Overview

In the early part of the 20th century, German biochemist Otto Warburg observed that tumor tissues and normal tissues metabolize glucose differently. Instead of relying on the citric acid cycle to extract maximal energy from a molecule of glucose, tumor cells rapidly convert glucose to lactate through glycolysis even when oxygen is abundant.

Known as the Warburg effect, this observation sits at the core of the field now known as cancer metabolomics. But for many years after Warburg's observation, scientists focused on separate mechanisms of oncogenesis without considering that these metabolic differences could drive the formation of new cancers or could speed their growth. More recently, cancer researchers have recognized that these metabolic changes help cancer cells build the macromolecules that support the rapid growth and proliferation of tumors.

Organized by Stephen S. Gross of Weill Cornell Medical College and Jennifer Henry of the Academy, the Cancer Metabolomics: Elucidating the Biochemical Programs that Support Cancer Initiation and Progression symposium held on February 3, 2012, is the latest in a series of meetings about cancer metabolomics. In an initial keynote address, Craig Thompson of Memorial Sloan Kettering Cancer Center gave an overview of the field and of the emerging links between oncogenic and metabolic pathways. Gary Siuzdak of Scripps Research Institute described metabolomics tools and the process of finding new cancer metabolites. As one slice of her research on sirtuin enzymes, Marcia Haigis of Harvard Medical School outlined how mitochondrial forms of these enzymes may be involved in cancer growth and proliferation. Joshua Rabinowitz of Princeton University explained fatty acid metabolism in cancer cells, and Eileen White of the Cancer Institute of New Jersey described autophagy in cancer cells. In a second keynote talk, Lewis Cantley of Beth Israel Deaconess Medical Center and Harvard Medical School discussed biochemical research to understand metabolic signals in cancer. In the final talk, Steven Lipkin of Weill Cornell Medical College described research linking the mechanisms of the primary chemotherapy in colorectal cancer, 5-fluorouracil, and a drug being tested for chemoprevention, difluoromethylornithine.

Use the tabs above to find a meeting report and multimedia from this event.

Presentations available from:
Lewis C. Cantley, PhD (Beth Israel Deaconess Medical Center and Harvard Medical School)
Marcia C. Haigis, PhD (Harvard Medical School)
Steven M. Lipkin, MD, PhD (Weill Cornell Medical College)
Joshua D. Rabinowitz, PhD (Princeton University)
Gary Siuzdak, PhD (The Scripps Research Institute, California)
Craig Thompson, MD (Memorial Sloan-Kettering Cancer Center)

Bronze Sponsors

Agilent Technologies

Academy Friends

Abcam

Agios Pharmaceuticals

Metanomics Health, a BASF Group company

Thermo Fisher Scientific

Waters Corporation

Image credit: Pathway diagram reproduced courtesy of Cell Signaling Technology, Inc.