The recent discovery of mutations affecting metabolic enzymes such as succinate dehydrogenase, fumarate hydratase, and isocitrate dehydrogenase provides genetic evidence that altered cellular metabolism can cause cancer. Moreover, it has become apparent that a number of proteins that regulate processes pertinent to cellular transformation, such as enzymes that affect chromatin structure, respond to specific cellular metabolites. Finally, technologies for monitoring cellular metabolism are improving rapidly including technologies that lend themselves to non-invasive imaging.
The goals of this meeting are to bring together a diverse group of scientists from academia and industry with basic and translational interests surrounding cancer metabolism. A particular focus will be on metabolic enzymes as potential targets for treating and/or imaging cancer cells.
Toward this end this meeting hopes to attract a diverse group of scientists including biologists, chemists, and engineers.
This meeting should provide participants with a greater understanding of the language and logic of cellular metabolism and provide a sense of the translational opportunities emerging from our growing knowledge of the role that altered metabolism plays in cancer.
The Summit provides a unique opportunity to gain the latest biomarker developments in three major therapeutic areas, formally organized in the following tracks and sessions:
- 7th Oncology Biomarkers
- 3rd Neurological Biomarkers
- 3rd Inflammatory / Immunological Biomarkers
A chronic low-grade inflammatory response is a defining feature of various metabolic diseases, including atherosclerosis, obesity, and type 2 diabetes. This smoldering inflammation in tissues, whether it is in the vascular bed, white adipose tissue or perivascular fat, is primarily mediated by the innate immune system.
Consequently, this Keystone Symposium on Innate Immunity, Metabolism and Vascular Injury will bring together leading investigators in areas of macrophage biology, vascular inflammation, atherosclerosis, and obesity-induced metabolic disease.
Sessions will encompass a broad range of topics highlighting the importance of and mechanisms by which innate immunity contributes to progression of metabolic diseases, including monocyte development and trafficking, macrophage activation in vascular bed and adipose tissues, and systems biology of myeloid cells. Exciting new developments in sensing of metabolic stress by inflammasomes, clearance of apoptotic cells by macrophages, and initiation of necrotic cell death programs will also be discussed.
These basic studies will be complemented by talks discussing new strategies for promoting plaque regression, and targeting innate inflammation to treat insulin resistance, type 2 diabetes, and coronary artery disease.