October 14 - 17, 2008
JW Marriott Ihilani Resort and Spa
Ko Olina, Oahu, Hawaii
Lisa M. Coussens, UCSF Comprehensive Cancer Center and Cancer Research Institute, San Francisco, CA
Michael Karin, Moores UCSD Cancer Center, La Jolla, CA
Lawrence J. Marnett, Vanderbilt University Medical Center, Nashville, TN
Recent clinical and experimental data have expanded the concept that inflammation is a critical component of solid tumor progression. Many cancers arise from sites of infection, chronic irritation, and inflammation; thus, it is now clear that the tumor microenvironment, which is largely orchestrated by inflammatory cells, is an indispensable participant in the neoplastic process altering not only the metabolic needs of the tissue, but also fostering DNA and protein damage, proliferation, survival, mutagenesis, migration and metastasis of malignant cells. Leukocytic infiltrates and pro-inflammatory cytokine/chemokine networks in premalignant tissues and tumors can be distinct depending upon the stage of malignant development and organ microenvironment. Current thinking is that activated immune cells provide both anti- and protumorigenic signals, thus representing targets to be harnessed or attacked for therapeutic advantage depending upon environmental and/or cellular context.
This AACR Special Conference examined critical cellular, molecular, and chemical mediators involved in regulating DNA and protein damage, pro- and anti-tumor immunity, and considered how balancing these dynamic programs may lead to more efficacious anti-cancer therapeutics. Nearly 250 researchers from over 20 different countries gathered in Hawaii for this AACR Special Conference that featured sessions on Reactive Oxidants/DNA Damage, Protein Modifications, Eicosanoids, Cytokines and Chemokines, Gastrointestinal Cancer, Innate Adaptive Cells, and Stroma/Angiogenesis. The program also featured two keynote presentations as well as two poster sessions.
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Please visit the AACR Meetings & Workshops Calendar for a complete list of upcoming programs.