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This meeting took place in 2005
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Inflammation and Cancer (B8)
Organizer(s) Raymond N. DuBois and Lisa M. Coussens
February 27—March 3, 2005
Beaver Run Resort • Breckenridge, Colorado USA
Abstract Deadline: Oct 27, 2004
Late Abstract Deadline:
Scholarship Deadline:
Early Registration Deadline: Dec 27, 2004
Supported by The Director's Fund
Summary of Meeting:
Chronic or recurrent inflammation is responsible for the development of many human cancers, including those affecting the liver, esophagus, stomach, large intestine, and urinary bladder [Coussens and Werb, [2002]]. Inflammation might influence the pathogenesis of cancers by (i) inflicting cell and genome damage, (ii) triggering restorative cell proliferation to replace damaged cells, (iii) elaborating a portfolio of cytokines that promote cell replication, angiogenesis and tissue repair [Coussens and Werb, [2002]]. Oxidative damage to DNA and other cellular components accompanying chronic or recurrent inflammation could increase risk by increasing the mutation rate. In response to infections, inflammatory cells produce a variety of toxic compounds designed to eradicate microorganisms. These include superoxide, hydrogen peroxide, singlet oxygen, as well as nitric oxide that can react further to form the highly reactive peroxynitrite. Some of these reactive oxygen and nitrogen species can directly interact with DNA in the host bystander cells, or react with other cellular components such as lipid, initiating a free radical chain reaction. If the damage is severe, these compounds can kill host bystander cells as well as pathogens, and can produce DNA damage and mutations among host cell survivors. As a consequence of an acquired defect in defenses against oxidant and electrophilic carcinogens associated with CpG island hypermethylation, normal epithelial cells may acquire a heightened susceptibility to oxidative genome damage in an inflammatory milieu, leading to neoplastic transformation and cancer progression.
View Scholarships/Awards
Chronic or recurrent inflammation is responsible for the development of many human cancers, including those affecting the liver, esophagus, stomach, large intestine, and urinary bladder [Coussens and Werb, [2002]]. Inflammation might influence the pathogenesis of cancers by (i) inflicting cell and genome damage, (ii) triggering restorative cell proliferation to replace damaged cells, (iii) elaborating a portfolio of cytokines that promote cell replication, angiogenesis and tissue repair [Coussens and Werb, [2002]]. Oxidative damage to DNA and other cellular components accompanying chronic or recurrent inflammation could increase risk by increasing the mutation rate. In response to infections, inflammatory cells produce a variety of toxic compounds designed to eradicate microorganisms. These include superoxide, hydrogen peroxide, singlet oxygen, as well as nitric oxide that can react further to form the highly reactive peroxynitrite. Some of these reactive oxygen and nitrogen species can directly interact with DNA in the host bystander cells, or react with other cellular components such as lipid, initiating a free radical chain reaction. If the damage is severe, these compounds can kill host bystander cells as well as pathogens, and can produce DNA damage and mutations among host cell survivors. As a consequence of an acquired defect in defenses against oxidant and electrophilic carcinogens associated with CpG island hypermethylation, normal epithelial cells may acquire a heightened susceptibility to oxidative genome damage in an inflammatory milieu, leading to neoplastic transformation and cancer progression.
View Scholarships/Awards
No registration fees are used to fund entertainment or alcohol at this conference
SUNDAY, FEBRUARY 27
MONDAY, FEBRUARY 28
TUESDAY, MARCH 1
WEDNESDAY, MARCH 2
THURSDAY, MARCH 3
Conference Program Print | View meeting in 12 hr (am/pm) time
SUNDAY, FEBRUARY 27
08:00—11:15
Innate Immunity and Malignancy
Meeting has ended...abstracts no longer viewable online.
Alberto Mantovani,
Humanitas University, Italy
Innate Immunity and Cancer
Innate Immunity and Cancer
Frances R. Balkwill,
Barts Cancer Institute, Queen Mary University of London, UK
The Role of Inflammatory Cytokines and Chemokines in Cancer Progression
The Role of Inflammatory Cytokines and Chemokines in Cancer Progression
Alison K. Bauer,
University of Colorado Anschutz Medical Campus, USA
Short Talk: A Protective Role for Toll-like Receptor (TLR)-4 in Butylated Hydroxytoluene (BHT)-Induced Mouse Pulmonary Inflammation and Tumorigenesis
Short Talk: A Protective Role for Toll-like Receptor (TLR)-4 in Butylated Hydroxytoluene (BHT)-Induced Mouse Pulmonary Inflammation and Tumorigenesis
*
Lisa M. Coussens,
Oregon Health & Science University, USA
Innate and Adaptive Immune Interactions Promote Cancer Development
Innate and Adaptive Immune Interactions Promote Cancer Development
P. Charles Lin,
Vanderbilt University, USA
Short Talk: Expansion of Myeloid Immune Suppressor Gr+CD11b+ Cells in Tumor-bearing Host Directly Promotes Tumor Angiogenesis
Short Talk: Expansion of Myeloid Immune Suppressor Gr+CD11b+ Cells in Tumor-bearing Host Directly Promotes Tumor Angiogenesis
Jeffrey W. Pollard,
Queen's Medical Research Institute, UK
Tumor-educated macrophages promote mammary tumor progression and metastasis
Tumor-educated macrophages promote mammary tumor progression and metastasis
17:00—19:00
Inflammatory Stressors and Cancer Progression
Meeting has ended...abstracts no longer viewable online.
*
Thea D. Tlsty,
University of California, San Francisco, USA
Epigenetic And Genetic Changes Control Tumorigenic Phenotypes and Occur In Vivo in Human Mammary Epithelia
Epigenetic And Genetic Changes Control Tumorigenic Phenotypes and Occur In Vivo in Human Mammary Epithelia
William L. Farrar,
National Cancer Institute, USA
Short Talk: Interleukin 6 (IL-6) Regulates and maintains Epigenetic Silencing of Tumor Suppressor and DNA Repair Genes in Human Multiple Myeloma Cells
Short Talk: Interleukin 6 (IL-6) Regulates and maintains Epigenetic Silencing of Tumor Suppressor and DNA Repair Genes in Human Multiple Myeloma Cells
Kathy Helzlsouer,
Johns Hopkins University, USA
C-Reactive Protein Levels and Subsequent Cancer Outcomes: Results from a Prospective Cohort Study and Implications for Prevention
C-Reactive Protein Levels and Subsequent Cancer Outcomes: Results from a Prospective Cohort Study and Implications for Prevention
08:00—11:00
Tumor Immunotherapy
Meeting has ended...abstracts no longer viewable online.
Olivera J. Finn,
University of Pittsburgh School of Medicine, USA
Premalignant lesions as targets for cancer vaccines
Premalignant lesions as targets for cancer vaccines
Brian P. Dolan,
Oregon State University, USA
Short Talk: Dendritic Cells Acquire Functional Peptide-MHC Complexes from Necrotic Tumor Cells
Short Talk: Dendritic Cells Acquire Functional Peptide-MHC Complexes from Necrotic Tumor Cells
Drew M. Pardoll,
Johns Hopkins University School of Medicine, USA
Molecular Immunology and Tumor Immunotherapy
Molecular Immunology and Tumor Immunotherapy
Ainhoa Perez-Diez,
NIAID, National Institutes of Health, USA
Short Talk: CD4 Cells Can Be More Efficient at Tumor Rejection Than CD8 Cells
Short Talk: CD4 Cells Can Be More Efficient at Tumor Rejection Than CD8 Cells
*
Glenn Dranoff,
Novartis Institutes for BioMedical Research, USA
Sequential Cancer Immunothherapy
Sequential Cancer Immunothherapy
17:00—19:00
Inflammation Fibrosis and Malignant Pathogenesis
Meeting has ended...abstracts no longer viewable online.
*
William G. Nelson,
Johns Hopkins School of Medicine, USA
Inflammation and Prostate Carcinogenesis
Inflammation and Prostate Carcinogenesis
Michael A. Hollingsworth,
University of Nebraska Medical Center, USA
MUC1 and the Pathogenesis of Pancreatic Cancer
MUC1 and the Pathogenesis of Pancreatic Cancer
Anna Moore,
Michigan State University, USA
Short Talk: UMUC-1 Tumor Antigen as an Imaging and Therapeutic Target
Short Talk: UMUC-1 Tumor Antigen as an Imaging and Therapeutic Target
Dafna Bar-Sagi,
New York University School of Medicine, USA
A Mouse Model of Hereditary Pancreatitis: Insights Into The Initiation of Pancreatic Cancer
A Mouse Model of Hereditary Pancreatitis: Insights Into The Initiation of Pancreatic Cancer
08:00—11:15
Host Response to Pathogens and Soluble Mediators
Meeting has ended...abstracts no longer viewable online.
*
Martin J. Blaser,
New York University School of Medicine, USA
Helicobacter pylori diversity and interaction with gastric epithelial cells.
Helicobacter pylori diversity and interaction with gastric epithelial cells.
Bernhard Homey,
Heinrich-Heine University Dussseldorf, Germany
Chemokine Receptors in Tumor Progression and Metastasis
Chemokine Receptors in Tumor Progression and Metastasis
Douglas McClain Noonan,
Università degli Studi dell'Insubria, Italy
Short Talk: Inflammation Associated Angiogenesis: A New Potential Target for Tumor Therapy
Short Talk: Inflammation Associated Angiogenesis: A New Potential Target for Tumor Therapy
M. Celeste Simon,
University of Pennsylvania, USA
Hypoxia, Angiogenesis, and Tumor Progression
Hypoxia, Angiogenesis, and Tumor Progression
Joseph S. Palumbo,
Cincinnati Children's Hospital Medical Center, USA
Short Talk: Mechanisms Linking Innate Hemostatic Factors and Innate Immunity to Metastatic Potential
Short Talk: Mechanisms Linking Innate Hemostatic Factors and Innate Immunity to Metastatic Potential
Thomas Doetschman,
University of Cincinnati, USA
TGFbeta, Inflammation and Colon Cancer Progression
TGFbeta, Inflammation and Colon Cancer Progression
17:00—19:00
Molecular Mechanisms for Cancer Prevention
Meeting has ended...abstracts no longer viewable online.
Michael Karin,
University of California, San Diego, USA
The IKK Complex: Providing a Link Between Inflammation and Cancer
The IKK Complex: Providing a Link Between Inflammation and Cancer
Ilan Stein,
Hebrew University of Jerusalem, Israel
Short Talk: NF-kappaB Functions as a Tumor Promoter in Inflammation-Associated Cancer
Short Talk: NF-kappaB Functions as a Tumor Promoter in Inflammation-Associated Cancer
George C. Prendergast,
Lankenau Institute for Medical Research, USA
Short Talk: IDO in Immune Suppression, Cancer, and Cancer Therapy
Short Talk: IDO in Immune Suppression, Cancer, and Cancer Therapy
*
Raymond N. DuBois,
Arizona State University, USA
COX-2, Inflammatory Mediators and Cancer Prevention
COX-2, Inflammatory Mediators and Cancer Prevention
*Session Chair †Invited, not yet responded.
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