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From Tumor Suppressors to Oncogenic Dynamics: The 2015 Dr. Paul Janssen Award Symposium

From Tumor Suppressors to Oncogenic Dynamics: The 2015 Dr. Paul Janssen Award Symposium

Wednesday, September 16, 2015

The New York Academy of Sciences

Presented By

Presented by the Dr. Paul Janssen Award for Biomedical Research and the New York Academy of Sciences


Over the last several decades our knowledge of the molecular and genetic mechanisms of cancer development has dramatically advanced, resulting in improved therapeutics and diagnostics for treating this devastating disease. Much of the understanding of complex oncogenic processes at the genetic and molecular level would not have been possible without the groundbreaking research conducted by Dr. Bert Vogelstein over his distinguished forty-year career. Dr. Vogelstein’s pioneering work in understanding how the tumor suppressor gene TP53 promotes cancer development provided the groundwork for his discovery that cancer is a progressive, multi-step disease defined by a series of genetic alterations. This concept was further advanced when Dr. Vogelstein and his colleagues identified and characterized the Adenomatous Polyposis Coli (APC) genetic mutation in colorectal cancer, which had profound implications on how this prevalent form of cancer is diagnosed and treated. Ongoing research on the genomic landscape of cancer as well as the development of novel, cutting-edge research technologies will continue to solidify Dr. Vogelstein’s reputation as a leader in the field. For his extensive characterization of the underlying mechanisms of cancer and its resulting clinical impact, Dr. Vogelstein will receive the 2015 Dr. Paul Janssen Award for Biomedical Research.

This symposium will honor Dr. Bert Vogelstein, who will reflect on his influential work defining how cancer is studied, diagnosed, and treated, and share his vision for the future discoveries in the field. Following his Award lecture, fellow prominent scientists at the forefront of oncology research will discuss emerging concepts and technologies in both basic and clinical cancer research.


Bert Vogelstein, MD

Johns Hopkins School of Medicine
Howard Hughes Medical Institute

Registration Pricing

This event is free, but registration is required. To attend, please click on the "Register Now" button in the grey box at the top of this page. Your registration will be complete upon receipt of a confirmation email. If you do not receive a confirmation, please contact for assistance.

This symposium is made possible with support from

  • Janssen Award
  • Johnson & Johnson


* Presentation titles and times are subject to change.

September 16, 2015

8:00 AM

Registration and Breakfast

9:00 AM

Welcome and Introductory Remarks
Seema Kumar, Johnson & Johnson
Ellis Rubinstein, The New York Academy of Sciences

Session I: Understanding the Molecular Landscape of Cancer: From Basic Mechanisms to Clinical Intervention

9:15 AM

2015 Dr. Paul Janssen Award for Biomedical Research Announcement
William N. Hait, MD, PhD, Janssen Research & Development

2015 Dr. Paul Janssen Award for Biomedical Research Lecture

9:30 AM

Cancer Genomics & the Wars Against Cancers
Bert Vogelstein, MD, The Johns Hopkins University

10:20 AM

Coffee and Networking Break

Session II: Expanding the Scientific Tool Kit for Enhancing Cancer Diagnostics and Therapeutics

Session Chair: Brooke Grindlinger, PhD, The New York Academy of Sciences

10:50 AM

Engineering T Cells: Moving Beyond Leukemia
Carl June, MD, University of Pennsylvania

11:20 AM

Modular Characterization of Circulating Tumor Cells
Daniel A. Haber, MD, PhD, Massachusetts General Hospital

11:50 AM

Copper is Required for Oncogenic BRAF Signaling and Tumorigenesis
Christopher Counter, PhD, Duke University School of Medicine

12:20 PM

The Path to New Medicines: The K-RAS Story
Peter Lebowitz, MD, PhD, Janssen Research & Development

12:50 PM

Panel Discussion: The Future of Cancer Therapy



Brooke Grindlinger, PhD, The New York Academy of Sciences



Bert Vogelstein, MD, The Johns Hopkins University
Carl June, MD, University of Pennsylvania
Daniel A. Haber, MD, PhD, Massachusetts General Hospital
Christopher Counter, PhD, Duke University School of Medicine
Peter Lebowitz, MD, PhD, Janssen Research & Development

1:15 PM


2:15 PM



Christopher Counter, PhD

Duke University School of Medicine

Dr. Counter undertook his PhD with Drs. Harley and Bacchetti at McMaster University and his postdoctoral fellowship with Dr. Weinberg at the Whitehead Institute, where he studied the role of telomeres and telomerase on cell immortalization and cancer. He began an Assistant Professorship in the Department of Pharmacology & Cancer Biology at Duke University, where he exploited the ability of telomerase to immortalize human cells as an experimental platform to explore oncogenic RAS signaling, which is now a major focus of the lab. Dr. Counter is currently a Professor in the Department of Pharmacology & Cancer Biology at Duke University and has active leadership roles in the Duke Cancer Institute.

Brooke Grindlinger, PhD

The New York Academy of Sciences

Daniel A. Haber, MD, PhD

Massachusetts General Hospital

Dr. Daniel Haber is Director of the MGH Cancer Center and the Isselbacher/Schwartz Professor of Oncology at Harvard Medical School. His laboratory interests have focused on the area of cancer genetics, including the etiology of the pediatric kidney cancer Wilms tumor and genetic predisposition to breast cancer. Recently, his laboratory reported that lung cancers with activating mutations in the epidermal growth factor receptor (EGFR) are uniquely sensitive to tyrosine kinase inhibitors that target this receptor. This observation has had important implications for the genotype-directed treatment of non-small cell lung cancer, and more broadly for strategies to identify critical genetic lesions in cancers that may serve as an "Achilles heel" and be suitable for molecular targeting. In collaboration with Dr. Mehmet Toner’s laboratory, Dr. Haber’s laboratory has recently established the application of a novel microfluidic technology for quantifying and purifying circulating tumor cells from the blood of patients with various epithelial cancers. This new application has potentially profound implications for early diagnosis of cancer and for noninvasive molecular profiling of cancers during the course of therapy.  

William N. Hait, MD, PhD

Janssen Research & Development

Carl June, MD

University of Pennsylvania

Carl June is the Richard W. Vague Professor in Immunotherapy in the Department of Pathology and Laboratory Medicine. He is currently Director of Translational Research at the Abramson Cancer Center at the University of PA, and is an Investigator of the Abramson Family Cancer Research Institute. He is a graduate of the Naval Academy in Annapolis, and Baylor College of Medicine in Houston, 1979. He had graduate training in Immunology and malaria with Dr. Paul-Henri Lambert at the World Health Organization, Geneva, Switzerland from 1978-79, and post-doctoral training in transplantation biology with Dr. E. Donnell Thomas and Dr. John Hansen at the Fred Hutchinson Cancer Research Center in Seattle from 1983-1986. He is board certified in Internal Medicine and Medical Oncology. He founded the Immune Cell Biology Program and was head of the Department of Immunology at the Naval Medical Research Institute from 1990 to 1995 before joining the faculty of the Perelman School of Medicine in 1999. He maintains a research laboratory that studies various mechanisms of lymphocyte activation that relate to immune tolerance and adoptive immunotherapy for cancer and chronic infection. In 2014, Dr. June is considered the most influential academic scientist in the biopharmaceutical industry according to FierceBiotech.

Peter Lebowitz, MD, PhD

Janssen Research & Development

Bert Vogelstein, MD

Johns Hopkins School of Medicine
Howard Hughes Medical Institute

Dr. Vogelstein obtained a B.A. degree in mathematics from the University of Pennsylvania and an M.D. degree from the Johns Hopkins University School of Medicine. He performed his internship and residency in pediatrics at the Johns Hopkins Hospital and completed a post-doctoral fellowship at the National Cancer Institute. He is currently the Clayton Professor of Oncology and Pathology and Co-Director of the Ludwig Institute at the Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins. He is an Investigator of the Howard Hughes Medical Institute and a Scholar of the Lustgarten Foundation for Pancreatic Cancer Research. His work focuses on the molecular genetic basis of human tumorigenesis and its implications for the diagnosis and treatment of patients with cancer.

Additional speakers to be announced.


Promotional Partners

Sandra and Edward Meyer Cancer Center

Weill Cornell Medical College

This symposium is made possible with support from

  • Janssen Award
  • Johnson & Johnson


Cancer Genomics & the Wars Against Cancers
Bert Vogelstein, MD, The Johns Hopkins University

The realization that cancers are, in essence, genetic diseases has profound implications for understanding these illnesses and mitigating morbidity and mortality from them.  Research over the last decade has revealed the genetic landscapes of nearly all tumors at unprecedented depth.   Cancers generally contain thousands of mutations distributed throughout their genomes.  However, only a few of these alterations confer selective growth advantages that “drive” tumorigenesis, considerably simplifying the otherwise complex picture that emerges.   These driver gene mutations provide extraordinary opportunities for interfering with, or reversing, the tumorigenic process.   The opportunities include drug-based pathway inhibition, immunotherapies, and novel diagnostic measures.  The potential impact of these approaches, as well as their current limitations, will be outlined in the context of the underlying genetics and with a view towards future reductions in cancer deaths.

Molecular Characterization of Circulating Tumor Cells
Daniel A. Haber, MD PhD1,3

Circulating Tumor Cells (CTCs) are shed from primary and metastatic cancers into the bloodstream, where they contribute to the metastatic spread of cancer to distant organs. Even in patients with advanced cancer, CTCs are rare and surrounded by abundant normal blood cells, thus requiring advanced technologies for their isolation and characterization. Such analyses hold the key to understanding the process of blood-borne metastasis, and as CTCs are derived from multiple tumor loci, they also provide tools for noninvasively monitoring cancer during response to therapy or tumor progression. We have developed a microfluidic chip, which effectively depletes normal blood cells from a clinical specimen, thereby revealing unlabeled CTCs without selection bias. We demonstrate two applications of this technology: first, we apply single cell RNA sequencing to individual CTCs, demonstrating remarkable heterogeneity among CTCs from individual patients with advanced prostate cancer, including differential expression of Androgen Receptor splice variants and novel mechanisms of anti-androgen resistance, that are not evident in bulk tumor populations. Second, we establish long-term cultures of CTCs, which allow matching acquired somatic mutations in heavily treated patients with breast cancer with the drug sensitivity patterns of CTCs. Acquired mutations in the ESR1, PIK3CA and FGFR genes predict sensitivity to their respective targeted inhibitors, alone or in combination, which can be effectively modeled in vitro and in mouse xenografts. Together, these studies point to the utility of CTCs to interrogate tumor biology in “real time” from patients undergoing treatment for cancer.
Coauthors: Shyamala Maheswaran, PhD1, Ravi Kapur, PhD2 and Mehmet Toner, PhD2
1 Massachusetts General Hospital Cancer Center
2 Center for Bioengineering in Medicine, Harvard Medical School, Boston, Massachusetts, United States
3 Howard Hughes Medical Institute, Chevy Chase, Maryland, United States


Copper is Required for Oncogenic BRAF Signaling and Tumorigenesis
Christopher M. Counter, PhD1

The mitogen-activated protein (MAP) kinase BRAF is mutated, typically Val 600®Glu (V600E), to induce an active oncogenic state in a large fraction of melanomas, thyroid cancers, hairy cell leukemia and, to a smaller extent, a wide spectrum of other cancers. BRAFV600E phosphorylates and activates the MAP kinase kinases MEK1 and MEK2, which in turn phosphorylate and activate the MAP kinases ERK1 and ERK2 to promote cancer. Targeting MEK1/2 is proving to be an important therapeutic strategy. In this regard, we previously found that copper (Cu) influx enhances MEK1 phosphorylation of ERK1/2 through a Cu–MEK1 interaction. We now present evidence that reducing the levels of the high-affinity Cu transporter 1 (CTR1), or mutations in MEK1 that disrupt Cu-binding decrease BRAFV600E-driven signaling and tumorigenesis.  Conversely, a MEK1–MEK5 chimaera that phosphorylates ERK1/2 independently of Cu restored tumor growth of murine cells lacking Ctr1.  Finally, we find that Cu chelators used in the treatment of Wilson disease decrease tumor growth of human or murine cells transformed by BRAFV600E or engineered to be resistant to BRAF inhibition, and most recently, provide a survival advantage in mice genetically engineered to develop melanoma.  Taken together, these results suggest that Cu-chelation therapy could be repurposed to treat cancers containing the BRAFV600E mutation. (Adapted from Brady DC et al., (2014) Nature 509:492-6)
Coauthors: Donita C. Brady, PhD1, Matthew S. Crowe, BS1, Michelle L. Turski, PhD1, G. Aaron Hobbs,PhD2, Xiaojie Yao, PhD3, Apirat Chaikuad, BS4, Stefan Knapp, PhD4, Kunhong Xiao, PhD3, Sharon L. Campbell, PhD2, Dennis J. Thiele, PhD1
1 Department of Pharmacology and Cancer Biology, Duke University Medical Center, Durham, North Carolina 27710, USA
2 Department of Biochemistry and Biophysics, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina 27599, USA
3 Department of Medicine, Duke University Medical Center, Durham, North Carolina 27710, USA
4 Nuffield Department of Clinical Medicine, Target Discovery Institute and Structural Genomics Consortium, University of Oxford, Oxford OX3 7DQ, UK


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