, Spain
Snail and EMT in Renal Fibrosis

Gregory J. Goodall, SA Pathology, Australia
Reversible Control of Cell State by the miR-200/ZEB/TGF-beta Signaling Loop

Katja Brückner, University of California, San Francisco, USA
Short Talk: A Drosophila Cell Culture Model for BMP-Induced Epithelial Plasticity

Jessica R. Seifert, New York University Langone Medical Center, USA
Short Talk: The Role of Endodermal EMT during Drosophila Germ Cell Migration

19:15—20:15
Social Hour with Lite Bites

Waterfront Ballroom AB
19:30—22:00
Poster Session 1

Waterfront Ballroom AB

SUNDAY, JANUARY 23

07:00—08:00
Breakfast

Mackenzie Ballroom
08:00—11:15
EMT in Early Development
Meeting has ended...abstracts no longer viewable online.
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
David R. McClay, Duke University, USA
Ingression of the Skeletogenic Cells of the Sea Urchin Embryo is Driven by Task-Specific Transcription Factor Control

Christopher M. Ward, University of Manchester, UK
The Function of E-Cadherin in Embryonic Stem Cells

Raymond E. Keller, University of Virginia, USA
EMT as a Force Generating Machine During Amphibian Gastrulation: A Tale of Two Blastopores

* Marianne Bronner-Fraser, California Institute of Technology, USA
Gene Regulatory Interactions Mediating Neural Crest Emigration

Margot L.K. Williams, University of Virginia, USA
Short Talk: Mechanisms of Primitive Streak Formation in the Mouse Embryo

Rodney A. Stewart, University of Utah Huntsman Cancer Institute, USA
Short Talk: EMT Mechanisms Regulating Neural Crest Development and Metastasis in Zebrafish

09:20—09:40
Coffee Break

Waterfront Foyer
11:15—13:00
Poster Setup

Waterfront Ballroom AB
13:00—22:00
Poster Viewing

Waterfront Ballroom AB
11:15
On Own for Lunch and Recreation

16:30—17:00
Coffee Available

Waterfront Foyer
17:00—19:15
Molecular Mechanisms: Signaling and Transcription II
Meeting has ended...abstracts no longer viewable online.
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
Morag Park, McGill University, Canada
Met Receptor Tyrosine Kinase: Signaling to EMT and Breast Cancer

* Amparo Cano Garcia, Instituto de Investigaciones Biomédicas, Spain
Regulation of Epithelial Plasticity and Metastasis of Basal-Like Breast Carcinomas by Lysyl Oxidase-Like 2 (LOXL2)

Aristidis Moustakas, Uppsala University, Sweden
Regulation of Epithelial to Mesenchymal Transition by Signaling Mediators under the Control of TGFbeta

Matthias Nees, VTT Technical Research Centre of Finland, Finland
Short Talk: Epithelial Plasticity, GPCRs & Bioactive Lipids in Prostate Cancer

Manti Guha, University of Pennsylvania, USA
Short Talk: Mitochondrial Retrograde Stress Signaling Induces an Epithelial to Mesenchymal Like Transition

19:15—20:15
Social Hour with Lite Bites

Waterfront Ballroom AB
19:30—22:00
Poster Session 2

Waterfront Ballroom AB

MONDAY, JANUARY 24

07:00—08:00
Breakfast

Mackenzie Ballroom
08:00—11:15
Epithelial Plasticity in Cancer
Meeting has ended...abstracts no longer viewable online.
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, Massachusetts Institute of Technology, USA
EMT and Cancer Stem Cells

* John Condeelis, Albert Einstein College of Medicine, USA
Molecular Mechanisms of EMT that also Contribute to Metastasis in Breast Tumors

Derek Radisky, Mayo Clinic, USA
Rac1b and Matrix Metalloproteinase-induced EMT in Lung Fibrosis and Cancer

David M. Epstein, Duke NUS, Graduate Medical School Singapore, Singapore
EMT in Context of Cancer Therapy

David Dornan, Genentech, Inc., USA
Short Talk: TRPS1 Targeting by miR-221/222 Promotes the Epithelial-Mesenchymal Transition in Breast Cancer

L. Eric Huang, University of Utah, USA
Short Talk: Long-term Hypoxia Promotes A Perpetual Mesenchymal Phenotype via Genetic Alterations for Malignant Progression

09:20—09:40
Coffee Break

Waterfront Foyer
11:15
On Own for Lunch and Recreation

14:30—15:00
Coffee Available

Waterfront Foyer
15:00—17:15
EMT in Tissue Differentiation
Meeting has ended...abstracts no longer viewable online.
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
Peter ten Dijke, Leiden University Medical Center, Netherlands
TGF-beta Signaling in Breast Cancer Cell Invasion & Endothelial to Mesenchymal Transition

* Raymond Runyan, University of Arizona, USA
Runx2-1 and Noelin1 are Essential Components of EMT in the Embryonic Heart

Ulrich Tepass, University of Toronto, Canada
Short Talk: Enhanced Requirement to Stabilize Epithelial Polarity and Adherens Junctions Results from EMT-Induced Morphogenetic Stress

Silva Krause, Children's Hospital Boston, USA
Short Talk: Embryonic Mesenchyme is Able to Revert the Mammary Cancer Cell Phenotype

Qihong Huang, Wistar Institute, USA
Short Talk: Functional Genomics Screen for the Regulators of Epithelial-Mesenchymal Transition and Metastasis

Odile Filhol, INSERM, France
Short Talk: Unbalanced Expression of Protein Kinase CK2 Subunits Induces Epithelial -to -Mesenchymal Transition and Contributes to Stemness

17:15—18:15
Social Hour with Lite Bites

Waterfront Ballroom AB

TUESDAY, JANUARY 25

07:00—08:00
Breakfast

Mackenzie Ballroom
08:00—11:15
EMT in Fibrosis
Meeting has ended...abstracts no longer viewable online.
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
Harold A. Chapman, University of California, San Francisco, USA
Regulation of EMT by Integrins

* Anna Mae Diehl, Duke University Medical Center, USA
Hedgehog Pathway Activation Promotes Epithelial-to-Mesenchymal Transitions and Other Events that Expand Myofibroblast Populations in Injured Livers

Raghu Kalluri, University of Texas MD Anderson Cancer Center, USA
Kidney Fibrosis: The Biology of Fibroblasts and the Role of ALK3 and BMP-7

Volker H. Haase, Vanderbilt University, USA
Hypoxic Signaling in the Development of Kidney Fibrosis

Damian Medici, Harvard Medical School, USA
Short Talk: Role of Endothelial-Mesenchymal Transition in Heterotopic Ossification

Melody L. Stallings-Mann, Mayo Clinic, USA
Short Talk: Matrix Metalloproteinase-3 (MMP-3) Induces Epithelial Cell Activation and Epithelial-Mesenchymal Transition during Lung Fibrosis Development

09:20—09:40
Coffee Break

Waterfront Foyer
11:15
On Own for Lunch and Recreation

16:30—17:00
Coffee Available

Waterfront Foyer
17:00—19:00
EMT in Cancer Invasion and Metastasis
Meeting has ended...abstracts no longer viewable online.
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
Shoukat Dedhar, British Columbia Cancer Research Centre, Canada
Tumor Hypoxia, Metastasis and Plasticity of Cancer Stem Cells: Critical Role of Carbonic Anhydrase IX, a HIF Induced pH Regulator

* 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
Epithelial Mesenchymal Plasticity in Human Breast Cancer Cell Lines: The Path Forward?

19:00—20:00
Social Hour with Lite Bites

Waterfront Ballroom AB
20:00—23:00
Entertainment

Waterfront Ballroom AB

WEDNESDAY, JANUARY 26

 
Departure


*Session Chair †Invited, not yet responded.



We gratefully acknowledge support for this conference from:


Directors' Fund


These generous unrestricted gifts allow our Directors to schedule meetings in a wide variety of important areas, many of which are in the early stages of research.

Click here to view all of the donors who support the Directors' Fund.



We gratefully acknowledge the generous grant for this conference provided by:


National Institutes of Health

Grant No. 1R13HL104795-01




We gratefully acknowledge additional in-kind support for this conference from those foregoing speaker expense reimbursements:



Astellas Pharma Inc.


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