Past Meeting | Keystone Symposia

This meeting took place in the past. Here is a list of meetings that are related:
Inflammation, Infection and Cancer (2014X1)
The Role of Inflammation during Carcinogenesis (2012E2)
Molecular and Cellular Biology of Immune Escape in Cancer (2010J6)
Role of Inflammation in Oncogenesis (2010J5)
Extrinsic Control of Tumor Genesis and Progression (2009C8)
Inflammation, Microenvironment and Cancer (2008D2)
Mechanisms Linking Inflammation and Cancer (2007B6)

Web Desc
Inflammation and Cancer Organizer(s): Raymond N. DuBois and Lisa M. Coussens Date: February 27 - March 03, 2005 Location: Beaver Run Resort, Breckenridge, CO, USA 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. Discounted Abstract Deadline: October 27 2004 Discounted Registration Deadline: December 27 2004 We gratefully acknowledge additional support for this conference from: We appreciate the organizations that provide Keystone Symposia with additional support, such as marketing and advertising: Click here to view more of these organizations Special thanks to the following for their support of Keystone Symposia initiatives to increase participation at this meeting by scientists from underrepresented backgrounds: Click here to view more of these organizations

Web Desc

Inflammation and Cancer

Organizer(s): Raymond N. DuBois and Lisa M. Coussens

Date: February 27 - March 03, 2005
Location: Beaver Run Resort, Breckenridge, CO, USA

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.

Discounted Abstract Deadline: October 27 2004

Discounted Registration Deadline: December 27 2004

We gratefully acknowledge additional support for this conference from:

We appreciate the organizations that provide Keystone Symposia with additional support, such as marketing and advertising:

Click here to view more of these organizations

Special thanks to the following for their support of Keystone Symposia initiatives to increase participation at this meeting by scientists from underrepresented backgrounds:

Click here to view more of these organizations

Program


Sunday, February 27 \| 3:00PM - 7:30PM Registration Room: Foyer
Sunday, February 27 \| 6:30PM - 7:30PM Refreshments Room: Foyer
Sunday, February 27 \| 7:30PM - 8:30PM Keynote Address Room: Peaks 4-5 Speaker 1 of 1 Harold F. Dvorak, Beth Israel Deaconess Medical Center, USA Inflammation And Cancer Induce Neovascular Stroma By Common Mechanisms.
Monday, February 28 \| 7:00AM - 8:00AM Breakfast Room: Peaks 6-12
Monday, February 28 \| 8:00AM - 11:15AM Innate Immunity and Malignancy Room: Peaks 4-5 Speaker 6 of 6 Jeffrey W. Pollard, Queen's Medical Research Institute, UK Tumor-educated macrophages promote mammary tumor progression and metastasis
Monday, February 28 \| 8:00AM - 11:15AM Innate Immunity and Malignancy Room: Peaks 4-5 Speaker 5 of 6 P. Charles Lin, Vanderbilt University, USA Short Talk: Expansion of Myeloid Immune Suppressor Gr+CD11b+ Cells in Tumor-bearing Host Directly Promotes Tumor Angiogenesis
Monday, February 28 \| 8:00AM - 11:15AM Innate Immunity and Malignancy Room: Peaks 4-5 Speaker 4 of 6 * Lisa M. Coussens, Oregon Health & Science University, USA Innate and Adaptive Immune Interactions Promote Cancer Development
Monday, February 28 \| 8:00AM - 11:15AM Innate Immunity and Malignancy Room: Peaks 4-5 Speaker 3 of 6 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
Monday, February 28 \| 8:00AM - 11:15AM Innate Immunity and Malignancy Room: Peaks 4-5 Speaker 2 of 6 Frances R. Balkwill, Barts Cancer Institute, Queen Mary University of London, UK The Role of Inflammatory Cytokines and Chemokines in Cancer Progression
Monday, February 28 \| 8:00AM - 11:15AM Innate Immunity and Malignancy Room: Peaks 4-5 Speaker 1 of 6 Alberto Mantovani, Humanitas University, Italy Innate Immunity and Cancer
Monday, February 28 \| 9:20AM - 9:40AM Coffee Break Room: Foyer
Monday, February 28 \| 11:15AM - 1:00PM Poster Setup Room: Peaks 1-3
Monday, February 28 \| 1:00PM - 10:00PM Poster Viewing Room: Peaks 1-3
Monday, February 28 \| 4:30PM - 5:00PM Coffee & Snacks Available Room: Foyer
Monday, February 28 \| 5:00PM - 7:00PM Inflammatory Stressors and Cancer Progression Room: Peaks 4-5 Speaker 4 of 4 Kathy Helzlsouer, Johns Hopkins University, USA C-Reactive Protein Levels and Subsequent Cancer Outcomes: Results from a Prospective Cohort Study and Implications for Prevention
Monday, February 28 \| 5:00PM - 7:00PM Inflammatory Stressors and Cancer Progression Room: Peaks 4-5 Speaker 3 of 4 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
Monday, February 28 \| 5:00PM - 7:00PM Inflammatory Stressors and Cancer Progression Room: Peaks 4-5 Speaker 2 of 4 * Thea D. Tlsty, University of California, San Francisco, USA Epigenetic And Genetic Changes Control Tumorigenic Phenotypes and Occur In Vivo in Human Mammary Epithelia
Monday, February 28 \| 5:00PM - 7:00PM Inflammatory Stressors and Cancer Progression Room: Peaks 4-5 Speaker 1 of 4 Curtis C. Harris, NCI, National Institutes of Health, USA Radical Causes of Human Cancer
Monday, February 28 \| 7:00PM - 8:00PM Social Hour Room: Peaks 1-3
Monday, February 28 \| 7:30PM - 10:00PM Poster Session 1 Room: Peaks 1-3
Tuesday, March 01 \| 7:00AM - 8:00AM Breakfast Room: Peaks 6-12
Tuesday, March 01 \| 8:00AM - 11:00AM Tumor Immunotherapy Room: Peaks 4-5 Speaker 3 of 5 Drew M. Pardoll, Johns Hopkins University School of Medicine, USA Molecular Immunology and Tumor Immunotherapy
Tuesday, March 01 \| 8:00AM - 11:00AM Tumor Immunotherapy Room: Peaks 4-5 Speaker 2 of 5 Brian P. Dolan, Oregon State University, USA Short Talk: Dendritic Cells Acquire Functional Peptide-MHC Complexes from Necrotic Tumor Cells
Tuesday, March 01 \| 8:00AM - 11:00AM Tumor Immunotherapy Room: Peaks 4-5 Speaker 1 of 5 Olivera J. Finn, University of Pittsburgh School of Medicine, USA Premalignant lesions as targets for cancer vaccines
Tuesday, March 01 \| 8:00AM - 11:00AM Tumor Immunotherapy Room: Peaks 4-5 Speaker 4 of 5 Ainhoa Perez-Diez, NIAID, National Institutes of Health, USA Short Talk: CD4 Cells Can Be More Efficient at Tumor Rejection Than CD8 Cells
Tuesday, March 01 \| 8:00AM - 11:00AM Tumor Immunotherapy Room: Peaks 4-5 Speaker 5 of 5 * Glenn Dranoff, Novartis Institutes for BioMedical Research, USA Sequential Cancer Immunothherapy
Tuesday, March 01 \| 9:20AM - 9:40AM Coffee Break Room: Foyer
Tuesday, March 01 \| 11:00AM - 1:00PM Poster Setup Room: Peaks 1-3
Tuesday, March 01 \| 1:00PM - 10:00PM Poster Viewing Room: Peaks 1-3
Tuesday, March 01 \| 4:30PM - 5:00PM Coffee & Snacks Available Room: Foyer
Tuesday, March 01 \| 5:00PM - 7:00PM Inflammation Fibrosis and Malignant Pathogenesis Room: Peaks 4-5 Speaker 1 of 4 * William G. Nelson, Johns Hopkins School of Medicine, USA Inflammation and Prostate Carcinogenesis
Tuesday, March 01 \| 5:00PM - 7:00PM Inflammation Fibrosis and Malignant Pathogenesis Room: Peaks 4-5 Speaker 2 of 4 Michael A. Hollingsworth, University of Nebraska Medical Center, USA MUC1 and the Pathogenesis of Pancreatic Cancer
Tuesday, March 01 \| 5:00PM - 7:00PM Inflammation Fibrosis and Malignant Pathogenesis Room: Peaks 4-5 Speaker 3 of 4 Anna Moore, Michigan State University, USA Short Talk: UMUC-1 Tumor Antigen as an Imaging and Therapeutic Target
Tuesday, March 01 \| 5:00PM - 7:00PM Inflammation Fibrosis and Malignant Pathogenesis Room: Peaks 4-5 Speaker 4 of 4 Dafna Bar-Sagi, New York University School of Medicine, USA A Mouse Model of Hereditary Pancreatitis: Insights Into The Initiation of Pancreatic Cancer
Tuesday, March 01 \| 7:00PM - 8:00PM Social Hour Room: Peaks 1-3
Tuesday, March 01 \| 7:30PM - 10:00PM Poster Session 2 Room: Peaks 1-3
Wednesday, March 02 \| 7:00AM - 8:00AM Breakfast Room: Peaks 6-12
Wednesday, March 02 \| 8:00AM - 11:15AM Host Response to Pathogens and Soluble Mediators Room: Peaks 4-5 Speaker 1 of 6 * Martin J. Blaser, New York University School of Medicine, USA Helicobacter pylori diversity and interaction with gastric epithelial cells.
Wednesday, March 02 \| 8:00AM - 11:15AM Host Response to Pathogens and Soluble Mediators Room: Peaks 4-5 Speaker 2 of 6 Bernhard Homey, Heinrich-Heine University Dussseldorf, Germany Chemokine Receptors in Tumor Progression and Metastasis
Wednesday, March 02 \| 8:00AM - 11:15AM Host Response to Pathogens and Soluble Mediators Room: Peaks 4-5 Speaker 3 of 6 Douglas McClain Noonan, Università degli Studi dell'Insubria, Italy Short Talk: Inflammation Associated Angiogenesis: A New Potential Target for Tumor Therapy
Wednesday, March 02 \| 8:00AM - 11:15AM Host Response to Pathogens and Soluble Mediators Room: Peaks 4-5 Speaker 4 of 6 M. Celeste Simon, University of Pennsylvania, USA Hypoxia, Angiogenesis, and Tumor Progression
Wednesday, March 02 \| 8:00AM - 11:15AM Host Response to Pathogens and Soluble Mediators Room: Peaks 4-5 Speaker 5 of 6 Joseph S. Palumbo, Cincinnati Children's Hospital Medical Center, USA Short Talk: Mechanisms Linking Innate Hemostatic Factors and Innate Immunity to Metastatic Potential
Wednesday, March 02 \| 8:00AM - 11:15AM Host Response to Pathogens and Soluble Mediators Room: Peaks 4-5 Speaker 6 of 6 Thomas Doetschman, University of Cincinnati, USA TGFbeta, Inflammation and Colon Cancer Progression
Wednesday, March 02 \| 9:20AM - 9:40AM Coffee Break Room: Foyer
Wednesday, March 02 \| 4:30PM - 5:00PM Coffee & Snacks Available Room: Foyer
Wednesday, March 02 \| 5:00PM - 7:00PM Molecular Mechanisms for Cancer Prevention Room: Peaks 4-5 Speaker 1 of 4 Michael Karin, University of California, San Diego, USA The IKK Complex: Providing a Link Between Inflammation and Cancer
Wednesday, March 02 \| 5:00PM - 7:00PM Molecular Mechanisms for Cancer Prevention Room: Peaks 4-5 Speaker 2 of 4 Ilan Stein, Hebrew University of Jerusalem, Israel Short Talk: NF-kappaB Functions as a Tumor Promoter in Inflammation-Associated Cancer
Wednesday, March 02 \| 5:00PM - 7:00PM Molecular Mechanisms for Cancer Prevention Room: Peaks 4-5 Speaker 3 of 4 George C. Prendergast, Lankenau Institute for Medical Research, USA Short Talk: IDO in Immune Suppression, Cancer, and Cancer Therapy
Wednesday, March 02 \| 5:00PM - 7:00PM Molecular Mechanisms for Cancer Prevention Room: Peaks 4-5 Speaker 4 of 4 * Raymond N. DuBois, Arizona State University, USA COX-2, Inflammatory Mediators and Cancer Prevention
Wednesday, March 02 \| 7:00PM - 8:00PM Social Hour Room: Copper top
Wednesday, March 02 \| 8:00PM - 11:00PM Entertainment Room: Copper top
Wednesday, March 02 \| 8:00PM - 11:00PM Cash Bar Room: Copper top
Thursday, March 03 \| 10:26AM - 10:26AM Departure *Session Chair.