Targeting Cancer Cell Metabolism

 

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The fact that cancer cells have an altered glucose metabolism has sparked new interest in the pharmaceutical industry. Reversing the increased glucose consumption in cancer cells is an important step and has great potential for therapeutic drug developments. This meeting is designed to shed light on current strategies of how to change the metabolism in cancer cells and the resulting opportunities for developing new molecular drug targets.

MONDAY, OCTOBER 1

7:00 am Conference Registration and Morning Coffee


Perspectives and Progress

8:30 Chairperson’s Opening Remarks

Elizabeth Maher, M.D., Ph.D., Associate Professor, Theodore H. Strauss Professorship in Neuro-Oncology, Southwestern Medical Center


» 8:40 KEYNOTE PRESENTATION 

Integrating Cancer Metabolism, Autophagy, and the Tumor Microenvironment to Achieve Personalized Cancer Treatment

Michael P. Lisanti, M.D., Ph.D., Professor, Director, Breakthrough Breast Cancer Research Unit, Muriel Edith Rickman Chair in Breast Oncology, Faculty Institute of Cancer Sciences, Paterson Institute for Cancer Research, The University of Manchester

Dr. Lisanti will discuss a new model of cancer metabolism, which is paradigm shifting.


9:10 Metabolism as a Key Component of Systems Biology for Targeting Cancer

Michael Su, Ph.D., Senior Vice President, R&D, Agios Pharmaceuticals

This presentation provides a better understanding of the pioneering research being conducted in the space and the first-in-class anticancer drugs that will “starve” cancer cells by interrupting the metabolic processes that fuel their growth. It will be presented how this new frontier of boundary-breaking science has the potential to uncover treatments with the potential to change patients’ lives.

9:40 A New View of Cancer

David W. Moskowitz, M.D., M.A., FACP, CEO, GenoMed, Inc.

The prevailing view of sporadic cancer is that it arises from mutations in somatic cells, and that the secret to curing cancer lies in the tumor. We have found thousands of cancer-associated SNPs in the germline of cancer patients. This suggests that cancer arises when tissue stem cells, sensing tissue atrophy, begin proliferating but fail to differentiate properly. Differentiation within the adult  rganism is more difficult than in the embryo because of the absence of fields of transcription factors. Our SNPs provide targets for non-toxic differentiation therapy.

10:10 Grand Opening Coffee Break in the Exhibit Hall with Poster Viewing


Targeting Glucose Metabolism

10:40 Glucose Metabolism in Human Brain Tumors

Elizabeth Maher, M.D., Ph.D., Associate Professor, Theodore H. Strauss Professorship in Neuro-Oncology, Southwestern Medical Center


EMD Millipore 11:10 Multiplex Analysis of Cellular Metabolism Pathways Using MILLIPLEX® MAP PanelsKelly Barrett, Field Application Scientist, EMD Millipore Corporation Cellular metabolism is the set of processes that convert biochemical energy into ATP. Significant progress has been made in understanding links between cellular metabolic pathways and diverse conditions (i.e. diabetes, AD, PD, cancer, aging). These pathways have drawn renewed interest in the research community. EMD Millipore has developed a series of innovative multiplex immunoassay panels based on the Luminex® xMAP® platform. These panels enable quantitative detection of multiple proteins simultaneously and are valuable tools in the study of diverse biological processes. We will provide an overview of the multiplex technology and present application data from selected MILLIPLEX® MAP Cellular Metabolism panels, such as PDH Complex, FAO, and OXPHOS.


11:25 Sponsored Presentation (Opportunity Available) 

11:40 Chloroacetaldehyde, an Ifosfamide Metabolite, Inhibits Cell Proliferation and Glucose Metabolism without Decreasing Cellular ATP Content in Human Breast Cancer Cells MCF7

Gabriel Baverel, Ph.D., Professor, CEO, CSO, Metabolomics, Metabolys, Inc.

Chloroacetaldehyde, a metabolite of the widely used anticancer drug ifosfamide, inhibits cell proliferation and specific steps of glucose metabolism but does not decrease cellular ATP content in human breast cancer cells MCF7.

12:10 pm Glycolytic Cancer Cells Lacking 6-Phosphogluconate Dehydrogenase Metabolize Glucose to Induce Senescence

Barden Chan, Ph.D., Instructor, Medicine, Beth Israel Deaconess Medical Center

We show that knockdown of 6-phosphogluconate dehydrogenase (6PGD) of the pentose phosphate pathway (PPP) inhibits growth of gefitinib-resistant lung cancer cells (H1975) by senescence induction. This inhibition is not due to a defect in the oxidative PPP per se. Significantly, G6PD knockdown rescues proliferation of cells lacking 6PGD, suggesting accumulation of growth inhibitory glucose metabolics in cells lacking 6PGD. Therefore, 6PGD inhibition may provide a novel strategy to treat glycolyic tumors such as lung cancer.

12:40 Lunch on Your Own


The Warburg Effect

2:20 Chairperson’s Remarks

Gabriel Baverel, Ph.D., Professor, CEO, CSO, Metabolomics, Metabolys, Inc.

2:25 The Use of Warburg Effect Indicators Such as FDG PET Avidity to Identify Lymphoma Patients Who May Be Candidates for Definitive Ultra Low Dose (2 Gy X 2) Radiotherapy

Roger Macklis, M.D., Professor of Medicine, Radiation Oncology, Cleveland Clinic

The absence of the Warburg switchover in cell metabolism is an indicator of potentially intact p53 status and may thus be a proxy for high cellular radiosensitivity and immunoresponsiveness in patients with sensitive disease.

Targeting the Mitochondrial Metabolism

2:55 Targeting Mitochondrial Bioenergetics Potently Induces Cell Death in Stem-Like Ovarian Cancer Cells

Ayesha B. Alvero, M.D., M.S., Associate Research Scientist, Department of Obstetrics, Gynecology and Reproductive Sciences, Yale University School of Medicine

Ovarian tumors are comprised of a heterogenous population of cells with distinct growth and survival requirements as well as unique chemoresistant characteristics. CD44+ ovarian cancer cells exhibit stem-like properties and are inherently chemoresistant to currently available agents. Elaboration of a unique mitochondrial and metabolic profile in these cells identifies a novel therapeutic option.

3:25 Refreshment Break in the Exhibit Hall with Poster Viewing

4:05 Targeting Mitochondria for Cancer Therapy: Exploiting Cancer Cell Metabolism to Develop Combination Therapy

Charles E. Wenner, Ph.D., Professor, Member, Molecular and Cellular Biology, Roswell Park Cancer Institute

Recent advances in the understanding of the role of sirtuins in metabolic diseases such as cancer offer new opportunity to develop therapeutic approaches which are based on reprogramming of the Warburg Effect.

4:35 Lipoate Analogs: Powerful Chemotherapeutic Agents Attacking Cancer Cell Metabolism

Paul M. Bingham, Ph.D., Vice President, Research, Cornerstone Pharmaceuticals; Professor, Biochemistry and Cell Biology, Stony Brook University

Lipoate is a uniquely pivotal molecule, having both indispensable catalytic and regulatory functions in mitochondrial metabolism. These regulatory functions include components systematically reconfigured during malignant transformation, allowing analogs of lipoate to selectively attack tumor cell metabolism. I will discuss progress on the mechanism and clinical efficacy of this novel drug family.

5:05 Interactive Breakout Discussion Groups

Strategic Planning of How to Starve a Tumor

Moderator: Michael Su, Ph.D., Senior Vice President, R&D, Agios Pharmaceuticals

Challenges of Targeting the Mitochondrial Metabolism

Moderator: Paul Bingham, Ph.D., Vice President, Research, Cornerstone Pharmaceuticals

  • What is our current best picture of tumor metabolism, including cancer-specific changes that might be universal and those that are idiosyncratic to individual patients?
  • Of potentially universal tumor metabolic changes, which minority healthy cells (stem cells, cells in healing wounds, for example) might share these properties?
  • What has deep sequencing of tumor genomes taught us about the relative importance of metabolic and regulatory targets in chemotherapy?
  • What are the relative merits of targeting cytosolic and mitochondrial metabolic processes for cancer chemotherapy?

Understanding the “Biology” of Novel Ligand Binding Sites

Moderator: Marc O’Reilly, Ph.D., Associate Director, Structural Biology, Astex Pharmaceuticals

  • How do you identify novel ligand binding sites
  • How do you determine the biological relevance of novel ligand binding site
  • Challenges of drugging novel ligand binding sites
  • Are certain target classes more amenable to being ‘drugged’ using novel ligand binding sites than others
 

6:15 – 7:30 Welcoming Reception in the Exhibit Hall with Poster Viewing



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Cellecta 

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SPONSORSHIPS & EXHIBITS 

The exhibit hall was sold out in 2013, so please contact us early to reserve your place. To customize your sponsorship or exhibit package for 2014, contact:

Jon Stroup
Business Development Manager
781-972-5483
jstroup@healthtech.com 

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