SCRIPPS DISCOVERS
Accele rating Discove r ies, S a ving L ives
A Newsletter for Philanthropists Published Quarterly by The Scripps Research Institute
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VOL 7
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NO 4
California-Florida
R E S E A R C H U P D AT E
Scripps Research Scientists Find ‘Brake-Override’
Proteins that Enable Development of Some Cancers
Scripps Research Institute scientists have discovered a basic mechanism that can enable developing
cancer cells to sustain abnormal growth. The finding is expected to lead to the targeting of this mechanism
with drugs and diagnostic techniques.
The study illuminates the roles of two nearly identical proteins, Cks1 and Cks2. These proteins were
known to be overexpressed in many cancers, but scientists hadn’t understood why. Now it appears that
Cks proteins’ overexpression enables cancerous growth by nullifying a natural defense against uncontrolled
cell division.
“An initial cancer-promoting gene mutation can push a cell to grow faster, but the cell often detects
that something is wrong and sends a signal to its DNA replication machinery to slow down,” said Steven
I. Reed, a professor in the Scripps Research Department of Molecular Biology and senior author of the
study. “We found that when the Cks proteins are overexpressed, they cause incipient cancer cells to ignore
that braking signal.”
Reed’s lab focuses on the basic biology of cell division, and Cks proteins are known to be involved in
normal cell division from embryogenesis onwards. Recently, in a routine investigation of the function of
continued on page 2
Inside:
3
. . . Scientist Profile: Erica
Ollmann Saphire
5
. . . Baldwin and Maximov
Receive Baxter Foundation
Early Career Awards
5
. . . Scripps Institutions Join
National Tumor Consortium
6
. . . Grant Funds Genomic
Research to Find Root Cause
of Heart Attack
7
. . . Hua Lu Awarded Damon
Runyon Cancer Research
Fellowship
7
. . . Supporting Scripps Research
Through a Bequest in Your Will
BACK COVER:
Partners, Contact Us
Professor Steven Reed
Team Sheds New Light on How
Blood Clots Form
> Scripps Research Institute scientists have discovered new elements of
the blood clot-formation process. The findings could lead to better drugs
for preventing heart attacks and other clot-related conditions.
The work, which was published by the Journal of Clinical Investigation in an advance,
online edition June 13, 2011, helps to establish a new model of clot formation.
According to the old model, an injury to the wall of blood vessels causes smooth muscle
cells to expose a clot-organizing protein called tissue factor. “In the emerging new model,
tissue factor exists on the surfaces of these smooth muscle cells, as well as on circulating immune
cells, but in an inactive state,” said Scripps Research Professor Wolfram Ruf. “In this study,
we’ve shown that cell-surface receptor P2X7, which was known to promote inflammation
when stimulated, also plays a major role in the clot-forming process by activating tissue factor.”
To better understand clot formation, Ruf and his colleagues performed a set of experiments
on cultured mouse cells and transgenic mouse models. The team’s investigation began with the
P2X7 receptor, because of its known role in the inflammatory response that can lead to excessive
clotting in sepsis, a severe illness in which the bloodstream is overwhelmed by bacteria.
continued on page 2
Cancer,
CONTINUED
Cks proteins in cells, Reed’s team used a chemical known as
thymidine to temporarily halt the cell division process, to
artificially synchronize the growth of two different groups of
cells—one with normal Cks expression, and the other with Cks
overexpression. To the researchers’ surprise, the Cks-overexpressing
cells failed to stop dividing.
“That was a serendipitous observation,” said Reed.
“It led us to hypothesize that these Cks proteins, when
overexpressed, are preventing cells from responding to
a normal growth-braking signal.”
As a dividing cell unravels its chromosomes, replicates them,
and becomes two new cells, it encounters safety “checkpoints,”
at which the cell division process should stop if the correct
signals are not in place. Thymidine inhibits cell division by
producing a stop signal at what is known as the “intra-S-phase
checkpoint.” But somehow, Cks overexpression causes cells to
speed past that checkpoint.
Reed and his team observed that the checkpoint-override
effect turned out to require a Cks expression level three to four
times higher than normal—the same Cks overexpression level
they observed in cell lines derived from human breast tumors.
“That’s probably not a coincidence,” said Reed.
Blood Clots,
Reed’s team created a simple model of Cks’s function in
cancer, inserting a mutant, cell-division-promoting “oncogene”
into human breast-derived cells. The oncogene’s protein product,
known as cyclin E, pushed the cell towards uncontrolled division,
which—as expected—triggered an intra-S-phase checkpoint
response, so that the rate of cell division went sharply down.
“When we overexpressed Cks, the cell division rate went back
up again,” said Reed.
Sampling real breast cancer cells from a tumor bank, Reed’s
team found that cells with high levels of cyclin E also tended to
have high levels of Cks. Since neither protein directly influences
the level of the other, the implication was that an initial oncogenic
overactivation of cyclin E must in most cases be followed by Cks
overexpression to keep a cell on the path to full-blown cancerous
growth. “The statistical link between the cyclin-E and Cks levels
was so strong that it could not have been a coincidence,” said Reed.
Cks’s cancer-enabling potential appears to be a broad one.
When Reed’s team looked at incipient cancer cells whose growth
was driven by a different oncogene, h-Ras, they again found that
the oncogene provoked checkpoint-dependent slower growth,
whereas Cks overexpression partially nullified it and allowed cell
division to proceed almost as normal.
In recent years, other researchers have noted that an initial
oncogene activation can trigger a slightly different kind of growth
arrest in cells. The phenomenon, known as oncogene-induced
continued on page 4
CONTINUED
Normally, when cells are damaged,
they release large quantities of energystorage molecules known as adenosine
triphosphate (ATP). Previous research
had hinted that when this freed ATP
encounters passing immune cells, it serves
as a damage signal, stimulating the
immune cells’ P2X7 receptors and causing
the release of “microparticles” exposing
the clot-promoting tissue factor. The
new study showed that ATP can affect
P2X7 receptors on both immune cells
and smooth muscle cells.
To confirm the significance of the
P2X7 receptor in the clot-forming
process, the team bred transgenic mice
that lacked functional P2X7 receptors,
and found that these P2X7-knockout
mice failed to form stable arterial
blood clots when the vessel wall was
exposed to a clot-inducing substance.
Importantly, these mice did not suffer
from uncontrollable bleeding.
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“This suggests that clot-preventing drugs
targeting the P2X7 pathway might not
have unacceptable side effects,” said Ruf.
In the cell experiments, the team
found that the cascade of molecular
events following P2X7 stimulation alters
the activity of a thiol-targeting enzyme
known as protein disulfide isomerase
(PDI), which Ruf 's previous studies had
implicated as a possible activator of tissue
factor. In the new study, the scientists
demonstrated the importance of PDI in
this process by showing that they could
block clot formation in normal mice with
anti-PDI antibodies.
Targeting the top of the clot-formation
pathway by blocking the P2X7 receptor
might have even broader beneficial effects,
since the activation of this receptor occurs
in a number of inflammatory disorders.
“Cardiovascular disease and heart
attacks are caused by chronic inflammation
as well as clot formation,” said Ruf,
“so possibly P2X7 is a major explanation
for the link between inflammation and
thrombosis, as well as a good target for
preventing these conditions.”
This work was supported by the
National Institutes of Health and the
American Heart Association.
Professor Wolfram Ruf
SCIENTIST PROFILE
Erica Ollmann Saphire: Fighting Deadly Viruses
in the Deep Reaches of the African Jungle
> Biomedical researchers in search of knowledge about the workings of the human body and the viruses
and diseases they fight typically make their discoveries in labs. But for Scripps Research Associate
Professor Erica Ollmann Saphire, the key to understanding deadly viruses is meeting them in their den –
the deep reaches of the African jungle.
rica has several times traded her climate-controlled
La Jolla lab for the 95 degree humidity of the West
African jungle, where she has tracked the Ebola virus,
Lassa hemorrhagic fever, and other hemorrhagic fevers, such
as Marburg virus – the subjects of her research for the past
eight years.
“It is an opportunity to see where these viruses live,” said
Erica. “In the lab, we use biochemistry and biophysics to
visualize and understand their component molecules. But these
molecules are made this way so they can function not in a lab,
but in a rainforest, cave or hut. In order to fully understand
their function, you have to put yourself in that rainforest, cave
and hut. You can do great science in the lab but the real goal is
to translate this science into use in the real world.”
Back in her lab, Erica applies this close-up look at these
viruses to her efforts to characterize them on the molecular level.
“Our goal is to get a road map for how to understand and
conquer these viruses, which have been largely undefeatable,”
said Erica.
The Ebola virus is among the more horrific known to
humankind, and there is currently no cure for Ebola hemorrhagic
fever, which inflicts a death rate as high as 90 percent of those
infected. It spreads when people come into contact with the
bodily fluids of an infected individual. Symptoms first include
a sudden fever, headache, and sore throat, then progress to
vomiting, diarrhea, rash, and kidney and liver failure. In the
final stages, massive hemorrhaging causes heavy bleeding from
body openings and internal organs.
E
Erica made headlines as the woman who broke open the
secrets of the Ebola virus. Her breakthrough study on Ebola
appeared on the cover of the journal Nature, lifting the veil
from the virus’s spike-shaped protein, a critical step in
understanding how Ebola works and an essential step for
any potential development of a treatment or a vaccine.
The Ebola virus glycoprotein itself, the one thing that is
necessary for attaching to and infecting a host, has been a
therapeutic target for more than 10 years. But because the structure
was unknown, no one knew how to take advantage of it.
The structure uncovered by Erica’s lab gives researchers
weaknesses to target in developing any potential therapeutic.
In her five-year quest to uncover the structure of the key
protein that resides on the surface of the Ebola virus and allows
it to enter human cells, Erica and her colleagues produced more
than 50,000 crystals, as part of the team’s use of a technique
called x-ray crystallography to determine the atomic structure
of molecules.
“We uncovered chinks in the virus’s elaborate armor that we
can target specific antibodies against,” said Erica.
Support for Erica’s work on this research was provided
partially by a Career Award from the Burroughs Wellcome
Fund, as well as funding from the Skaggs family to recruit and
support postdoctoral fellows. In the past, she has also received
private funding for her work on Dengue Virus through a New
Initiatives Award in Global Infectious Disease from The Ellison
Medical Foundation.
“Private philanthropic support has provided us with the seed
money for risky projects,” said Erica. “With these funds, we’ve
been able to do the big initial work and make discoveries that
then set up the next ten years for federal funding.”
On her most recent trip to Africa, Erica visited the hospital
with which her lab is collaborating to investigate the virus that
causes Lassa hemorrhagic fever. The goal of this joint initiative
is to provide field diagnostics as well as critical templates for
therapeutics and vaccines by understanding how Lassa virus
infects cells. Her trip was part of a project with Tulane University
aimed at developing new ways to treat and prevent Lassa fever.
Lassa fever, a huge public health threat, is an often deadly
viral disease that threatens hundreds of thousands of people
annually in West Africa. In some areas of Sierra Leone, up to
16 percent of people admitted to hospitals have Lassa fever.
Lassa fever is also associated with occasional epidemics, during
which the fatality rate can reach 50 percent.
“If you catch Lassa early enough, it’s treatable,” said Erica,
“but you need cheap, fast, and simple diagnostics. Local hospitals
only have electricity every other day, the local lab technicians
might not be well trained, the country was ravaged by civil war,
roads can be impassable, few vehicles are available, and the
average working person ears far less than $100 a year. If the test
costs more than pennies, is complicated or can only be run in
a laboratory, it’s not going to be useful.”
Erica and her team have learned how to make recombinant
protein both inexpensively and cleanly, and are working to
develop it into a diagnostic, somewhat like a pregnancy test
dipstick. This early diagnostic allows the fever to be identified
and treated in time to save the patient’s life.
SCRIPPS RESEARCH INSTITUTE
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Saphire,
CONTINUED
“By looking at the structure of the core nucleoprotein of
Lassa, we discovered a whole new function of the protein that
no one knew it had before,” said Erica. “This is the first step in
being able to design drugs to combat the virus.”
The village chief of the village of Yawei was so grateful for
the team’s work on trapping rodents that helped rid their village
of Lassa, that he gave them a goat, a prized possession that
normally costs a year’s salary, as a gift in gratitude.
“The fact that the chief and village were so thankful for our
work is a huge motivator for our team,” said Erica. “It gives our
work more meaning than just a paper in a journal.”
Born in Baton Rouge, Louisiana, and raised in Austin, Texas,
Erica wanted to be a journalist in high school. Journalism held
the allure of a career with the potential of seeing new things,
maybe experiencing some adventure, and having a decent
chance to figure things out. Her parents were teachers and she
remembers they often spent their summers traveling to national
parks. In college at Rice University in Houston, is where she
first took up science, studying biochemistry in the lab and the
ecology of East Texas wetlands in the field for species restoration
and food production.
Erica continued to pursue science in graduate school,
enrolling in what is now the Scripps Research Kellogg School
of Science and Technology due to the program’s focus on research
and discovery. Working in the Scripps Research laboratory of
Professor Ian Wilson, she took on a difficult and ambitious
project involving another infamous and deadly virus – human
immunodeficiency virus (HIV) – as part of a larger effort to
help develop a vaccine against AIDS. After she received her
Ph.D. in 2000, Erica chose to stay at Scripps Research where
she now heads her own lab.
Erica was recently honored at the White House
where she received a Presidential Early Career
Award for Scientists and Engineers, the highest
honor bestowed by the United States government
for young professionals at the outset of their
independent research careers.
Associate Professor Erica Ollmann Saphire with Stu the Goat
Cancer,
The award winners are selected based on two criteria:
innovative research at the frontiers of science and technology,
and community service demonstrated through scientific
leadership, education, or community outreach.
Erica credits her fellow faculty members at Scripps Research,
as well as the postdoctoral fellows and graduate students working
in her lab with much of her success. “My faculty colleagues are
bright, interesting, and collaborative – they’re all doing important
work and are on top of their fields. They’re willing to share ideas,
which inspires me,” said Erica. “And our students and postdocs
here work extremely hard and share my mission to defeat these
viruses – they’re willing to put in the extra work to make our
discoveries possible.”
C O N T I N U E D F R O M PA G E 2
cellular senescence, is believed to underlie the slow or stopped growth of skin moles and some benign cancers. “It has been shown that
this induced senescent state depends in part on the persistent activation of cell-cycle checkpoints, so presumably it is related to the
process affected by Cks,” said Reed.
Reed and his team are now trying to determine the precise molecular events through which Cks proteins exert their checkpointnullifying effect in cancer. At the same time, they are looking for ways to use their new knowledge against Cks-overexpressing cancers.
The most direct strategy would be to treat cancer, or prevent it in people with inherited predispositions, simply by using a drug to reduce
the activity of Cks proteins.
“We know that we can delete half of the Cks genes from mice without any deleterious effects, and this reduces the frequency of tumor
formation,” said Reed. “So the chances are we could find a way to reduce Cks proteins’ activity enough to prevent their checkpoint-override
effect while still allowing their essential cell functions.”
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AWARDS AND HONORS
Kristin Baldwin and Anton Maximov Receive
Baxter Foundation Early Career Awards
ssistant Professors in the Department of Cell Biology Kristin Baldwin
and Anton Maximov have been named recipients of the 2011 Baxter
Foundation Early Career Award. The award is funded by a Donald E. &
Delia B. Baxter Foundation endowment to Scripps Research. The two Department
of Cell Biology investigators will use the award to fund risky projects of potentially
high impact that have not yet been funded by more traditional mechanisms.
Baldwin’s lab aims to improve stem cell and reprogramming technologies
to better understand brain development and generate models of neurological
disease. Maximov’s lab seeks to define the basic mechanisms underlying
synaptic development and function, and to elucidate the links between synaptic
abnormalities and heritable disease. The two laboratories, situated nearby in
the Dorris Neuroscience Center, will use the Baxter Awards to enhance existing
synergies between the research groups.
Founded in 1959, the Baxter Foundation was established initially in memory
of Donald Baxter, who developed and manufactured the first commercially
prepared intravenous solutions.
A
Assistant Professor
Kristin Baldwin
Assistant Professor
Anton Maximov
Scripps Institutions Join National Tumor Consortium
he Scripps Research Institute, Scripps Health, and Scripps
Translational Science Institute (STSI) have announced they
have joined a national consortium of research institutions
headed by The Jackson Laboratory ( JAX) that is building a library
of primary human tumors with the goal of developing highly
targeted cancer therapies.
“By joining this consortium, we will contribute to and share
in a tumor library that will vastly exceed what any institution
could build on its own,” said Nicholas J. Schork, professor at
Scripps Research and director of bioinformatics and biostatistics
at STSI. “This shared resource ultimately will greatly expand
research capacity for all consortium members, with the goal of
accelerating drug development for individualized approaches to
each type of tumor.”
JAX launched the Primary Human Tumor Consortium in
2009. Consortium members provide solid human tumor samples
to JAX, which performs their initial genomic characterization and
grafts them into mouse models for scientific study. Consortium
scientists then have access to the models to conduct research on
how to better understand and treat cancer, including the potential
for tumor-specific therapies.
Mouse models that can accept newly resected human
tumors offer a highly productive way to develop and test cancer
treatments. Mouse models of virtually any kind of cancer can be
developed, providing a more individualized approach to finding
new treatments.
This approach stands in stark contrast to the standard way of
discovering new therapies for cancer, which relies on the use of
tumor cell lines. The tumor cell-line approach can be problematic,
since genetic mutations naturally occur as those cells divide and
reproduce. Consequently, the cells may drift into a different
T
genetic profile and any treatments designed to target the original
tumor won't work. Also, the cell-line approach provides insights
into which therapies are ineffective, but doesn't predictably prove
which ones are effective.
“The biomedical research community needs a common, readily
accessible resource to support this vital effort,” said JAX Executive
Vice President and Chief Operating Officer Chuck Hewett. “No
single cancer center has a sufficiently broad patient population to
meet this need, so we must work together.”
Located at The Jackson Laboratory’s JAX-West facility in
Sacramento, California, the Primary Human Tumor Consortium
seeks additional health care and research partners to speed the
development of this tumor library resource. Other participating
institutions outside San Diego include the University of Florida,
the Swedish Neuroscience Institute in Seattle, and UC Davis
Cancer Center.
To date, the consortium
has engrafted 172 tumors,
with tumor sites including
prostate, pancreas, lung,
kidney, colon, breast,
brain and bladder.
Professor Nicholas Schork
SCRIPPS RESEARCH INSTITUTE
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$7.9 Million NIH Grant Funds
‘Disease in a Dish’ Genomic Research
to Find Root Cause of Heart Attack
> Researchers looking to find a root cause for heart attacks and coronary artery disease will soon begin
using a novel investigative approach as they work toward preventing the nation's number one killer.
he National Institutes of Health (NIH) has awarded a
$7.9 million grant to the Scripps Translational Science
Institute (STSI) of The Scripps Research Institute
and Scripps Health in San Diego and Sangamo BioSciences
(NASDAQ: SGMO) of Richmond, California, to conduct the
nation’s first-ever, heart-based “disease in a dish” research.
The study will involve the use of induced pluripotent stem
cells (non-embryonic stem cells created from mature cell types,
such as skin cells) to recreate participants’ own heart artery-lining
cells in a dish, along with genome-editing technology aimed at
potentially directing certain cells away from a disease state.
T
Medical research confirms that the human
genome’s 9p21 “gene desert” region, which
everyone possesses, is strongly linked to
people’s risk of developing heart disease.
But researchers don’t understand what takes place in this
trouble spot that causes some people’s cells to eventually become
diseased. This portion of genetic code is known as a “gene desert”
because there are no genes in this region.
“We’re trying to figure out for the first time how this region
works and which other parts of the genome or genes it’s interacting
with to make some people’s cells become diseased,” said Scripps
Research Professor of Translational Genomics Eric J. Topol, the
study’s principal investigator and director of STSI.
In the study, scientists will recreate artery-lining cells for two
distinct patient groups, each totaling approximately 1,000 people.
The first group includes those who already have coronary artery
disease, which is a precursor to heart attack. The second cohort
comprises those who have lived to at least age 80 without any
heart disease or other major illnesses.
“We’ll take people whose 9p21 region of the genome says
they’re at risk for coronary artery disease, and then compare the
stem cells from that individual to a healthy elderly person who
may also have risk in that region, but somehow doesn’t have the
disease,” said Samuel Levy, the study’s lead investigator, director
of genomic sciences with STSI and professor of molecular and
experimental medicine at Scripps Research. “The crux of our
research is to figure out which genes, or which other parts of the
genome, are interacting with the 9p21 region. There are no genes
in the 9p21 region, which is a big part of our challenge.”
The “disease in a dish” heart study brings together two emerging
research strategies that, to date, have largely developed separately
—induced pluripotent stem cells to create relevant cells and a
sophisticated genome-editing technology, which acts like scissors
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to cut and replace pieces of the genome. The research will also
leverage extensive data from genome-wide association studies.
“Genome editing allows us to do an experiment no one has
ever tried; that is, if you change someone’s genetics, can you make
their cells revert away from acquiring a disease?” said Levy. “Using
zinc finger nucleases (ZFNs) that act like molecular scissors, we
can actually take this risk region out of a person’s genome and see
what happens to his cells if that region is present or absent. This
editing allows us to basically recreate the disease or take it away.”
Scientists will take skin or blood cells from participants and
reprogram them to create induced pluripotent stem cells, which
have the capacity to become any cell type in the body. These stem
cells then will be transformed into three different types of heart
artery-lining cells: smooth muscle cells, endothelial cells, and
cardio myocytes.
Researchers will characterize participants’ artery-lining cell
types as a way of trying to understand how someone with the
9p21 allele of risk ultimately goes on to acquire cells that are
diseased. Once scientists understand the cells’ underlying biology,
they’ll employ a genome-editing process using zinc finger proteins
to cut the genome and replace parts of it with DNA with a
different sequence. This will enable researchers to decipher how
this gene desert region functions.
Learning the root defect in the genome would open the door
to potentially developing new drugs or identifying existing ones
that could help a person’s cells revert away from the path of
developing a heart attack or coronary artery disease later in life.
According to Topol, this study will address the biggest
deficiency in genomics today. “We don’t know the so-called
functional genomics,” he said. “We only know there’s this zip code
in the genome that’s a problem spot, but we don’t know what’s
going on in this zip code of hundreds of thousands of letters.
We don’t know which is the offending letter or group of letters.
Genome editing will allow us to edit each one and analyze which
ones are the culprits.”
Professor Eric Topol
Hua Lu Awarded Damon Runyon
Cancer Research Fellowship
Hua Lu, research associate in the Schultz lab, has been named a 2011 Damon Runyon Fellow, a
prestigious award presented by the Damon Runyon Cancer Research Foundation to recognize earlycareer researchers.
According to the foundation, the fellowship “encourages the nation’s most promising young scientists
to pursue cancer research by providing them with independent funding to work on innovative projects.”
The 18 newly announced fellows each receive a three-year grant to pursue their research.
A research associate in the laboratory of Professor Peter G. Schultz, Lu has focused his scientific
investigation on developing antibody-drug conjugates that can specifically recognize and kill acute myeloid
leukemia cancer cells. Lu aims to generate highly specific ADCs to attack tumor cells without harming
normal cells. His work may lead to identifying new clinical candidate drugs.
Since its founding in 1946, the Damon Runyon Cancer Research Foundation has invested more than
$235 million in funding more than 3,250 young scientists. Among past foundation fellows are eleven
Nobel Prize winners, heads of cancer centers, and leaders of renowned research programs, according to the
foundation. Fewer than 10 percent of fellowship applicants are funded in the competitive award program.
Hua Lu
Supporting Scripps Research Through
a Bequest in Your Will
Remembering us in your will is the most enduring statement you can make about your belief in our mission. Here you will learn how easy it
is to extend the support you have offered throughout your lifetime for years to come.
Q – I want to remember Scripps Research in my will; how do I accomplish this?
A – The process of making a provision in your will for The Scripps Research Institute is simple. You can include a charitable bequest
when you create your will, or you may add or update a bequest later with a codicil, a formal amendment to your will. With a bequest,
you can give away property, securities or real estate without worrying about whether you will need those assets, because the giving of
them won’t actually take place until after your lifetime.
Q – What are the benefits of making a bequest?
A – Bequests are:
· Easy. A few sentences in your will or living trust complete the gift.
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a percentage of your estate.
Q – How do I put a bequest in place?
A – Take these three simple steps:
· Decide what amount or percentage you want to give.
· Take the sample bequest language (listed below) to your estate planning attorney to add to your will.
· Notify us of your intention, if you would like (we will honor your preferences regarding anonymity), so our staff can thank you for
your future gift, include you in The Scripps Legacy Society, and keep you informed of ongoing activities.
Selected Language to Remember Us in Your Will
If you would like to support our mission after your lifetime, ask your estate planning attorney to add this suggested wording to your will
or living trust:
Example of unrestricted bequest language:
I give (insert dollar amount, property to be given, percentage of the estate or “the remainder of my estate”) to The Scripps Research
Institute, a nonprofit corporation, tax identification number 33-0435954, headquartered at 10550 N. Torrey Pines Road, La Jolla, CA 92037,
for its general use and purposes.
Example of restricted bequest language:
I give (insert dollar amount, property to be given, percentage of the estate or “the remainder of my estate”) to The Scripps Research
Institute, a nonprofit corporation, tax identification number 33-0435954, headquartered at 10550 N. Torrey Pines Road, La Jolla, CA 92037,
to support (insert designation or purpose) at The Scripps Research Institute.
To learn more about supporting Scripps Research through a gift in your will, please contact William Burfitt in our California office,
(858) 784-2037 or burfitt@scripps.edu, or Alex Bruner in our Florida office, (561) 228-2013, or abruner@scripps.edu, at no obligation.
We would also be happy to discuss how your gift will help treat devastating diseases.
SCRIPPS RESEARCH INSTITUTE
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Partners
1
A private event for over 75 clients
of PNC Wealth Management,
Palm Beach, was held recently on
the Scripps Florida campus. Attendees
enjoyed a short presentation on aging by
Professor Roy Smith, founding chairman
of the Department of Metabolism and
Aging, an overview of Scripps Florida
from Barbara Noble, a behind-the-scenes
tour of several research laboratories, and
a lavish luncheon in the Founders Room.
PNC Wealth Management is a longtime, dedicated supporter of Scripps
Research. Pictured (l to r) are Mark
Stevens, Executive Vice President and
Managing Director of PNC Wealth
Management, with his wife, Sonya; and
Chairman Roy Smith, Ph.D., with his
wife, Jane. (top photo)
2
This year, Scripps Florida’s high
school and undergraduate summer
interns represented thirteen Palm
Beach County high schools, and five
colleges and universities from across the
United States. The undergraduate Kenan
Fellows are seeking degrees in the sciences
and are past participants of the six-week
high school program. This summer, they
returned to Scripps Florida laboratories
to complete a ten-week summer research
internship. Now in its seventh year, the
Kenan Fellows program at Scripps Florida
is made possible through the generous
support of The William R. Kenan, Jr.
Charitable Trust, and lead by Deborah
Leach-Scampavia, Director of Education
Outreach Programs. The 2011 Kenan
Fellows are pictured here. (bottom photo)
3
The Saul and Theresa Esman
Foundation has made a new pledge
for $832,000 to fund a postdoctoral
fellowship under the direction of Professor
Philip LoGrasso in the Department
of Molecular Therapeutics at Scripps
Florida. When combined with prior gifts,
the Foundation becomes our newest
$1 million benefactor. This gift is an
example of the ardent commitment by
Theresa Esman (pictured above) and
the Esman Foundation to basic science
research. Scripps Research is now the
leading recipient of the Foundation’s
philanthropic support of disease research.
(middle photo)
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• For more information about Scripps Research,
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cutting-edge research, please contact:
CALIFORNIA
(858) 784.2037 or (800) 788.4931
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(561) 228.2013
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