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National Cancer Institute (NCI),
Division of Cancer Biology (DCB)
Workshop on Defining the Epigenome: Addressing
the Value and Scope of a Human Epigenome Project
Andrew P.
Feinberg and Peter A. Jones, Co-Chairs
Grace Ault,
NCI Organizer
Epigenetics is
the study of modifications of DNA, other than the primary DNA sequence, plus
associated protein factors, that have information content and are maintained
during cell division. Unlike genetic information, the epigenome, or sum of genome-wide
epigenetic patterns, distinguishes and defines one tissue from another, stem
cells from somatic cells, and aged from young cells. We now appreciate that
age, diet, inflammation, gender, genotype and drug exposures can alter the
epigenome and cause disease, with the cancer epigenome being the best studied
example. Two compelling influences are driving epigenomics research today—the
appreciation that epigenetics changes are likely to mediate many human disease,
and recent technical advances that allow genome-wide studies of epigenetic
regulation.
Recognizing
the importance of the field of epigenetics, the National Cancer Institute
convened a workshop on defining the epigenome on November 28-29, 2005, attended
by 25 distinguished scientists in epigenetics, representing diverse research
interests including cancer, environmental health, neuroscience, aging,
developmental biology, model organisms and basic research in chromatin. This international
convocation of epigeneticists was prompted by the recognition by the community
of an urgent need to establish a foundation for systematic epigenomics research.
In particular, while great progress has been made in understanding epigenetics
at the single gene/single cell level, little is known of the comprehensive epigenome,
or of the variations in the epigenome that distinguish one cell type from
another, or normal from diseased tissue. Prior to the meeting, there was a
consensus among investigators that defining the epigenome would require an
organized effort, to ensure both cost efficiency and maximal translational
impact.
The Workshop responded
to a recommendation from the Think Tank in Epigenetics organized by the NCI
Division of Cancer Biology in May 2004, and followed a Conference on an
Epigenome Project held by the American Association for Cancer Research in June
2005. The purpose of the current workshop was to answer three questions: (1)
What would be the value of a comprehensive organized Epigenome Project, over
that which can be done by regular investigator-initiated research? (2) What
would be the scope of an Epigenome Project, i.e.
what did the group feel needs to be defined? (3) What are the tools that can be
brought to bear toward this effort, and in particular are they mature enough
for such a project to be launched? The purpose was to incorporate the responses
to these three questions in a draft outline of how a Human Epigenome Project
could be structured—not necessarily to produce a final polished plan but to
come up with a first draft.
The Workshop
developed consensus support for an Epigenome Project, endorsing its value,
addressing its scope, and defining the types of tools that could be applied
toward this goal.
(1) Value of an Epigenome Project
During the
session devoted to assessing the value of an epigenome project, it was clearly agreed
that a comprehensive approach to defining the epigenome is critical to
understanding stem cell biology, aging, development, and important diseases
that have been relatively resistant to therapy, including cancer and
psychiatric illness. Understanding the epigenome and knowing how it works in an
integrated fashion would have major public health implications across NCI and
NIH. Benefits of an Epigenome Project identified by the panelists include:
·
The need to discover the unexpected: we simply do not know
the landscape of most of the epigenome. A comprehensive Human Epigenome Project
will reveal the loci and patterns of modifications on which the broad community
of researchers can focus in studying human diseases. This comprehensive
approach will allow studies of the normal function and role in disease of
modifications whose existence we would not otherwise know. Traditional
epigenetics research is directed at what we already know or suspect, and a
comprehensive epigenomics approach will open windows into the unknown,
including:
o
A window to understanding the mechanism of cellular reprogramming,
and the maintenance of stable patterns of transcriptional activation and
repression.
o
A foundation for regenerative medicine, since epigenetics is
fundamental to the difference between stem cells and somatic cells
o
Fundamental insights into the mechanisms of aging, a problem
which is still almost completely opaque.
o
The role of the environment and nutrition in disease, as
both have been shown to alter the epigenome.
o
A much better understanding of mental retardation, since
several important common syndromes are caused or mediated by epigenetic
changes.
o
Fundamental insights into psychiatric diseases, some of
which show parent of origin effects, or respond to epigenome modifying
compounds, yet the epigenetics of the brain are essentially unknown.
In addition,
an Epigenome Project will provide:
·
Shared and standardized resources, such as good monoclonal
antibodies and normal reference tissues for analysis.
·
Cost efficiency from economy of scale, and downward cost
pressure from the Project itself.
·
The development of new technologies to allow more
comprehensive and cost-efficient whole-genome epigenomic analyses.
·
The ability to integrate epigenetic information across
experimental platforms, across types of epigenetic modification, and with
phenotypic data such as pharmacological responses.
·
Creation of a bioinformatics infrastructure defining a data
exchange format for epigenomics data.
The large amount of noncoding sequence, and epigenetic
variation:
Epigenetic variation and the environment:
Value for stem cell biology and cancer: Speakers
during this session included Steven Baylin, Andrew Feinberg, and Thea Tlsty,
all of whom emphasized the importance of understanding the epigenetics of stem
cells, in order to understand the epigenetics of cancer. Steve Baylin pointed
out that cancer genes are useful models to understand chromatin generally. In
cancer in particular, it is critical to identify epigenetic changes in normal
cells that control stem cell function, and likely precede the development of
mutations, and genetic changes.
(2) Scope of an Epigenome Project
This session
addressed the substrates for analysis, discussion of levels of resolution, and
model organisms.
Substrates for analysis: Since there are many epigenomes
and they vary according to developmental stage, age, etc., a key concept to emerge was that it would only be possible to
perform comprehensive analyses for a limited number of epigenomes to begin with.
By studying embryonic stem cells and a panel of differentiated cells from
humans, focusing on samples acquired from young individuals to control for age
effects, the variability of the epigenomic landscape will be captured. One
thing that all agreed was that understanding the epigenome in embryonic stem
cells would be critical, since these really represent the ground state of the
epigenome. Significantly, ES cells were
appealing as a baseline because they are relevant and useful to all areas of
research and all organ systems. Convincing cases were also made for the use of
mouse embryonic stem cells since they can be experimentally manipulated so that
alterations in the epigenome with respect to differentiation can be better
understood. In this regard this project would have strong overlap with ongoing
projects funded by the European Union which are mostly focused on the mouse. It
would also be feasible, and indeed highly desirable, to define the epigenome in
a human embryonic stem cell line. It will be critical to agree on a single stem
cell line so that the data obtained can be integrated across studies. With respect to human differentiated tissues,
human epidermal keratinocytes and dermal fibroblasts obtained from newborn
foreskins are a promising system that could provide a useful source of
information allowing for comparisons to be made between differentiation
lineages.
Ben Tycko
noted the importance of defining normal tissue very carefully, requiring expert
panels in the selection of each tissue type that will be analyzed. He also
noted that an additional value of studying stem cells is that it helps to
clarify the differences that distinguish one differentiated tissue type from
another. Thea Tlsty emphasized that we should include all known marks, all “players”
in the epigenetic program with no preconceived notions. She defined a set of
requirements for sample collection: ample material, easy to sample, easy to
visualize, easy to genetically and chemically manipulate. They should behave in
a reproducible fashion, provide insight into key questions, with defined
differentiation models (normal to disease, or ES to differentiated cells).
Ideally, one would want to be able to do tissue reconstruction, so the in vitro
situation faithfully recapitulates in vivo growth. She suggested dermal keratinocytes, or dermal
fibroblasts, and hematopoietic cells (B lymphocytes). There are models for skin
growth, e.g. culture for burn victims, and these are easy to sample. For
lymphocytes, there are excellent in vitro systems and in vivo correlates, and
many relevant diseases. Keratinocytes and fibroblasts together would give
insight into epithelium and stroma relationship, and might easily be obtained
from newborn circumcisions. Another source of material she suggested is the
HMEC (human mammary epithelial cells) system, which would allow comparison of
epigenomic with known genomic and gene expression data, as well as the
relationship to in vivo tumor progression.
Finally, it
was agreed that expert committees must be assembled to recommend those human
tissues to be studied as normal references for comparison with cells from
patients with diseases, and to set the standards by which the samples will be
defined.
Levels of resolution: It was agreed that the eventual
goal of an epigenome project should be one base pair of resolution of DNA
methylation, similar to the human genome project. The consensus was that it
would be best to start with analysis of the selected reference epigenomes at
the currently-feasible lower level of resolution (between 100 - 1,000 base
pairs) to enable focused single-locus studies in the near term. Meanwhile, a
major focus of the project would be to encourage the development of technology
and methodologies capable of high level resolution.
Peter Jones
pointed out that unlike the human genome sequencing project, more material will
be needed for the reference epigenome samples, because of the need to examine
primary cells rather than cloned libraries.
He also stressed the importance of model organisms. As he pointed out,
we must deal with imperfect materials, because there is no perfect reference
epigenome. We also must do this work comprehensively across the genome, like
the human genome project was done, or we will miss critical information. He
made the point that a “reference” should start with normal tissue so as to form
the basis for understanding the changes in each cancer. After some number of normal tissues are done
as reference epigenomes, less intensively evaluated epigenomes to reflect age,
diseases, other tissues, etc, can be layered on top. A large scale project to
produce this baseline can be complemented by R01-funded projects that provide
these additional layers.
Model organisms: Several speakers convincingly argued
for the necessity of including key model organisms. Model organisms provide a
means of getting from correlation to causality by intervening experimentally in
ways not possible in humans, testing the functional consequences of gene
knock-outs or substitution of mutant copies as well as over-production of gene
products. Shelley Berger pointed out that yeast is an outstanding developmental
model. One could use a process for a
reference, such as transcription as a model of changes over time, e.g.
GAL1/HIS3. Questions would be asked such as, is there epigenetic similarity
among members of a group of coordinately regulated genes? Are there epigenetic differences profound or
subtle between groups of coordinately regulated genes? One could also examine
DNA damage (UV/IR induced), to look at changes over time. We could learn how
broad are the regions of alteration around the breaks. Does the extent vary
depending on chromosomal location? Are there permanent changes? An intriguing
example is sporulation (gametogenesis), a developmental epigenetic state. Aging
is another, as yeast has a finite life span.
The
participants concurred on the short-term feasibility of understanding the yeast
and Drosophila epigenomes
particularly since both genomes are relatively small and neither of these organisms
have substantial cytosine methylation. However, understanding how chromatin
functions on a genome-wide level in these organisms would have considerable
impact for understanding the human epigenome. Sarah Elgin discussed the
advantages of including Drosophila as a developmental model. Advantages include
the high quality genome sequence and
heterochromatin analysis being done in D.
melanogaster, similar gene organization (intron/exon patterns), good
annotation (FlyBase), a complex organ-based body plan (>70% human disease
genes have orthologues), on-going work on insulators, and the accessibility of
polytene chromosomes. Past work has also
made Drosophila a model for population and quantitative genetic approaches..
ChIP on chip is already established as a method, as well as nucleosome mapping
using tagged histones, DNase hypersensitive site mapping has been done for
specific genes, and should be possible on a genome-wide basis. She raised the
question of the organization of the genome and presence of repeats. This could
have great relevance to understanding epigenome regulation, as the type of
repeats, rather than density of repeats appears to be important in epigenetic
regulation in flies.
(3) Tools for Epigenome Analysis
The unanimous
opinion of the Workshop participants was that the tools for epigenome analysis
are available now for a pilot project. Peter Jones noted that bisulfite
conversion can be followed by locus-specific PCR and possibly shotgun
sequencing. The major limitation at this time is cost, although Steve Henikoff
noted that in some ways methylation sequencing is simpler than DNA sequencing
since it involves a resequencing effort, and only cytosines followed by
guanines need be interrogated, and there are only two possible bases at these
sites, C (if methylated prior to bisulfite treatment) and T (if unmethylated
prior to treatment). The major limitation to bisulfite sequencing of all of the
reference genomes is cost, although that will likely be driven down
substantially by the project itself, similar to the history of DNA sequencing.
Furthermore, the panelists agreed that we should not specify one particular
method over another, as emerging technologies may drive the cost down further.
Largely
because of the cost issue, the group felt that a lower resolution (1 kb)
analysis should be performed immediately. At this level for DNA methylation
studies, several exciting and workable technologies were discussed. These
included restriction enzyme based platforms, as described by
Peter Laird
described the robustness and low cost of techniques such as MethylLight, but
emphasized that rather than choose a particular approach, there is a wealth of
technology to choose from. Another approach that might be used for the CpG
island component is hybridization-based array analysis, as described by Tim
Huang.
Finally, Bing
Ren noted that ChIP on chip technology is fairly mature and productive in
complex genomes already, in studying both cell lines and tissues. He noted that
50% of known promoters have RNA Pol II in a set of 5 tissues examined, and 5%
in only 1 tissue, but novel promoters show Pol II binding in only 1 tissue in
36% of cases. There is also relatively low CpG island content in
tissue-specific genes, supporting the idea that many tissue-specific genes are
normally methylated at their promoters. The bottlenecks are antibody quality,
data analysis tools, standards, the large amounts of materials, and the costs
of genome-wide tiling arrays, all of which would be ameliorated if not
eliminated by a comprehensive epigenome project.
(4) Ongoing Epigenome Efforts and Relevant Projects
A special session
was held to hear from other interested and related groups, in the hope that an
Epigenome Project would be broadly connected to the community, as well as to
ongoing research efforts. Paula Kim, a patient advocate, emphasized the
importance of reaching out to many constituencies, through patient education,
research committees, public policy/advocacy, and direct funding. Translating Research Across Communities (TRAC)
is an organization that she founded to harness the scientific/industrial/social
will to accelerate discoveries into accessible and meaningful clinical
applications. Another organization with a similar goal is the AACR
scientist-survivor program. She stressed that we must emphasize the discoveries
that are relevant to patient care, and how the Epigenome Project will get us
there.
Peter Jones,
as the President of AACR, described how AACR has played a significant role in
the development of the field of epigenetics. It has organized three special
conferences on cancer epigenetics and recently sponsored a workshop held at
Bing Ren
described the overlapping goals of the ENCODE project in the areas of conserved
sequence, transcribed, DNase hypersensitive, transcriptional regulatory
elements, chromatin structure, and DNA methylation (including ChIP-on-chip).
The focus of ENCODE has been on identifying the DNA sequence elements, not a
reference epigenome. However, there have been intense discussions in NHGRI Council
and the ENCODE scientific advisory committee on identifying biological
functions for each of the functional elements being studied. Thus there could
be considerable overlap in the interests of ENCODE and the epigenome community
going forward. For example, both groups recognize the need for standardized reagents
(antibodies, in particular) and bioinformatics infrastructure. The ENCODE Project
is considering issues of scale-up, and one aspect of scale up is the question
of which cells should be examined. Certainly a dialogue on this issue
between the two groups would seem useful. Given the financial strictures
of the times, it would seem worthwhile to try to construct these projects to
support the congruence of interests where that is possible.
Daniella
Gearhart (NCI) discussed the Human Cancer Genome Project pilot, a 3 yr / $100M effort
that will be focused on clinically important but biologically not too
complicated tumors. There is discussion of examining one solid tumor and one
liquid tumor. There is also an RFA to be issued on biospecimen availability.
The focus will be on gene targets as well as regulatory sequences, chromosomal
regional changes, and the integration of biological information.
(5) Next Steps
There was
unanimous consensus among the workshop participants of the necessity for a
Human Epigenome Project, and that the technology and rationale exist now to
move forward. The Epigenome Project is critical for understanding the nature of
stem cells, the differences among tissues during development, and many
pathological states including cancer, neurological and psychiatric disease, and
aging. The National Institutes of Health should take the lead in international
efforts to develop scientifically and organizationally a Human Epigenome
Project.
The Workshop
participants agreed on the following mission statement for the Epigenome
Project:
- The long term goal is to
achieve 1 bp resolution of DNA methylation, and a comprehensive analysis
of chromatin, including modifications (such as H3K9 and H3K4 methylation),
chromatin factor binding (such as polycomb, HP1), and structural change
(such as DNase hypersensitivity), to be performed on normal human
embryonic stem cells, fibroblasts and epithelial cells derived from
newborns, and a panel of 10 normal tissues, corresponding to targets of
common human disease, to be selected by experts in the tissue biology.
- The short term goal is to
analyze DNA methylation and chromatin (as defined above) in the same
target tissues at a 1kb resolution.
- Much added value would come
from a comparative epigenomics arm to the project to harness the power of
model organisms, specifically mouse, including mouse ES cells, Drosophila
and yeast. The project will develop cross-organism investigator groupings
and an organizational structure for cross-fertilization, rapid application
to model organisms and back to human and translational biology.
- The project should develop
new tools for epigenome analysis, including reference reagents such as
validated monoclonal antibodies for chromatin, and bioinformatics tools to
allow information generated by multiple investigators to be assembled and
compared for quantitative multi-platform epigenome analysis.
List
of Participants
Andrew P. Feinberg,
M.D., M.P.H. (Co-chair)
King
Fahd Professor of Medicine, Oncology, and Molecular Biology & Genetics
Director,
Phone:
(410) 614-3489
Fax:
(410) 614-9819
E-mail:
afeinberg@jhu.edu
Peter A. Jones,
Ph.D (Co-chair)
Director
Phone:
(323) 865-0816
Fax:
(323) 865-0102
E-mail:
jones_p@ccnt.hsc.usc.edu
Stephen B. Baylin, M.D.
Ludwig Professor of Oncology
Chief, Cancer Biology Division
The Johns Hopkins University School of Medicine
1650 Orleans Street
Suite 541
Baltimore, MD 21231
Phone:
(410) 955-8506
Fax: (410) 614-9884
E-mail:
sbaylin@jhmi.edu
Shelley L. Berger, Ph.D.
Associate
Professor
The Wistar Institute
3601 Spruce Street, Room 207
Philadelphia, PA
19104
Phone:
(215) 898-3922
Fax:
(215) 898-0663
E-mail:
berger@wistar.upenn.edu
Bradley Bernstein, M.D., Ph.D.
Assistant Professor
Massachusetts General Hospital and Harvard Medical
School
146 Larch Road
Cambridge, MA
02138
Phone:
(617) 256-5520
Fax:
(617) 495-0751
E-mail:
bbernstein@partners.org
Aravinda Chakravarti, Ph.D
Professor and Director
The John Hopkins University
733 North Broadway, Suite 571
Baltimore, MD
21205
Phone:
(410) 502-7525
Fax:
(410) 502-7544
E-mail:
aravinda@jhmi.edu
Joseph F. Costello,
Ph.D.
Associate
Professor
2340 Sutter, Room N225
Phone:
(415) 514-1183
Fax:
(415) 502-6779
E-mail:
Sarah Elgin, Ph.D.
Professor of Biology
Biology Department, CB-1229
Phone:
(314) 935-5348
Fax:
(314) 935-5125
E-mail:
Manel Esteller, M.D.,
Ph.D.
Director, Cancer Epigentics
Centro Nacional de Investigaciones Oncologica
Melchor Fernandez Almagro, 3
Phone:
+34-91-224-6940
Fax:
+34+61-224-6923
E-mail:
Margaret Foti, Ph.D.,
M.D.
Chief Executive Officer
American Association for Cancer Research
17th Floor
Phone:
(215) 440-9300
Fax:
(215) 440-9322
E-mail:
Thomas R. Gingeras,
Ph.D.
Vice President Biological Research
Affymetrix Laboratories
3380 Central Expressway
Phone:
(408) 731-5069
Fax:
(408) 481-0422
E-mail:
tom_gingeras@affymetrix.com
Michael Goggins, M.D.
Associate Professor of Pathology, Medicine and
Oncology
The
632 Ross Building
Phone:
(410) 955-3511
Fax:
(410) 614-0671
E-mail:
John M. Greally,
M.D., Ph.D.
Assistant Professor
Phone:
(718) 430-2875
Fax:
(718) 824-3153
E-mail:
Professor
Phone:
(206) 667-4515
Fax:
(206) 667-5889
E-mail:
Hui-Ming T. Huang, Ph.D.
Professor
Human Cancer Genetics, Medical
Research Facility
Phone:
(614) 688-8277
Fax:
(614) 292-5995
E-mail:
Assistant Professor
Children's Hospital
Phone:
(617) 919-2104
Fax:
(617) 730-0168
E-mail:
Professor
Phone:
(919) 684-2770
Fax:
(919) 684-5584
E-mail:
Paula Kim
President
Translating Research Across Communities
10720 Columbia Pike #500
Phone:
(866) 261-2295
Fax:
(310) 388-1524
E-mail:
Peter W. Laird,
Ph.D.
Associate Professor
NOR 6418, MC 9176
Phone:
(313) 865-0650
Fax:
(323) 865-0158
E-mail:
Jared M. Ordway,
Ph.D.
Scientist
Orion Genomics
Phone:
(314) 633-1847
Fax:
(314) 615-6975
E-mail:
Bing Ren, Ph.D
Assistant Professor
Cellular and Molecular Medicine
Phone:
(858) 822-5766
Fax:
(858) 534-7750
E-mail:
Thea D. Tlsty,
Ph.D
Professor
Phone:
(415) 502-6116
Fax:
(415) 502-6163
E-mail:
Benjamin Tycko, M.D., Ph.D.
Associate Professor of Pathology
630
Phone:
(212) 851-5280
Fax:
(212) 851-5284
E-mail:
Toshikazu Ushijima, M.D.,
Ph.D.
Chief
National Cancer Center Research Institute
Chuo-ku
Phone:
81-3-3547-5240
Fax:
81-3-5565-1753
E-mail:
Patrick Varga-Weisz, Ph.D.
European Epigenome Network of Excellence
Babraham Institute
Phone:
(011) (44) 1223 496 434
Fax:
(011) (44) 1223 496 22
E-mail:
patrick.varga-weisz@bbsrc.ac.uk
Stephen T. Warren,
Ph.D.
Professor of Human Genetics
Whitehead Biomedical
615 Michael Street., NE.,
Phone:
(404) 727-5979
Fax:
(404) 727-3949
E-mail:
swarren@emory.edu
Bernard E. Weissman,
Ph.D.
Professor
Phone:
(919) 966-7533
Fax:
(919) 966-9673
E-mail:
weissman@med.unc.edu
National Institutes of Health Attendees
Grace S. Ault, Ph.D. (NCI Organizer)
Program Director
Division of Cancer Biology
National Cancer Institute
National
Institutes of Health
6130 Executive Boulevard
EPN 5000
Rockville, MD 20852
Phone:
(301) 435-1878
Fax:
(301) 480-0864
E-mail:
ga5k@nih.gov
Anthony D.
Carter, Ph.D.
Program
Director
Division
of Genetics and Developmental Biology
National
National
Institutes of Health
Room
2A5-25R, MSC 6200
Phone:
(301) 594-0943
Fax:
(301) 480-2228
E-mail:
cartera@nigms.nih.gov
John S. Cole III, Ph.D.
Program Director
Division of Cancer Biology
National Cancer Institute
National
Institutes of Health
6130 Executive Boulevard
Suite 5000
Rockville, MD 20852
Phone:
(301) 496-1718
Fax:
(301) 496-2025
E-mail:
jc121b@nih.gov
Jennifer Couch, Ph.D.
Program Director
Division of Cancer Biology
National Cancer Institute
National
Institutes of Health
EPN 5004
Phone:
(301) 435-5226
Fax:
(301) 480-2854
E-mail:
couchj@mail.nih.gov
Elise Feingold, Ph.D
Program Director, Genome Analysis
National Human Genome Research Institute
National
Institutes of Health
MSC 9305
Phone:
(301) 496-7531
Fax:
(301) 480-2770
E-mail:
ef5j@nih.gov
Daniela Gerhard, Ph.D
Director
Office of Cancer Genomics
National Cancer Institute
National
Institutes of Health
Room 10A07
Phone:
(301) 451-8027
Fax:
(301) 480-4368
E-mail:
gerhardd@mail.nih.gov
Peter Good, Ph.D.
Program Director
National Human Genome Research Institute
National Institutes of Health
Phone:
(301) 496-7531
Fax:
(301) 480-2770
E-mail:
goodp@mail.nih.gov
Mark S. Guyer,
Ph.D
Director, Extramural Research
National Human Genome Research Institute
National
Institutes of Health
Phone:
(301) 496-7531
Fax:
(301) 480-2770
E-mail:
guyerm@exchange.nih.gov
Kevin Howcroft, Ph.D.
Program Director
Division of Cancer Biology
National Cancer Institute
National
Institutes of Health
EPN 5060
Phone:
(301) 496-7815
Fax:
(301) 480-2844
E-mail:
howcrofk@mail.nih.gov
John Ilekis, Ph.D
Program Director
National
National Institutes of Health
PPB, Room 4B0C
Phone:
(301) 435-6895
Fax:
(301) 496-3790
E-mail:
ilekisj@mail.nih.gov
Carol MacLeod, Ph.D.
Program Director
Division of Cancer Biology
National Cancer Institute
National
Institutes of Health
EPN 5066
Phone:
(301) 435-1878
Fax:
(301) 480-0864
E-mail:
cm465d@nih.gov
Susan McCarthy, Ph.D.
Program Director
Division of Cancer Biology
National Cancer Institute
National
Institutes of Health
Room 5058
Phone:
(301) 594-8785
Fax:
(301) 480-2844
E-mail:
mccarths@mail.nih.gov
Anna McCormick, Ph.D
Branch Chief
National Institute on Aging
National
Institutes of Health
Phone:
(301) 496-6402
Fax:
(301) 402-0010
E-mail:
mccormia@nia.nih.gov
Judy Mietz, Ph.D.
Branch Chief
Division of Cancer Biology
National Cancer Institute
National
Institutes of Health
EPN 5028
Phone:
(301) 496-9326
Fax:
(301) 496-1224
E-mail:
jm166o@nih.gov
Suresh Mohla, Ph.D.
Branch Chief
Division of Cancer Biology
National Cancer Institute
National
Institutes of Health
EPN 5038
Phone:
(301) 435-1878
Fax:
(301) 480-0864
E-mail:
mohlas@mail.nih.gov
Allan R. Mufson, Ph.D.
Branch Chief
Division of Cancer Biology
National Cancer Institute
National
Institutes of Health
EPN 5062
Phone:
(301) 496-7815
Fax:
(301) 496-2844
E-mail:
rm2300@nih.gov
Paul Okano, Ph.D.
Program Director
National Cancer Institute
National
Institutes of Health
Phone:
(301) 496-9326
Fax:
(301) 496-1224
E-mail:
Brad
Ozenberger, Ph.D.
Program
Director
Division
of Extramural Research
National
Human Genome Research Institute
National
Institutes of Health
Phone:
(301) 496-7531
Fax:
(301) 480-2770
E-mail:
bozenberger@mail.nih.gov
Jane Peterson, Ph.D.
Associate Director of Extramural Research
National Human Genome Research Institute
National
Institutes of Health
Phone:
(301) 496-7531
Fax:
(301) 480-2770
E-mail:
petersonj@exchange.nih.gov
William C. Reinhold
Biologist
Division of Genomics and Bioinformatics Group
National Cancer Institute
National
Institutes of Health
9000 Rockville Pike
Building 37, Room 5056
Phone: 301-496-9572
Fax: 301-402-0752
E-mail: wcr@mail.nih.gov
Neeraja Sathyamoorthy, Ph.D.
Program Director
Division of Cancer Biology
National Cancer Institute
National
Institutes of Health
Phone:
(301) 435-1878
Fax:
(301) 294-5030
E-mail:
sathyamn@mail.nih.gov
Dinah Singer, Ph.D.
Director
Division of Cancer Biology
National Cancer Institute
National
Institutes of Health
EPN 5044
Phone:
(301) 496-8636
Fax:
(301) 496-8656
E-mail:
ds13j@nih.gov
John Sogn, Ph.D.
Deputy Director
Division of Cancer Biology
National Cancer Institute
National
Institutes of Health
Room 5050
Phone:
(301) 594-8782
Fax:
(301) 496-8656
E-mail:
sognj@mail.nih.gov
Daniel J. Sussman, Ph.D.
Program Director
Division of Cancer Biology
National Cancer Institute
National
Institutes of Health
Phone: (301) 435-1878
Fax: (301) 496-8656
E-mail: sussmand@mail.nih.gov
Susan T. Taymans,
Ph.D.
Program Director
National
National Institutes of Health
Room 8B01
Phone:
(301) 496-6517
Fax:
(301) 496-0962
E-mail:
taymanss@mail.nih.gov
Frederick L. Tyson, Ph.D.
Scientific Program Administrator
Suspectibility and Population Health
National Institute of Environmental Health Science
National
Institutes of Health
MD EC-21
Research
Phone:
(919) 541-0176
Fax:
(919) 316-4606
E-mail:
tyson2@mail.nih.gov
May Wong, Ph.D.
Program Director
Cancer Etiology Branch
National Cancer Institute
National
Institutes of Health
Room 5010, MSC 7398
Phone:
(301) 496-1953
Fax:
(301) 496-2025
E-mail:
mw132k@nih.gov
Senior Investigator
National Cancer Institute
National
Institutes of Health
Phone:
(301) 496-9571
Fax:
(301) 402-0752
E-mail:
jw4i@nih.gov
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