Inflammation and Cancer
Organizer(s): Raymond N. DuBois and Lisa M. CoussensDate: February 27 - March 03, 2005
Location: Beaver Run Resort, Breckenridge, CO, USA
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, ]. 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, ]. 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: