Summer Symposium 2012

Scott Armstrong, M.D., Ph.D.

Associate Professor of Pediatrics
Dana Farber Cancer Institute

Dr. Armstrong is a leader in the fields of cancer stem cell and genomics research with a focus on leukemia. His work has led to several findings that point to potential new therapies. Among his most notable achievements are genomic characterization of infant leukemia, and identification of the FLT3 receptor tyrosine kinase as important in this disease. This work led to the development of new therapeutic approaches that are now being tested in patients. Dr. Armstrong’s most important fundamental discovery was the demonstration that leukemia stem cells can be distinct from normal blood stem cells, and defined by dependence on stem cell associated pathways activated in an inappropriate developmental context. His group also recently identified epigenetic changes as a critical initial step in leukemia stem cell development which has led to the discovery of small molecules that can reverse this process and eradicate leukemia cells. He has been recognized with several awards including the McCulloch and Till Award from the International Society of Experimental Hematology (2009), which recognizes international leaders in stem cell biology and the Paul Marks Prize for Cancer Research from Memorial Sloan Kettering Cancer Center (2011). His current work is focused on defining how enzymes that control the epigenetic states of cancer stem cells can be leveraged for therapeutic purposes.

Stephen Baylin, M.D.

Deputy Director, Professor of Oncology and Medicine
Chief of the Cancer Biology Division and Director for Research
The Sidney Kimmel Comprehensive Cancer Center
John Hopkins University

For the last 25 years, Dr. Stephen Baylin has studied the role of epigenetic gene silencing in the initiation and progression of human cancer. He and his colleagues have fostered the concept that DNA hypermethylation of gene promoters, and associated transcriptional silencing, can serve as an alternative to mutations for producing loss of tumor suppressor gene function. They have described some of the classic genes involved, invented approaches to randomly screen the cancer genome for such genes and to demonstrate their functional role in cancer progression, helped begin unravel the molecular mechanisms responsible for the initiation and maintenance of the gene silencing, and worked to utilize all of their findings for translational purposes. Dr. Baylin has authored or co-authored over 375 full-length publications on the above and other areas of cancer biology.

Laurie Boyer, Ph.D.

Sizer Career Development Assistant Professor of Biology
Department of Biology
Massachusetts Institute of Technology

Laurie A. Boyer, Ph.D., earned her doctorate in biochemistry from the University of Massachusetts Medical School. Her graduate work with Craig Peterson focused on dissecting the biochemical mechanisms of chromatin remodeling enzymes. She then joined the laboratories of Rudolf Jaenisch and Rick Young at Whitehead Institute for Biomedical Research as a postdoctoral fellow, where she pioneered the development of high-throughput platforms for genome wide analysis of transcription factors and chromatin regulators in stem cells. In particular, Dr. Boyer discovered how three key transcription factors -Oct4, Sox2, and Nanog- comprise a core transcriptional regulatory network that controls embryonic stem cell (ESC) pluripotency. She also illuminated a key role for chromatin modifying enzymes, such as Polycomb group proteins, in regulating cell fate decisions during ESC differentiation. In 2006, Laurie was recognized as one of the world’s 50 top leaders in research by Scientific American for her innovative work in understanding the genome of human ESCs. In 2007, she joined the Biology Department at the Massachusetts Institute of Technology and is currently the Sizer Career Development Associate Professor of Biology. The Boyer lab investigates how gene expression programs are precisely coordinated during lineage commitment and how failure to establish proper gene expression states can contribute to developmental failure and disease. Dr. Boyer is a Pew Scholar in the Biomedical Sciences and is the recipient of several early career awards including those from the Smith Family Foundation for Excellence in Biomedical Research as well as the Massachusetts Life Sciences Center.

Jay Bradner, M.D.

Staff Physician, Hematologic Malignancies
Dana-Farber Cancer Institute
Assistant Professor of Medicine, Harvard Medical School

James Bradner is a Staff Physician in Hematologic Malignancies at Dana-Farber as well as an Assistant Professor in Medicine at Harvard Medical School.  The research focus of his laboratory concerns the discovery/optimization of prototype drugs targeting cancer gene regulation.  Clinically, the Bradner group strives to deliver novel therapeutics for human clinical investigation in hematologic diseases. Dr. Bradner is a member of the American Society of Clinical Investigation, the American Society of Hematology, the American Chemical Society and the American Association of Cancer Research.  His recent research has been published in Nature, Cell, Nature Chemical Biology and the Journal of the American Chemical Society. He has authored sixteen United States Patent applications, licensed to five pharmaceutical companies, and is a scientific founder of Acetylon Pharmaceuticals, SHAPE Pharmaceuticals and Tensha Therapeutics.

John Dick, Ph.D.

Senior Scientist, Campbell Family Cancer Research Institute
Ontario Cancer Institute
Professor of Molecular Genetics, University of Toronto

Dr. Dick's research has focused on understanding normal and leukemic human stem cells. One of the most important achievements was developing a system for transplanting normal and leukemic human stem cells into immune-deficient mice; an assay that has revolutionized the study of human hematopoiesis. His group characterized many of the properties of normal repopulating cells with this assay system. His lab also established that only a small proportion of human leukemic cells were capable of initiating human leukemia within the immune-deficient mice. Purifying these leukemia-initiating cells provided direct evidence for the cancer stem cell hypothesis. Dr. Dick is currently a Senior Scientist, at the Campbell Family Cancer Research Institute, Ontario Cancer Institute, Princess Margaret Hospital, University Health Network and the McEwen Centre for Regenerative Medicine and Professor of Molecular Genetics at the University of Toronto. He is also Director of the Program in Cancer Stem Cells at the Ontario Institute of Cancer Research (OICR). Dr. Dick’s seminal contributions to the fields of molecular hematology, stem cell biology and oncology have been recognized by numerous prestigious awards at the provincial, national and international levels.

Kristian Helin, Ph.D.

Director of the Biotech Research & Innovation Centre (BRIC)
University of Copenhagen

Kristian Helin is the founding director of the Biotech Research & Innovation Centre (BRIC) at the University of Copenhagen.  He is also the director of the Danish National Research Foundation’s Centre for Epigenetics, professor of Biomedical Gene Technology at the University of Copenhagen and a PI in the Danish Stem Cell Center.  Dr. Helin is a co-founder of the biotech company EpiTherapeutics, where he is member of the board of directors and chair of the scientific advisory board. Dr. Helin obtained his PhD from the University of Copenhagen in 1991, and performed post-doctoral work at Harvard Medical School, where he cloned the first member of the E2F transcription factor family.  Subsequently, Dr. Helin was a group leader at the Danish Cancer Society in Copenhagen and a Division Director at the European Institute of Oncology from 1995-2004.  Professor Helin is an elected member of the European Molecular Biology Organisation and the Royal Danish Academy of Science and Letters.

Peter W. Laird, Ph.D.

Director of the USC Epigenome Center
Professor of Surgery, Biochemistry and Molecular Biology
University of Southern California

Dr. Peter W. Laird is Director of the USC Epigenome Center and Professor of Surgery, Biochemistry and Molecular Biology at the University of Southern California. He earned his B.S. and his M.S., Cum Laude, from the University of Leiden, The Netherlands. He received his Ph.D. from the University of Amsterdam with Dr. Piet Borst, Netherlands Cancer Institute, and postdoctoral training with Dr. Anton Berns, Netherlands Cancer Institute, and with Dr. Rudolf Jaenisch, at the Whitehead Institute for Biomedical Research in Cambridge, Massachusetts. He received the Lily Opas Research Career Development Award from Stop Cancer Foundation, a Career Development Award from the USC Liver Disease Research Center, and the USC Mellon Mentoring Award. He published the first demonstration of a causal role for DNA methylation in oncogenesis (Cell,1995). This work was cited as a “milestone” in cancer by Nature magazine (Nature Cancer Milestones, April, 2006). He developed two widely used DNA methylation analysis techniques, COmbined Bisulfite Restriction Analysis (COBRA) and MethyLight. His research findings include the report of a close link between DNA methylation and BRAF mutation in colorectal cancer (Nature Genetics, 2006), the discovery that embryonic stem cell Polycomb repressor targets are predisposed to abnormal DNA methylation in cancer (Nature Genetics, 2007), the identification of a novel epigenetic subtype of glioma (G-CIMP), tightly associated with IDH1 mutation (Cancer Cell, 2010), and the link between nuclear architecture and domains of epigenetic instability in cancer (Nature Genetics, 2011). He is a member of the AACR Stand Up To Cancer Epigenetics “Dream Team”. He is Principal Investigator for all epigenomic data production and analysis for The Cancer Genome Atlas (TCGA), together with Dr. Stephen B. Baylin (Nature, 2008, 2011, 2012).

Jacqueliine Lees, Ph.D.

Professor of Biology
Associate Director
Koch Institute for Integrative Cancer Research
Massachusetts Institute of Technology

Jacqueline Lees’ research is focused on identifying the proteins and pathways that play a key role in tumorigenicity and establishing the mechanism of their action in both normal and tumor cells. Her lab approaches this using a combination of molecular and cellular analyses, mutant mouse models, and genetic screens in zebrafish.  Her lab has cloned a family of transcription factors, called E2F, that control the expression of genes that are essential for cellular proliferation. The activity of the E2Fs is regulated by their interaction with a second family of proteins called the pocket proteins, which includes the retinoblastoma protein, a tumor suppressor that is functionally inactivated in all human tumors. Lees current goal is to understand how the interplay between the various E2F and pocket proteins mediates the appropriate control of cell cycle entry and exit that is required for normal development and tumor suppression. Jacqueline Lees conducted her graduate work at the Imperial Cancer Research Fund (now Cancer Research, UK) at Lincoln’s Inn Fields, London and received her Ph.D. degree in Biochemistry from the University of London in 1990.  From 1990 to 1994, Dr. Lees was a postdoctoral fellow in the laboratory of Ed Harlow, initially at the Cold Spring Harbor Laboratories (CSHL) and then at Massachusetts General Hospital Cancer Center and Harvard Medical School.  Here, she made key contributions to our understanding of the retinoblastoma protein (pRB) tumor suppressor. In 1994, Dr. Lees became a faculty member in the MIT Center for Cancer Research and Department of Biology. She is now a Full Professor of Biology, a Daniel K. Ludwig Scholar, and Associate Director of the Koch Institute for Integrative Cancer Research.

Victoria Richon, Ph.D.

Vice President of Biological Sciences
Epizyme

Victoria M. Richon, Ph.D. joined Epizyme, Inc.in 2008 as Vice President of Biological Sciences.  Epizyme is focused on the discovery and development of small molecule histone methyltransferase (HMT) inhibitors, a new class of personalized therapeutics for the treatment of genetically-defined cancer patients, based on breakthroughs in the field of epigenetics. Dr. Richon was a leading member of the scientific group that discovered the histone deacetylase inhibitor vorinostat (SAHA). This discovery was the basis of Aton Pharma, Inc., a company that Dr. Richon co-founded and for which she served as Executive Director of Biology. Dr. Richon led the discovery of selective inhibitors of histone deacetylases as well as the development of vorinostat.  Aton Pharma was acquired by Merck & Co, Inc in 2004 and Victoria continued supporting vorinostat through its approval by the U.S. FDA in October 2006 for the treatment of cutaneous manifestations in patients with advanced cutaneous T-cell lymphoma (CTCL), a form of non-Hodgkin's lymphoma. Marketed under the name Zolinza™, vorinostat is the first histone deacetylase inhibitor approved for the treatment of cancer.  In addition to supporting vorinostat at Merck, Dr. Richon served as the head of the department of Cancer Biology and Therapeutics.  In this role, Dr. Richon led the department’s efforts for the discovery and development of small molecule therapeutics for novel cancer targets. Dr. Richon received her BA in Chemistry from the University of Vermont and her PhD in Biochemistry at the University of Nebraska. Her thesis research focus was on the development of resistance to cisplatin.  Following her graduate work, she conducted post-doctoral research at Memorial Sloan-Kettering Cancer Center in New York.

Richard Young, Ph.D.

Member, Whitehead Institute
Professor of Biology
Massachusetts Institute of Technology