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Cancer Metabolomics: Elucidating the Biochemical Programs that Support Cancer Initiation and Progression

Cancer Metabolomics: Elucidating the Biochemical Programs that Support Cancer Initiation and Progression

Friday, February 3, 2012

The New York Academy of Sciences

Presented By


Since the 1920s, it has been recognized that cancer cells exhibit metabolic features that are distinct from those of 'normal' cells. However, a comprehensive picture of cancer metabolism and its molecular underpinnings has been essentially unapproachable—that is, until very recently. With the emergence of effective analytical strategies for broad-based metabolite profiling (both targeted and untargeted), the cancer cell 'metabolome' has now come into sight. Taking advantage of LC-MS-based analytical platforms, the participating speakers will describe new knowledge of metabolic pathways that distinguish cancer cells, signaling cascades that drive cancer-selective metabolic pathways and implications for the development of novel cancer chemotherapies.

Poster Session

The call for poster abstracts is now closed.

Registration Pricing

Student / Postdoc / Fellow Member:$10
Nonmember Corporate:$80
Nonmember Not for Profit:$60
Student / Postdoc / Fellow Nonmember:$40



* Presentation times are subject to change.

Friday, February 3, 2012

8:30 AM

Registration and Continental Breakfast

9:00 AM

Welcome and Introduction
Jennifer Henry, PhD, The New York Academy of Sciences
Steven S. Gross, PhD, Weill Cornell Medical College

9:15 AM

Keynote Presentation
Putting the Brakes on Cancer Cell Metabolism
Craig Thompson, MD, Memorial Sloan-Kettering Cancer Center

10:00 AM

Untargeted Metabolomics Reveals Shared Metabolic Changes for the Induction of Oncogenesis
Gary Siuzdak, PhD, The Scripps Research Institute, California

10:45 AM

Coffee Break

11:15 AM

SIRT3 Loss, Mitochondrial Oxidative Stress and HIF1-α Stabilization: A Triggering Cascade for Tumorigenesis and Warburg Metabolism
Marcia C. Haigis, PhD, Harvard Medical School

12:00 PM

How Do Cancer Cells Acquire Fatty Acids?
Joshua D. Rabinowitz, PhD, Princeton University

12:45 PM

Networking Lunch and Poster Session

2:00 PM

Role of Autophagy in Cancer Metabolism
Eileen P. White, PhD, The Cancer Institute of New Jersey, Rutgers University

2:45 PM

Keynote Presentation
Cancer Cell Metabolism
Lewis C. Cantley, PhD, Beth Israel Deaconess Medical Center and Harvard Medical School

3:30 PM

Coffee Break

4:00 PM

Metabolite Profiling Reveals Novel Insights into Mechanism of Action of DFMO, an Ornithine Decarboxylase Inhibitor Effective in Colon Cancer Chemoprevention
Steven M. Lipkin, MD, PhD, Weill Cornell Medical College

4:45 PM

Selected Poster Presentations

5:00 PM

Panel Discussion
All speakers and Steven Fischer, Agilent Technologies

A 1-hour networking reception will follow the symposium.



Steven S. Gross, PhD

Weill Cornell Medical College

Steven S. Gross is Professor of Pharmacology, Director of the Mass Spectrometry Core Facility and Director of Advanced Training in Pharmacology at the Weill Cornell Medical College. Dr Gross' primary research interest is in cell–cell communication, with a focus on nitric oxide (NO) and reactive molecules as mediators of cell signaling. In the late 1980s, Dr Gross and colleagues made the initial identification of L-arginine as the precursor of NO in blood vessels. They were also first to establish that NOS inhibition elevates blood pressure in animals, demonstrating that NO plays a physiological role in controlling blood pressure and vascular tone. Since then, research efforts have been directed toward elucidating the enzymes and mechanisms that regulate NO synthesis in cells. Results of these basic studies have provided fundamental insights into the therapeutic control of NO synthesis, resulting in core technologies for the creation of ArgiNOx Inc., a biotech start-up that seeks to develop novel NO-based drugs. Dr Gross' research is supported in part by a MERIT Award from the NHLBI. He is a founder and Board Director of the Nitric Oxide Society and chairs the Steering Committee of the Biochemcial Pharmacology Discussion Group (BPDG) at NYAS. Dr Gross received his PhD in Biomedical Science from the Mount Sinai School of Medicine in New York City.

Jennifer Henry, PhD

The New York Academy of Sciences

Keynote Speakers

Lewis C. Cantley, PhD

Beth Israel Deaconess Medical Center and Harvard Medical School

Lewis Cantley, PhD is the William Bosworth Castle Professor of Medicine at Harvard Medical School and Director of the Cancer Center at Beth Israel Deaconess Hospital. Throughout his career, Dr. Cantley has been interested in the biochemical mechanisms by which growth factors and hormones control cell growth and cell metabolism and the defects in these control mechanisms that lead to diseases such as diabetes, immune disorders and cancers. In the course of this work, Dr. Cantley discovered a cell growth pathway involving the enzyme Phosphoinositide 3-Kinase (PI3K). This pathway is now known to be the most frequently mutated pathway in human cancers. His discoveries have led to the development of drugs to target this pathway for treating cancers. In recognition of his contributions to the understanding of human diseases, Dr. Cantley was elected to the American Academy of Arts and Sciences (1999) and the National Academy of Sciences (2001). He has received numerous awards, including the ASBMB Avanti Award for Lipid Research (1998), the Heinrich Weiland Preis for Lipid Research (2000), the Caledonian Prize from the Royal Society of Edinburgh (2002), the American Association of Cancer Research/Pezcoller Award for Cancer Research (2005), the Rolf Luft Award for Diabetes and Endocrinology Research (2009) and the Pasarow Award for Cancer Research (2011).

Craig Thompson, MD

Memorial Sloan-Kettering Cancer Center

Craig B. Thompson, MD (age 58) became President and Chief Executive Officer of Memorial Sloan-Kettering Cancer Center (MSKCC) on November 1, 2010. He came to MSKCC from the University of Pennsylvania, where he had served since 2006 as Director of the Abramson Cancer Center and Associate Vice President for Cancer Services of the University of Pennsylvania Health System. Dr. Thompson is a board-certified internist and medical oncologist with extensive research experience in cancer, immunology, and translational medicine. His current research focuses on the role that metabolic changes play in the origin and progression of cancer. Dr. Thompson is a member of the Institute of Medicine, the National Academy of Sciences, the American Academy of Arts and Sciences, and the Medical Advisory Board of the Howard Hughes Medical Institute.


Marcia C. Haigis, PhD

Harvard Medical School

Marcia C. Haigis, PhD is an Assistant Professor in the Department of Cell Biology at Harvard Medical School and a member of the Paul F. Glenn Laboratories for Medical Research. Dr. Haigis received her Ph.D. from the University of Wisconsin in 2OO2 and completed postdoctoral research at MIT. Her current work contributes to the understanding of how mitochondrial sirtuins regulate tumor cell metabolism. Dr. Haigis has received a Brookdale Leadership in Aging Award, the Ellison Medical Foundation New Scholar Award and an American Cancer Society Research Scholar Award.

Steven M. Lipkin, MD, PhD

Weill Cornell Medical College

Dr. Lipkin is an Associate Professor Medicine and Genetic Medicine at Weill Cornell Medical Center. Major interests of his include genetic factors that increase colorectal cancer risk, and chemoprevention for pancreatic and colorectal cancer.

Joshua D. Rabinowitz, PhD

Princeton University

Joshua Rabinowitz grew up in Chapel Hill, North Carolina. In 1994, he earned B.A. degrees in Mathematics and Chemistry from the University of North Carolina. From there, he moved west to Stanford, where he earned his Ph.D. in Biophysics in 1999, followed by his M.D. in 2001. As he was completing his M.D. degree, he co-founded Alexza Pharmaceuticals, now a public company with its first product awaiting FDA approval. After four years leading R&D efforts at Alexza, Joshua joined the faculty of Princeton University, where he is currently Professor of Chemistry and Integrative Genomics. His work applies mass spectrometry to study metabolism and its regulation across a diversity of organisms from E. coli to humans. He is particularly interested in quantitative analysis of metabolic flux.

Gary Siuzdak, PhD

The Scripps Research Institute, California

Gary Siuzdak is Director of the Scripps Center for Metabolomics and Professor of Chemistry and Molecular Biology at The Scripps Research Institute in La Jolla, California ( He is also Faculty Guest at Lawrence Berkeley National Laboratory and served as Vice President of the American Society for Mass Spectrometry. His research includes developing novel mass spectrometry-based approaches in metabolomics, nanostructure-based imaging, microorganism analysis, and enzyme activity assays. He has over 170 peer-reviewed publications and two books, "Mass Spectrometry for Biotechnology" and the "The Expanding Role of Mass Spectrometry in Biotechnology", 2006 Edition.

Eileen White, PhD

Rutgers University

Dr. Eileen White received a BS from Rensselaer Polytechnic Institute and a PhD in Biology from SUNY Stony Brook. She was a Damon Runyon Postdoctoral fellow in the laboratory of Dr. Bruce Stillman at Cold Spring Harbor Laboratory. She is currently the Associate Director for Basic Science at the Cancer Institute of New Jersey (CINJ), Professor of Molecular Biology and Biochemistry at Rutgers University, and Adjunct Professor of Surgery at UMDNJ. Dr. White has served on the Board of Scientific Counselors of the National Cancer Institute (NCI) and the Board of Directors of the American Association for Cancer Research (AACR). She has revieved a MERIT Award from the NCI, an Investigatorship from the Howard Hughes Medical Institute (HHMI), the Red Smith Award from the Damon Runyon Cancer Research Foundation, an Achievement Award from the International Cell Death Society, and a Career Award from the European Cell Death Organization. Dr. White is also an elected Fellow of the American Society of Microbiology (ASM) and the American Association for the Advancement of Science (AAAS). Dr. White currently serves on the Scientific Review Boards for the Starr Cancer Consortium and the Cancer Prevention Research Institute of Texas (CPRIT), and is a member of the Board of Scientific Advisors for the AACR. Dr. White is a member of Dr. Varmus's "Big Questions Project" to guide future of the NCI. Editorial Boards memberships include of Genes & Development, the Journal of Cell Biology, Oncogene, Cancer Prevention Research, Molecular Cancer Research, Autophagy, Cell Death and Disease, and Cancer Discovery.


Steven Fischer

Agilent Technologies

Steven Fischer received his bachelors in chemistry (1981) and masters in chemistry (1991) at California State University, Hayward. In 1986, he joined Agilent Technologies in Santa Clara (previously part of Hewlett-Packard Company), where he has designed and applied HPLC/MS instrumentation for analytical problems for 20 years. He has over 40 United States issued patents in the field of mass spectrometry. He was the 2007 Bill Hewlett Award recipient for outstanding instrument design innovation. He currently is the Marketing Manager, Metabolomics and Proteomics, responsible for Agilent’s world wide metabolomics and proteomics program. In that position, he has focused his attention on developing solutions to metabolomics and proteomics analysis with the goal of using the experimental data synergistically to yield deeper biological insight.


Putting the Brakes on Cancer Cell Metabolism
Craig B. Thompson, MD, Memorial Sloan-Kettering Cancer Center

Proliferating cancer cells exhibit a robust but seemingly wasteful metabolism. Two nutrients, glucose and glutamine, are consumed by tumor cells at rates in vast excess of their utilization by non-transformed cells. The uptake of each of these nutrients is under the control of distinct oncogenes. The PI3K/Akt/TOR signaling pathway plays the primary role in directing cellular glucose uptake and metabolism. Deregulation of this pathway in cancer can be imaged in vivo by FDG-PET scans. In contrast, the myc family of oncogenes direct glutamine uptake and mitochondrial catabolism in transformed cells. Glutamine and glucose metabolism facilitate distinct mitochondrially-dependent synthetic reactions required for growth. Recent evidence suggests tumor suppressors are counter-regulators of mitochondrial biosynthesis. In the case of hypoxia, conversion to anaerobic glycolysis is induced by activation of HIF-1α. In the case of glucose limitation, conversion to fatty acid oxidation is mediated by activation of p53. In addition, a role for intracellular metabolites in oncogenic signaling has also been recently suggested through studies of succinate dehydrogenase and fumarase mutations in cancer. The discovery of cancer-associated mutations in isocitrate dehydrogenase that produce a novel metabolite, 2-hydroxyglutarate, provides the most compelling example of this principle to date. With these new discoveries in mind, the roles of oncogenes and tumor suppressors in the regulation of metabolic pathways will be discussed. Therapeutic strategies to selectively impair tumor metabolism will be considered.

Untargeted Metabolomics Reveals Shared Metabolic Changes for the Induction of Oncogenesis
Gary Siuzdak, PhD, The Scripps Research Institute, California

Untargeted metabolomics, the quantitative global analysis of endogenous metabolites from cells, tissues, fluids and whole organisms, is becoming an integral part of functional genomics efforts as well as a tool for understanding fundamental biochemistry. Our experimental aim is to obtain a comprehensive quantitative view of the metabolome in order to expand our understanding of what pathways are altered in specific diseases—a central question in the emerging field of therapeutic metabolomics. In order to accomplish this goal we have developed a novel mass spectrometry-based platform for metabolomics including XCMS data analysis combined with Metlin (a comprehensive MS/MS metabolite database) as well as nanostructure-initiator mass spectrometry (NIMS) imaging. These technologies will be presented in the context of their application to discovering new therapeutic targets/pathways in oncology.

SIRT3 Loss, Mitochondrial Oxidative Stress and HIF1-α Stabilization: A Triggering Cascade for Tumorigenesis and Warburg Metabolism
Marcia C. Haigis, PhD, Harvard Medical School

One hallmark feature of tumor cells is a shift from oxidative to glycolytic metabolism, and this reliance on aerobic glycolysis to support cell growth is known as the Warburg effect. Mitochondrial sirtuins are NAD-dependent enzymes that bind and regulate numerous metabolic pathways within the mitochondria. For example, SIRT3 functions as an NAD-dependent deacetylase that binds and activates numerous oxidative pathways. We have discovered that SIRT3 has an additional effect on cellular metabolism by repressing cellular glycolysis through the regulation of HIF1 a transcription factor that increases gene expression of glycolytic targets. SIRT3 null cells exhibit metabolic and genetic features of the Warburg effect and enhanced tumorigenecity in vivo. Likewise, SIRT3 overexpression reduces glycolysis in tumor cells. In sum, a better understanding of sirtuin-mediated regulation may identify novel ways to therapeutically target tumor metabolism.

How Do Cancer Cells Acquire Fatty Acids?
Joshua D. Rabinowitz, PhD, Princeton University

Cell proliferation requires replication of the plasma membrane and internal lipid structures. How do cells acquire the required fatty acids? What is the impact of oncogenes on this process? Fatty acids are synthesized using three fundamental components: (i) acetyl-CoA, (ii) ATP, and (iii) NADPH. We have used liquid chromatography-mass spectrometry (LC-MS) and isotope tracers to investigate how each of these components is produced in cultured cells expressing activated Akt or Ras. In addition, to examine fatty acid biosynthetic reactions directly, we have developed a LC-MS method for long-chain and very-long-chain fatty acid analysis. The method enables quantitation of molecular ion peaks for all labeled forms of each fatty acid, and thereby isotope tracer-based analysis of fatty acid metabolism. Its application reveals substantial differences in fatty acid acquisition routes between Akt and Ras driven cells, with Akt favoring de novo lipogenesis and Ras favoring scavenging of serum lipids. The potential for these differences to impact the sensitivity of tumors to lipid metabolic enzyme inhibitors will be discussed.

Role of Autophagy in Cancer Metabolism
Eileen P. White, PhD, The Cancer Institute of New Jersey, Rutgers University

The cellular self-cannibalization process of autophagy is activated by stress and starvation to capture proteins and organelles and deliver them to the lysosomal compartment for degradation. The resulting breakdown products, such as amino acids, sugars, nucleosides, and lipids, are then released into the cytoplasm where they can be recycled to sustain metabolism or used for generation of new biomass. Normal cells use autophagy to survive interruptions in growth factor and nutrient availability and to eliminate damaged proteins and organelles, the accumulation of which is toxic. Autophagy has a dual role in cancer. Loss of autophagy normal tissue results in damage, inflammation and genome instability resulting from failure of protein and organelle quality control that can promote cancer initiation. In this context autophagy is a tumor suppression mechanism, particularly in the liver. In tumors, autophagy is activated by stress in the microenvironment and supports cancer cell survival. Autophagy is also upregulated in established cancers and supports metabolism, stress survival, therapy resistance and tumorigenesis. In these contexts autophagy is tumor promoting. The role of autophagy in the settings of cancer initiation, progression and therapy, and its functional role in protein and organelle quality control and in metabolism will be discussed. Insights from autophagy modulation in genetically engineered mouse models for cancer, and in the context of cancer therapy, will be addressed.

Cancer Cell Metabolism
Lewis C. Cantley, PhD, Beth Israel Deaconess Medical Center and Harvard Medical School

Cancer cells have a greater demand for NADPH than most non-cancerous cells because of an increased demand of this reducing potential to combat ROS and to synthesize fatty acids and nucleic acids. A failure to meet this demand can result in cell stasis or cell death. This greater demand for NADPH can be achieved by altering pathways for glucose and glutamine metabolism to increase NADPH production, at the expense of decreased ATP synthesis. The particular way that a cancer cell solves this metabolic problem is dictated by the mutational and epigenic changes that occur during tumor development. For example, mutations in the PI3K pathway typically drive tumors into higher rates of glucose consumption and lower rates of oxygen consumption (known as the Warburg Effect). An understanding of the links between oncogenic mutations and their consequent effects on metabolic flux should suggest novel approaches for therapies that combine inhibitors of signal transduction pathways with inhibitors of nodes in metabolic pathways.

Metabolite Profiling Reveals Novel Insights into Mechanism of Action of DFMO, an Ornithine Decarboxylase Inhibitor Effective in Colon Cancer Chemoprevention
Steven M. Lipkin, MD, PhD, Weill Cornell Medical College

Colorectal cancer (CRC) is the 2nd leading cause of cancer death. CRCs develop through a multi-step process that takes several years. The long duration of this process makes chemoprevention an attractive approach to reduce CRC mortality. The most effective CRC chemoprevention regimen to date includes the ornithine decarboxylase inhibitor α-difluoromethylornithine (DFMO), which reduces polyamine levels. However, in DFMO treated patients, mucosal polyamine levels do not correlate with CRC chemopreventative efficacy and the metabolic consequences of DFMO therapy are incompletely characterized. Here, we perform the first global, unbiased metabolomic profiling study of DFMO treated intestinal mucosa. Our study reveals that chronic DFMO therapy unexpectedly causes depletion of S-adenosylmethionine (SAM), which reduces one-carbon metabolism and thymidine synthesis both in vitro and in vivo. Reduced thymidine levels impair cellular proliferation. Thymidine repletion rescues this defect. Since 5-fluorouracil reduced cellular thymidine is the cornerstone of anti-CRC chemotherapy, this study reveals the first shared mechanism for CRC chemoprevention and therapy and suggests commonalities between pre-malignant and malignant colonocytes. Our study also raises an unanticipated concern that dietary folate and SAM could reduce DFMO efficacy and confound an ongoing FDA registrational CRC chemoprevention trial of DFMO and sulindac.


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