October 30, 2008
Westin Gaslamp Quarter Hotel
San Diego, CA
Cancer therapies increasingly are relying on agents which modify the inflammatory response including anti-inflammatory agents such as glucocorticoids and COX2 inhibitors as means of cancer prevention. In addition vaccine and cytokine strategies are applied to enhance inflammation to enable tumor eradication. There has been increasing evidence that inflammation in particular is a double-edged sword with regard to cancer, both promoting and inhibiting tumor formation. There is also increased awareness of the need for better diagnostic and prognostic markers in cancer both for therapy selection and for monitoring efficacy through the use of genetic analysis. The use of immunotherapeutic approaches has been widely considered the best chance for successful eradication of disseminated cancers. Developing clarity about diagnostic strategies and biomarkers and surrogates to help guide the field and enable both early diagnosis and monitoring during therapy would seem to be critical. The use of biologic approaches to modify inflammation has significant scientific, regulatory and legal issues which require extensive interactions among investigators for their development and optimization in the clinic. Issues concerning trial design, tumor and patient selection, immune monitoring, safety, and increasing efficacy all need to be continually addressed. This is particularly critical now with more use of anti-inflammatory therapies. This meeting will allow for:
iSBTc is unique among societies in that it represents a cross section of basic scientists, clinicians, regulatory agencies and the pharmaceutical industry that allows for these issues to be addressed. The Annual Meeting allows for exchange of the most cutting edge preclinical and clinical data on the use biological therapies in cancer. Workshops on clinical trial design, navigating the regulatory issues, and well as the most current concepts on biologic and immunotherapeutic approaches will occur. This will promote scientific exchange and collaboration. The plenary Workshop will be on “Cancer and Inflammation” will cover the most recent data using inhibition of inflammation to both prevent cancer development and also increase the efficacy of cancer treatments. Other workshops will cover the most recent promising data on suppression of the immune system by the tumor as well as the use of adoptive immunotherapy in cancer. This meeting will allow various investigators to share and build on their data. Ultimately this will lead to better patient outcomes in cancer.
The response to pathogens and damage in plants and animals involves a series of carefully orchestrated, highly evolved, molecular mechanisms resulting in pathogen resistance and wound healing. In metazoans, molecules executing precise intracellular tasks are also able to exert disparate functions when released into the extracellular space and include Damage or Pathogen Associated Molecular Pattern Molecules (DAMPs, PAMPs). The emergent consequence for both inflammation and wound healing of the abnormal extra-cellular persistence of these factors may underlie many clinical disorders including cancer. DAMPs/PAMPs are recognized by hereditable receptors including the Toll-like receptors (TLRs), the NOD1-like receptors (NLRs) and RIG-I (retinoic-acid-inducible gene I)-like receptors (RLRs), as well as the receptor for advanced glycation end products (RAGE). These host molecules ‘sense’ not only pathogens but also misfolded/glycated proteins or exposed hydrophobic portions of molecules, activating intracellular cascades that lead to an inflammatory response. Equally important are means to not only respond to these molecules but also to eradicate them. Their destruction through oxidative mechanisms normally exerted by myeloid cells such as neutrophils and eosinophils or their persistence in the setting of pathologic extracellular reducing environments maintained by exuberant necrotic cell death and/or oxidoreductases represent important molecular means enabling chronic inflammatory states and promoting the development of cancer.