winter 2009

VOLUME 6 NUMBER 4 | WINTER 2009

From Research, The Power to Cure

InsIde >BURNhaM REsEaRch >PhIL aNThROPy

The Year in Translation

B U r n h a m R E P O R T

BL aIR BLUM Senior Vice President External Relations

ELIzaBETh GIaNINI Vice President External Relations

EdGaR GILLENWaTERs Vice President External Relations

chRIs LEE Vice President External Relations

aNdREa MOsER Vice President Communications

O N T h E c O V E R

It is the central tenet

of modern biology: The

information in our DNA

(right) is translated into

RNA (center), which

moves these coded

instructions from the

cellular nucleus and trans-

lates them into proteins

(upper left). In turn,

proteins are the machines that power virtually all aspects

of biology. Burnham scientists spend their careers studying

these interactions. Each year they learn more about how

cells function and what can go awry to cause disease.Burnham Institute for Medical Research10901 North Torrey Pines Road, La Jolla, CA 92037 • 858.646.3100

Burnham Institute for Medical Research at Lake Nona 6400 Sanger Road, Orlando, FL 32827 • 407.745.2000

Founders

WILLIaM h. F IshMaN, Ph.d. L ILLIaN FIshMaN

honorary Trustees

JOE LEWIs cONRad T. PREBys T. dENNy saNFORd

Trustees and Officers

GREG LUcIER Chairman

aL aN GLEIchER Vice Chairman

JOhN c. REEd, M.d. , Ph.d. President & Chief Executive Officer Professor and Donald Bren Presidential Chair

GaRy F. RaIsL, Ed.d. Executive Vice President Chief Administrative Officer Chief Financial OFficer Treasurer

MaRGaRET M. dUNBaR Secretary

Trustees

Mary BradleyBrigitte BrenArthur Brody

Trustees, continued

Malin BurnhamShehan Dissanayake, Ph.D.M. Wainwright Fishburn, Jr.Jeannie M. Fontana, M.D., Ph.D.David HaleJeanne Herberger, Ph.D.Brent JacobsJames E. Jardon II (Florida)Robert J. LauerFred Levine, M.D., Ph.D.Sheila B. LipinskyPapa Doug ManchesterRobert A. Mandell (Florida)Douglas H. ObenshainPeter PreussStuart TanzJan Tuttleman, Ph.D., MBAAndrew J. Viterbi, Ph.D.Kristiina Vuori, M.D., Ph.D.Bobbi WarrenAllen R. Weiss (Florida)Gayle E. WilsonDiane WinokurKenneth J. Woolcott

Ex-Officio

Raymond L. White, Ph.D.Chairman, Science Advisory Board

JOsh BaxT Editor, Burnham Report

GaVIN & GaVIN adVERTIsING Design

MaRk dasTRUPNadIa BOROWskI scOTTMELIssa JacOBsMaRTIN MaNNPhotography

Please address inquiries to: [email protected]

www.burnham.org

I N T h I s I s s U E

B U R N h a M R E s E a R c h

The Year in Translation 1

NCI-Designated Cancer Center 2

Del E. Webb Neuroscience, Aging and

Stem Cell Research Center 4

Infectious and Inflammatory Disease Center 6

Diabetes and Obesity Research Center 8

Sanford Children’s Health Research Center 10

Conrad Prebys Center for Chemical Genomics 11

UCSB-Burnham Center for Nanomedicine 12

P h I L a N T h R O P y

Meet Greg Lucier 14

The Power to Cure Gala 15

The Fishman Fund Awards 16

F I N a L T h O U G h T s

President’s Message 17

Partners in Science 18

The Year in Translation

Translation has a variety of definitions. It can mean translating one language into another. In scientific parlance, translation can describe how the information from our genetic code is converted into proteins. Also, translational research is the process by which basic scientific discoveries are moved from the laboratory to the clinic.

While these three defini-

tions describe very different

processes, they all apply

to the work being done at

Burnham. And 2009 was a

very good year for translation.

It is no secret that the

biological sciences have

a language all their own.

Complicated terminology is

often required to describe

complicated processes.

However, Burnham has

succeeded in making our

investigations more acces-

sible, and the world has

taken notice. In the past year,

Burnham science has been

described in the New York

Times, Wall Street Journal,

San Diego Union-Tribune and

Orlando Sentinel, as well as

on National Public Radio,

Fox Business News and many

other outlets. These stories

allow the world to see the

incredible work being done at

Burnham and help advance

scientific understanding.

In 2009, Burnham scien-

tists published more than

300 research papers, many

in high-profile journals. The

vast majority of these papers

illuminated some aspect

of translation. According

to Thompson Scientific, in

the past 10 years Burnham

research has received the

highest number of citations,

in biology and biochemistry,

of any institution publishing

more than 500 papers. In

other words, Burnham discov-

eries spark the creativity of

scientists around the world.

With the opening of

our new facility at Lake

Nona and a new Center

for Nanomedicine in Santa

Barbara, Burnham expands

both our basic and transla-

tional research capabilities.

New scientific and adminis-

trative leadership, as well as

multiple collaborations, will

advance the science and help

transform basic discoveries

into new medicines.

B U r n h a m d I a B E T E s R E s E a R c h

www.burnham.org | The BUrnham reporT 1

The Year in TranslationThe recently opened Conrad Prebys Center for Chemical Genomics facility at Lake Nona can conduct hundreds of thousands of assays to find chemical compounds that can alter protein function (see page 11).

B U r n h a m T h E y E a R I N T R a N s L a T I O N

2 The BUrnham reporT | www.burnham.org

BaTTLING METasTasIs

Metastasis is a word no one wants to hear. Cells that should

never leave their biological home migrate to distant parts of the

body. Many things have to go wrong with cellular checks and

balances for this to happen, yet it happens all too frequently.

To metastasize, cells must acquire a number of properties,

including the abilities to move,

survive in the bloodstream, cross

tissue boundaries and grow in

foreign organs. These last two

properties require the activity of

proteases, enzymatic proteins that

break down other proteins. Sara

A. Courtneidge, Ph.D., director

of the Tumor Microenvironment

Program, studies how the activity of

these proteases is controlled by cell

surface structures called invado-

podia. These finger-like projections

from the cell membrane are found

in metastatic cancer cells but not in

non-invasive cells. Dr. Courtneidge’s

laboratory discovered a protein,

called Tks5, which controls the formation of these invadopodia in

cancer cells.

Recently the Courtneidge laboratory showed, in an article

in Science Signaling, that reactive oxygens, such as superoxide

and hydrogen peroxide, play a key role in forming invadopodia.

Inhibiting reactive oxygen reduces invadopodia formation and

limits cancer cell invasion.

“Reactive oxygen has a complex cellular role,” says Dr.

Courtneidge. “Normal cells use reactive oxygen to signal, grow and

move. Immune cells, such as neutrophils, produce reactive oxygen

to destroy bacteria. Now we find that reactive oxygen is necessary

for invadopodia formation, which allows cancer cells to become

metastatic.”

ThE sEcRET WORLd OF PROTEINs

Ubiquitination is the process that marks proteins for destruc-

tion and is critical to cellular health. Recently, Dieter Wolf,

M.D., and colleagues, in an article in Molecular Cell, illuminated

how competition between proteins enhances diversity during

ubiquitination. Using S. pombe fission yeast as a model, the Wolf

laboratory uncovered an intricate relationship, in which an array of

proteins (called F-box proteins) alternately attach to and are kicked

off a protein called CRL1. There are 16 different types of F-box

proteins, and one of them must attach for CRL1 to fulfill its role of

marking a protein for destruction. If ubiquitination goes awry, aber-

rant proteins can accumulate and lead to diseases such as cancer.

Dr. Wolf ’s research shows that these proteins attach to CRL1

but are kicked off by the competing protein CAND1. F-box

proteins and CAND1 continue to trade places until they come in

contact with the appropriate part of the protein

being degraded.

“The tension between CAND1 and F-box

gives more F-box proteins the opportunity

to attach to CRL1,” says Dr. Wolf. “Without

CAND1, more prevalent F-box proteins would

dominate the process.”

Another way proteins communicate is

through enzymes called caspases (a type of

protease), which cleave, or nick, other proteins

to alter their function. Again, understanding

how this process works leads to a better under-

standing of how proteins collaborate and the

differences between healthy and diseased cells.

Using an advanced proteomic technique

called N-terminomics, Guy Salvesen, Ph.D.,

professor and director of the Apoptosis and

NCI-Designated Cancer Center

Dr. Sara A. Courtneidge

Invadopodia, seen as orange dots in this image, are found in metastatic cancer cells.

Cell Death Research

Program, graduate

student John Timmer

and others determined

the cleavage sites on

target proteins. Prior

to this study, published

in Nature Structural

and Molecular Biology,

scientists believed that

proteases primarily

cleave in unstructured

loops, unstable parts

of proteins that are

readily accessible. The

discovery that caspase-3

also cleaves α-helices contradicted that belief and offered new

insights into protein signaling pathways.

“This was a big surprise because there shouldn’t be anything

for a protease to grab onto in a helix,” says Dr. Salvesen. “We found

that the basic concept that they don’t cleave to helices is wrong.

However, though we’ve found that proteases can cleave helices, we

don’t believe that’s their biological function.”

Because they alter the functions of other proteins, proteases

like caspase-3 are critical to cell signaling. Understanding how

and where they interface with target proteins enhances our

ability to understand disease.

RENEWING ThE NcI -dEsIGNaTION

Every five years, Burnham’s Cancer Center competes for

renewal of its coveted NCI support grant. The process involves

a massive grant application, followed by a day-long site visit,

during which NCI sends experts to review the

Institute’s progress. This year, Burnham’s Cancer

Center received an overall rating of outstanding.

The NCI’s report noted:

“This center has many significant strengths in

terms of the quality of the basic science pursued

throughout its research programs and has made

noteworthy contributions to science that have

impacted cancer-related questions. Leadership

and planning and implementation mechanisms are

now in place to facilitate the synergy of its pool of

outstanding talent that can be directed at some of

the most fundamental processes driving the initia-

tion, growth and progression of cancer.”


www.burnham.org | The BUrnham reporT 3 www.burnham.org | The BUrnham reporT 3

Other Research HighlightskRIsTI INa VUORI, M.d. , Ph.d. , director of the

Burnham Cancer Center, and colleagues found that

Caspase-8, a protein long known to play a major role

in promoting programmed cell death (apoptosis), helps

relay signals that can cause cancer cells to proliferate,

migrate and invade surrounding tissues. For the first time,

Caspase-8 was shown to play a key role in relaying the

growth signals from the protein EGF that cause cell divi-

sion and invasion. Published in Cancer Research.

MINORU FUkUda, Ph.d. , and colleagues discovered

that specialized complex sugar molecules (glycans) that

anchor cells into place act as tumor suppressors in breast

and prostate cancers. These glycans play a critical role in cell

adhesion in normal cells, and their decrease or loss leads to

increased cell migration by invasive cancer cells. Published

in Proceedings of the National Academy of Sciences.

GaRy chIaNG, Ph.d. , and colleagues have

elucidated how the stability of the REDD1 protein is

regulated. The REDD1 protein is a critical inhibitor of the

mTOR signaling pathway, which controls cell growth and

proliferation. Published in EMBO Reports.

sTEFaN RIEdL, Ph.d. , and colleagues have deter-

mined the structure of the Fas/FADD protein complex

as the core component of the death inducing signaling

complex. This revealed a key mechanism in the induction

of programmed cell death and unraveled a novel mecha-

nism in receptor signaling. Published in Nature.

WEI J IaNG, Ph.d. , and colleagues have demon-

strated important new roles for the protein kinase complex

Cdc7/Dbf4 or Cdc7/Drf1 (Ddk) in

monitoring damage control during

DNA replication and reinitiating repli-

cation following DNA repair. Since

Ddk is often deregulated in human

cancers, this new understanding of its

role in DNA damage control could help

shape new cancer therapies. Published

in Molecular Cell.

Dr. Dieter Wolf

BURNHAM INSTITUTE for MEDICAL RESEARCH

Burnham recently published a report on our NCI-designated

Cancer Center. Progress on the Path to Cancer Cures is avail-

able by request. Contact Jane Langer at [email protected]

or 858-795-5288 to receive a copy.



The picture in the San Diego Union-Tribune showed a hand removing a sticker—a small action with deep significance. The sticker, and others like it, described federal restrictions on stem cell research. These rules dictated that federally funded equipment was off limits. When the restrictions were reversed, the stickers came off, and the promise of stem cell research could be pursued more effectively.

“The federal rules forced us

to operate kind of like a kosher

kitchen,” says Evan Snyder,

M.D., Ph.D., director, Stem

Cells and Regenerative Biology.

“We just couldn’t use federally

funded equipment, no matter

how inefficient that made the

science.”

When the ban was lifted,

world attention focused on

Burnham and other leaders in

stem cell research. The Wall

Street Journal, Fox Business

News, the BBC and many

other news outlets came to

Torrey Pines Mesa to find out

what these changes meant for

current science and future

treatments. For the scientists

who have dedicated their

careers to stem cell research,

this new freedom means

expanded opportunities to

translate stem cells into cures.

hOW dO sTEM cELLs FUNcTION?

One of the goals

of the Stem Cell and

Regenerative Biology

program is to under-

stand the processes

that help stem cells

decide whether to

differentiate, or not,

and what type of

tissue they should

differentiate into.

Alexey Terskikh,

Ph.D., is inves-

tigating the earliest neural

pathways taken by

differentiating embryonic

stem cells. He notes that cells

derived from the neural crest

(embryonic cells that give rise

to neurons, skeletal elements,

smooth muscle, etc.) become

peripheral cells throughout the

body—but how is that specifi-

cation acquired?

“When they start migrating,

they’re all the same. But then

they become specialized; they

know what they’re supposed to

do,” says Dr. Terskikh.

The ultimate goal is to

create cells for clinical use.

The Terskikh laboratory has

developed a protocol to rapidly

differentiate human embry-

onic stem cells into neural

progenitor cells that may be

ideal for transplantation. Their

research, published in Cell

Death and Differentiation,

could be adapted to produce

committed neural precursor

cells, one of the key require-

ments for clinical use.

TaRGETING BRaIN TUMORs

Recently, Evan Snyder,

M.D., Ph.D., in collaboration

with Mitchel Berger, M.D.,

chair of the UC San Francisco

Del E. Webb Neuroscience, Aging and

Stem Cell Research Center

When President Barack Obama reversed the federal restrictions on funding for

embryonic stem cell research, he raised the hopes of millions of people

around the world…Now that these unnecessary, indeed harmful, regulations have

been removed, American researchers can ethically and conscientiously pursue

these advances, accelerated by access to federal research funds.

Burnham President and CEO John C. Reed, M.D., Ph.D.,

in a March 27, 2009, op-ed in the San Diego Union-Tribune

Dr. Alexey Terskikh

Neural stem cells from the Terskikh laboratory.

Department of Neurosurgery, received a

disease team grant from the California

Institute for Regenerative Medicine.

The team, which includes the

Ludwig Institute, UC San Diego, and

UCLA, received more than $19 million

to study using neural stem

cells—genetically engineered

to contain a tumor-killing

gene—to home in on glio-

blastoma multiforme. This

approach is based on Dr.

Snyder’s discovery that stem

cells seek out cancer cells,

including primary and meta-

static brain tumor cells. In

addition, Dr. Snyder discov-

ered that stem cells could be

engineered to deliver a range

of genes, including tumor-

killing genes. The goal is to

launch a clinical trial within four years.

PROGREss ON NEUROdEGENERaTIVE dIsEasEs

There is a direct relationship between

how a protein is folded and what that

protein does. Many diseases can trace

their roots to problem proteins. This is

particularly true in neurodegenerative

diseases, which are commonly caused by

misfolded proteins.

Recently, Stuart Lipton, M.D.,

Ph.D., director of the Del E. Webb

Center for Neuroscience, Aging and

Stem Cell Research and colleagues

found that normal synaptic activity

in nerve cells (the electrical activity

in the brain that allows nerve cells to

communicate) protects the brain from

the misfolded proteins associated with

Huntington’s disease. They also found

that the drug Memantine, which is

approved to treat Alzheimer’s, success-

fully treated Huntington’s disease in

mice by preserving normal synaptic elec-

trical activity and suppressing excessive

extrasynaptic electrical activity.

“We show here, for the first time,

that electrical activity controls protein

folding, and if you have a drug that can

adjust the electrical activity to the correct

levels, you can

protect against

misfolding,”

says Dr. Lipton.

“This verifies

that appropriate

electrical

activity is

protective,

supporting the

concept of the

‘use it or lose

it theory’ of

brain activity at

the molecular

level. Published in Nature Medicine, this

finding may explain why epidemiologists

have found that ‘using’ your brain by

performing crossword puzzles and other

games can stave off cognitive decline in

diseases like Alzheimer’s.”

Burnham researchers also made prog-

ress in understanding Alzheimer’s disease.

Huaxi Xu, Ph.D., acting director of the

Neurodegenerative Disease Research

program, and others identified a novel

mouse gene that reduces the accumula-

tion of two toxic proteins that are major

players in Alzheimer’s: amyloid beta and

tau. Amyloid beta is responsible for the

plaques found in the brains of Alzheimer’s

patients. Tau causes the tangles found

within patients’ brain cells. The study

was published in Neuron.

“From the point of view of treating

Alzheimer’s disease, if we can express

the mouse gene in human brain cells,

we may be able to control the buildup

of amyloid beta and tau neurofibrillary

tangles,” says Dr. Xu.



Dr. Huaxi Xu

Other Research Highlights

Proteins play a key role in determining stem

cell fates, and phosphorylation (the biochemical

process that modifies proteins by adding a phos-

phate molecule) is central to protein activity.

EVaN sNydER, M.d., Ph.d., director of

Burnham’s Stem Cell and Regenerative Biology

program, and LaURENcE BRILL, Ph.d., and

others have catalogued 2,546 phosphorylation

sites on 1,602 phosphoproteins. Identifying these

sites will help us understand the mechanisms

that influence self-renewal and differentiation.

Published in Cell Stem Cell.

A great deal of work has been done on aging as

a systemic process throughout the body, but now

researchers are looking more closely at how aging

affects individual organs. ROLF BOdMER, Ph.d.,

director, Development and Aging, has found

that the protein d4eBP controls cardiac aging

in Drosophila (fruit flies). The team also found

that d4eBP protects heart function against aging.

Published in Aging Cell.

GREGG dUEsTER, Ph.d., xIaNLING zhaO,

Ph.d., and colleagues have clarified the role

that retinoic acid plays in limb development.

The study showed that retinoic acid controls the

development (or budding) of forelimbs, but not

hindlimbs, and that retinoic acid is not respon-

sible for patterning (or differentiation of the parts)

of limbs. This research corrects longstanding

misconceptions about limb development and

provides new insights into congenital limb defects.

Published in Current Biology.

ThE LIPTON LaBORaTORy has demonstrated

that attacks on the mitochondrial protein Drp1

by the free radical nitric oxide—which causes a

chemical reaction called S-nitrosylation—mediates

neurodegeneration associated with Alzheimer’s

disease. Prior to this study, the mechanism by which

beta-amyloid protein caused synaptic damage to

neurons in Alzheimer’s disease was unknown. These

findings suggest that preventing S-nitrosylation of

Drp1 may reduce or even prevent neurodegeneration

in Alzheimer’s patients. Published in Science.



NEW sTRaTEGIEs, NEW INsIGhTs

Viruses may have invented

planned obsolescence.

Humans, and other higher

organisms, have sophisticated

error-correction mechanisms

to carefully limit the number

of mutations in our DNA.

Not so with viruses. In fact,

they are designed to mutate

to better evade our immune

systems. But occasionally, a

viral protein is resistant to

mutation because its function

is so complex any changes

would render it useless.

In February, Robert

Liddington, Ph.D., director,

Infectious Disease Program,

along with collaborators at the

Dana-Farber Cancer Institute

and the Centers for Disease

Control, found such a vulner-

ability in the influenza virus.

The team identified human

monoclonal antibodies that

neutralize numerous influenza

viruses, including bird flu,

previous pandemic influenza

viruses and potentially H1N1.

The study was published

in Nature Structural and

Molecular Biology.

“The head portion of

hemagglutinin (the protein

that binds the virus to a cell)

is highly changeable, leading

to forms of the virus that can

evade neutralizing antibodies,”

says Dr. Liddington. “However,

the stem region of hemag-

glutinin is highly conserved

because it undergoes a dramatic

conformational change to allow

entry of viral RNA into the host

cell. It’s very difficult to get a

mutation that doesn’t destroy

that function,

which explains

why these

antibodies

neutralize

such a variety

of influenza

strains.”

The ripples

from this

paper were

felt worldwide.

With interna-

tional concern

over the

avian flu, the

possibility that

researchers

might have found a way to

target multiple influenza strains

garnered considerable interest.

Hundreds of news outlets,

including CNN, the New York

Times and Time Magazine,

reported on this breakthrough,

and interest continued for

several weeks.

As fall approached and

H1N1 (swine) flu became

a growing concern, there

was renewed interest in

this research. In October,

Burnham sponsored an

experts panel to sort fact from

fiction in the H1N1 discus-

sion. The panel featured Dr.

Liddington; Steve Waterman,

M.D., medical epidemiologist

for the Centers for Disease

Control; Patricia Skoglund,

R.N., administrative director

of Disaster Preparedness for

Scripps Health; and Nathan

Fletcher, state assemblyman

representing California’s 75th

District. The panel was moder-

ated by former San Diego

newscaster Carol LeBeau. The

Infectious and

Inflammatory Disease Center

Dr. Robert Liddington

Image of the influenza virus hemagglutinin bound to neutralizing antibodies (in red). Most antibodies

bind to the head region, which is highly variable. However, the stalk region cannot mutate because it

is part of a complex molecular machine required to enter the cell. Liddington laboratory



Other Research HighlightsaNdREI OsTERMaN, Ph.d. , in collaboration with the

University of Texas Southwestern Medical Center and University of

Maryland, demonstrated that an enzyme essential to the survival of

many bacteria can be targeted by chemical compounds that inhibit

the enzyme and suppress bacterial growth. These findings are essen-

tial to developing new antibiotics to overcome multidrug resistance.

Published in Chemistry and Biology.

GIOVaNNI PaTERNOsTRO, M.d., Ph.d., adjunct professor

in Burnham’s Cancer Center, and colleagues showed that search

algorithms used in digital communications can help scientists iden-

tify effective multi-drug combinations, particularly combinatorial

cancer therapies. As personalized medicine moves from the present

emphasis on diagnosis and prognosis to therapy, physicians will need

to find drug combinations that are uniquely suited to the genetic

and molecular profile of each patient. This research is a first step in

that direction. Published in PLoS Computational Biology.

ROBERT RIckERT, Ph.d. , and colleagues have provided

evidence that suppressing the PI3-kinase signaling pathway is a

hallmark of anergic (inactivated) B cells. This work sheds light on

the biochemical basis of B cell anergy and may provide insights into

human autoimmune diseases characterized by broad autoantibody

production. Published in Immunity.

sUMIT chaNda, Ph.d. , and colleagues have assembled

an encyclopedia of cellular proteins reported to be important for

HIV replication. Using interaction mapping and bioinformatic tools,

the team identified biochemical complexes and biological pathways

that were common to these studies. This study reconciles previously

published host/pathogen interaction data and provides an important

road map to develop host factor-mediated antivirals. Published in

PLoS Pathogens.

hour-long event discussed flu

dangers, distinctions between

flu varieties, vaccinations,

common sense precautions

and how state and local orga-

nizations and agencies are

preparing for the flu. The event

was videotaped by UCSD-TV

and can be found, along with

a web chat on the flu with Dr.

Liddington, at www.burnham.

org/pandemicflu.

MaPPING a PROTEIN NETWORk

There are various ways

to test a hypothesis: in vitro

methods use cells in a dish

or test tube; in vivo uses a

living organism. Burnham’s

Bioinformatics and Systems

Biology Program is helping

develop another method: in

silico, or in a computer. Adam

Godzik, Ph.D., with colleagues

at UC San Diego, The Scripps

Research Institute, Genomics

Institute of the Novartis

Research Foundation and

other institutions, recently

constructed a complete model,

including three-dimensional

protein structures, of the central

metabolic network of the bacte-

rium Thermotoga maritima (T.

maritima). Published in Science,

this is the first time researchers

have developed such a compre-

hensive model of a metabolic

network overlaid with an atomic

resolution of network proteins.

Combining biochemical

studies, structural genomics

and computer modeling, the

researchers deciphered the

shapes, functions and interac-

tions of 478 proteins that

make up T. maritima’s central

metabolism.

“We have built an actual

three-dimensional model of

every protein in the central

metabolic system,” says Dr.

Dr. Adam Godzik

Godzik, director, Bioinformatics

and Systems Biology Program.

“We got the whole thing. This

is analogous to sequencing an

entire genome.”

This information has the

promise to expand computer

modeling to allow investigators

to simulate the interactions

between proteins and various

compounds in an entire system.

Furthermore, the procedure

developed in this study could

be applied to study many other

organisms, including humans.

It could potentially help identify

both positive and adverse drug

reactions before pre-clinical and

clinical trials.

NEW FacILITy, NEW cOLLaBORaTIONs, NEW scIENcE

On October 8, more than 900 people, including Florida

Governor Charlie Crist, helped Burnham dedicate our new

175,000-square-foot scientific facility at Lake Nona in Orlando,

Florida. This is the first facility to open in Lake Nona’s Medical

City, which will be a hub for medical research to advance scien-

tific discoveries and breakthrough therapies.

“We have established a foundation by bringing new expertise

to the region and

forging strong

alliances that

will enhance and

accelerate scientific

opportunities,” said

John Reed, M.D.,

Ph.D., president

and CEO, professor

and Donald Bren

Presidential Chair.

“Burnham’s collab-

orative approach

has been very successful. We are transferring that model to the

Lake Nona campus in Orlando, where scientists are conducting

research in metabolic disorders, heart disease and cancer.”

Burnham’s Lake Nona facility was designed to maximize an

array of sophisticated technolo-

gies that will help researchers

answer some of the most funda-

mental questions about human

biology. The Conrad Prebys

Center for Chemical Genomics

facility at Lake Nona, like its

counterpart in La Jolla, will iden-

tify small molecule compounds

that can help regulate proteins implicated in disease (see page

11). In addition, the Cardiovascular Pathobiology and Metabolic

Signaling and Disease programs will study type 2 diabetes, heart

disease and other conditions. This will be supported by the

Cardiometabolic Phenotyping Core, which will study cardiovas-

cular complications and metabolic disturbances in mouse models

of human diseases.

METaBOLOMIcs

Researchers are particularly excited about the new facility’s

emerging metabolomics capability. Burnham is collaborating with

the Sarah W. Stedman Nutrition and Metabolism Center (Stedman

Center) at Duke University Medical Center to use metabolite

profiling to clarify the basic mechanisms of disease, identify

biomarkers for diagnosis and monitor treatment. The recent agree-

ment establishes an extension of Duke’s Stedman Center laboratory

at Burnham’s Lake Nona campus and combines the Stedman

Center’s metabolomics expertise with Burnham’s complementary

technologies. But what is metabolomics?

“Metabolomics is the survey of the small molecule metabolites

in the body,” says Stedman Center Director Christopher Newgard,

Ph.D. “I think a good way to describe it is the chemical fingerprint.

What we’re really talking about is the fundamental way that we

process genetic information. It starts at the gene, then you make

messenger RNA, you make proteins, but the end result of all of that

genetic machinery is to affect

the chemistry of the body.”

In short, metabolomics will

provide a rapid way to analyze

chemicals (metabolites)

in the body and determine

the processes that created

those chemicals. Once these

compounds have been traced

to their genetic source, clinicians will use these metabolite

profiles as a powerful diagnostic tool to uncover diseases at their

earliest stages and determine the specific nature of the disease.

Dan Kelly, M.D., Scientific Director of Burnham at Lake Nona,

sums up the importance of this technology: “How do we begin to,

identify the individual who’s most at risk for developing diabetes? Can



Diabetes and Obesity Research Center

Florida Governor Charlie Crist and Malin Burnham at the dedication ceremony

Burnham’s Lake Nona facility was designedto maximize an array of sophisticated

technologies that will help researchers answer some of the most fundamental questions about human biology.

Greg Lucier, Dr. John Reed, Malin Burnham and Dr. Daniel Kelly tour the Conrad Prebys Center for Chemical Genomics.

we come up with personalized markers? The Stedman Center has

already begun to find chemical markers that identify individuals who

might go on to develop insulin resistance and diabetes. This technology

could also be applied to heart disease and different forms of cancer—

both in making a diagnosis and looking at the severity of the disease.

“The bottom line is: how do we individualize treatment?”

cOLL aBORaTIONs

Collaborating with clinical institutions is a key element of

Burnham’s strategy to rapidly move discoveries from the laboratory to

the clinic. In fact, just prior to the dedication ceremony, the University

of Florida announced that they too will build a facility in the Medical

City. Their presence will add additional firepower to an already potent

lineup of Burnham partners, including M.D. Anderson Cancer Center

Orlando and the University of Central Florida.

The Florida Hospital-Burnham Translational Research Institute

(TRI) is a great example of how these basic research/clinical part-

nerships will work. The TRI combines scientists and clinicians with

incredible technologies to enhance translational research and bring

new treatments to patients. Recently, Steven R. Smith, M.D., was

recruited as the TRI’s executive director, one of many new faculty

brought to Lake Nona in 2009.

Dr. Smith’s work bridges the gap between cellular and molecular

biology and clinical care. His research is focused on obesity, diabetes

and the metabolic origins of cardiovascular disease. Specifically, Dr.

Smith investigates why some people burn fat when fed a fatty diet

while others fail to burn fat and develop health problems like diabetes.

He is also trying to understand how obesity leads to type 2 diabetes and

examining the relationship between inflammation and diabetes.

“We recently discovered that in some obese people, adipose

(fat) tissue becomes hypoxic (starved of oxygen) because there are

not enough small blood vessels,” says Dr. Smith. “This leads to

inflammation in adipose tissue. There is a growing body of science

that shows that inflammation is a major player in the development

of type 2 diabetes.”

On the clinical side, Dr. Smith wants to identify and validate

drugs to treat obesity and diabetes. His translational work has

demonstrated that everyone is unique at the molecular level,

suggesting new ways to match therapies to the individual—in

other words, personalized medicine.

“One new area that I will be working on in Florida is using anti-

obesity drugs to treat diabetes,” says Dr. Smith. “We know that the

first 10 to 15 pounds lost has a big impact on blood sugar control

and metabolism. Many diabetes drugs cause weight gain. Since

most people become diabetic because they are overweight, we

believe that weight gain is not a desirable effect of diabetes drugs.

Weight loss can also prevent the development of diabetes.”



Dr. Steven R. Smith

dR. daNIEL kELLy hONOREd FOR GROUNdBREakING REsEaRch

Burnham at Lake Nona’s Scientific Director Daniel

P. Kelly, M.D., has been awarded the American Heart

Association’s 2009 Basic Research Prize, which recognizes

his work on molecular biology and the physiology of cardiac

metabolism and his vision of how basic research can trans-

late into treatments.

Dr. Kelly’s research focuses on problems in cardiac

energy metabolism. His investigations outline metabolism

in normal and diseased hearts and the impact of obesity

and diabetes on cardiac function. His pioneering work in

fuel and energy metabolism is defining new classes of drug

targets and sets the stage for more personalized therapies.

Burnham at Lake Nona


Sanford Children’s Health Research Center

In late 2007, the Sanford Children’s Health Research Center was established at Burnham’s San Diego campus with a $20 million gift from South Dakota philanthropist Denny Sanford through Sanford Health. The gift was the foundation for a long-term collaboration between Sanford Health of Sioux Falls, South Dakota, and Burnham.

The collaboration combines world-class scientific talent with

state-of-the art technology to conquer childhood diseases like

type 1 diabetes, muscular dystrophy and many others. In addition

to the center in La Jolla, Sanford Health has created a Children’s

Health Research Center in Sioux Falls. Together, Burnham and

Sanford Health are establishing an integrated, academic/pediatric

research network.

Recently, Sanford researchers from Sioux Falls and La Jolla

met for the Second Annual Sanford Scientific Symposium to share

their research and discuss how best to move forward with efforts

to cure childhood diseases. Held at Burnham’s La Jolla campus,

the symposium addressed the convergence of basic scientific and

clinical research and how the collaborations between Burnham

and Sanford Health could lead to new treatments.

“This collaboration is working on many levels,” says Fred

Levine, M.D., Ph.D., director, Sanford Children’s Health

Research Center. “Scientists from Sioux Falls and Burnham are

periodically comparing research findings. One scientist from La

Jolla has been recruited to Sioux Falls, and others are applying

for positions there. So we are developing the cross-pollination we

hoped to achieve, and that will lead to new and important insights

into childhood diseases.”


Other Research HighlightsTaRIq RaNa,

Ph.d. , recently showed

how a microRNA (a

short, noncoding strand

of RNA) plays a key role

in controlling the HIV

life cycle by transporting

HIV messenger RNA to

processing bodies inside

cells, where it is stored

or destroyed. This results

in a reduction of viral

replication and infectivity.

While, on the surface, this may seem like a good result, Dr. Rana

believes that HIV may be co-opting this cellular defense mecha-

nism to help the virus hide from immune defenses and antiviral

drugs. Published in Molecular Cell.

PaMEL a ITkIN- aNsaRI , Ph.d. , and colleagues recently

demonstrated in mice that transplanted pancreatic precursor

cells are protected from the immune system when encapsu-

lated in polytetrafluorethylene, suggesting a new approach

to treating type 1 diabetes. Dr. Itkin-Ansari showed that the

precursor cells matured into functional beta cells that were

glucose-responsive and

controlled blood sugar levels.

Published in Transplantation.

yU yaMaGUchI, M.d. ,

Ph.d. , along with collabo-

rators at the University of

Connecticut Health Center,

showed that mice, in which

the gene Has2 was inactivated

in the limb bud mesoderm,

had shortened limbs, abnormal

growth plates and duplicated

bones in fingers and toes. The

Yamaguchi laboratory genetically modified the Has2 gene so that

the gene can be conditionally disrupted in mice. This is the first

time a conditional Has2 knockout mouse has been created, a

breakthrough that opens vast possibilities for future research.

Published in Development.

JOsé LUIs MILL áN, Ph.d. , studies a horrible and often

fatal disease called Infantile hypophosphatasia (HPP). A rare form of

rickets, HPP makes bones dangerously fragile. When HPP patient

“Baby Amy” was flown from her home in Ireland to Winnipeg,

Canada, she was transported in an insulated box to prevent her bones

from breaking. However, after receiving an enzyme replacement

therapy developed by Dr. Millán and others, she was healthy enough

to be held by her mother and make the trip home to Ireland.

Dr. Yu Yamaguchi

Dr. Tariq Rana

IN sEaRch OF NEW

MEdIcINEs

In 2001, Burnham leader-

ship, as part of the Institute’s

10-year plan, decided to pursue

the study of chemical genomics.

This decision was not without

risk, as creating the scientific

infrastructure would require a

large capital investment. On

the other hand, the potential

rewards were immense. Much

of the science at Burnham

involves asking important ques-

tions about how genes and

proteins function. Chemical

genomics is a powerful way

to answer many of those

questions.

Now, eight years later,

scientists at the Conrad

Prebys Center for Chemical

Genomics are carrying out

the formidable task of finding

chemical compounds that can

alter protein function. Robotic

screening systems test large

chemical libraries (with nearly a

half million compounds) against

biological material—like a

single protein or a specific type

of cancer cell. These screens

are intended to find the handful

of molecules that can regulate

a specific gene or protein by

turning it on or off.

A chemical “hit” can have a

number of uses. The ability to

manipulate a protein can help

researchers determine what that

protein does. In some instances,

a compound may have drug-like

properties that can be optimized

by medicinal chemists and

pharmacologists and perhaps

advanced to clinical trials.

a sOUNd dEcIsION

Burnham’s expertise in

chemical genomics has been

recognized nationwide and has

become a magnet for public

and private investment. In

September 2008, Burnham was

awarded a $98 million grant

to establish a comprehensive

screening center as part of the

National Institute of Health’s

Molecular Libraries Probe

Production Centers Network—

one of only four such screening

centers in the country.

In early 2009, Burnham

signed an assay develop-

ment and license agreement

with Johnson & Johnson

Pharmaceutical Research

and Development (J&JPRD),

Burnham’s first broad-based

partnership with a large phar-

maceutical company. Under this

multi-year agreement, Burnham

will provide J&JPRD with

access to screening technologies

to investigate drug targets for

inflammatory diseases.

In January 2009, Conrad

Prebys donated $10 million

to name the screening center.

For Prebys, a longtime San

Diego real estate developer, the

decision to support chemical

genomics was built on his desire

to make a significant impact.

“I lost four close friends

to cancer last year—one to a

leukemia I didn’t even know

existed,” said Prebys at the time

of his gift. “I have been very

blessed in my life, and some

times I wonder why. The only

answer I can come up with is

that I’m here to do some good in

the world.”

MOVING dIscOVERIEs

TO ThE cLINIc

Burnham recently

appointed Michael R. Jackson,

Ph.D., to the newly created

position of vice president

for Drug Discovery and

Development. In this role, Dr.

Jackson will oversee the chem-

ical biology and drug discovery

efforts at the Prebys Center

facilities in La Jolla and Lake

Nona. He will lead Burnham’s

efforts to identify drug candi-

dates—developing promising

chemical compounds into new

medicines and creating part-

nerships for preclinical and

clinical drug development.



Conrad Prebys Center for Chemical Genomics

“The idea of saving just one life is remarkable, but

the opportunity to use this technology to find cures

that will affect millions of people, that’s incredible.”

Conrad T. Prebys

Burnham’s expertise in chemical genomics has been recognized nationwide and has become a magnet for public and private investment.

Conrad T. Prebys

Nanoparticles, like this micelle, may be the future of medicine.

scIENcE aNd scIENcE FIcTION

Burnham distinguished

professor Erkki Ruoslahti,

M.D., Ph.D., sits in his

office at UC Santa Barbara

and ponders the relationship

between science and science

fiction. He is discussing Star

Trek’s sophisticated hand-held

medical devices and all they

could do for patients.

“Ideally, you would like to

have a device like Dr. McCoy’s

that could both diagnose and

treat,” says Dr. Ruoslahti.

“I think eventually we will

have devices like small MRI

machines that can do just

that.”

Though this level of

technology is still many years

off, Dr. Ruoslahti is leading

projects that might seem

like science fiction. A former

Burnham president and CEO,

Dr. Ruoslahti established

the Burnham connection to

UCSB in 2006. He is building

on his earlier discovery that

a peptide (a piece of protein)

called RGD is attracted to cell

attachment proteins called

integrins. What makes this so

important is that tumor blood

vessels express RGD-binding

integrins, allowing researchers

to custom-make peptides that

home in on tumors.

Taking that a step further,

Dr. Ruoslahti has been

collaborating with engineers

at UC Santa Barbara to build

medicine-containing nanopar-

ticles. By combining these two

technologies, researchers hope

to create therapeutic nanopar-

ticles that home directly to

a cancer and release their

therapeutic payloads inside

the tumor.

“We have

succeeded in

putting targeting

molecules on

nanoparticle

drugs and have

shown that they

are more effec-

tive and less

toxic,” says Dr.

Ruoslahti.

FILLING IN ThE PUzzLE

Jamey Marth,

Ph.D., who

directs the new

joint Center for Nanomedicine

established by Burnham and

UC Santa Barbara, began his

career studying genes. In fact,

he helped develop Cre-loxP

technology, which is used

by researchers worldwide

to selectively remove genes

to study their functions in

specific cells and tissues at

specific times. But over time,

Dr. Marth realized that there

was more to cells than what

DNA, RNA and proteins were

teaching us.

“We have been looking to

genes to find the origins of

disease,” says Dr. Marth, “but

genomic variation has not

explained the origins of many

common grievous diseases,

such as diabetes, autoimmune

conditions and various neuro-

degenerative disorders.”

When his research

revealed that mechanisms

responsible for at least some of

these diseases were attributed

to non-genetic alterations of

cells, Dr. Marth began to see

things differently.

“Genes and proteins are

important, but cells are also

made up of two other major

structural components:



UC Santa Barbara– Burnham Center for Nanomedicine

Dr. Erkki Ruoslahti

glycans (sugars) and lipids

(fats). We need to come to a

better understanding of how

they operate and malfunction

in causing disease.”

Dr. Marth notes that

glycans and lipids are much

more difficult to study because

they are not template-driven.

In other words,

a specific

sequence

of DNA is

a template

for a specific

sequence of

RNA, which

in turn creates

a sequence of

amino acids

that build a

protein. Lipids

and glycans,

on the other

hand, are not

so easy to

trace.

“There

will continue

to be profound discoveries in

the genome, but we’re going

to miss things if we don’t look

at the cell in a more holistic,

rigorous way,” says Dr. Marth.

“We need to develop high-

throughput structural analysis

of glycans and lipids so we

can see inside that black box.

Nanotechnology is the best

way to achieve this and incor-

porating these components

more broadly into nanomedi-

cine is expected to further

enrich our current approaches

to diseases that we still have

trouble treating effectively.”

a MaRRIaGE OF BIOLOGIsTs aNd ENGINEERs

One of the main reasons

Drs. Ruoslahti and Marth set

up labs at UC Santa Barbara

was to take advantage of

the university’s world-class

engineering.

“Because of my knowledge

of homing peptides, engineers

began approaching me about

using this technology to help

target nanoparticles,” says

Dr. Ruoslahti. “I realized

that molecular biology and

chemistry have made great

contributions to medicine, but

we needed to do more. It was

time to also focus on physics.”

When the UCSB-Burnham

Center for Nanomedicine

was created in summer 2009,

it was built on the idea that

fruitful collaborations between

biologists, chemists, physicists,

engineers and others could

lead to amazing breakthroughs.

“The typical approach has

been to start from the biomed-

ical side by cherry-picking a

few talented engineers and

moving them out of their

comfort zone into a biomedical

research environment,” says

Dr. Marth. “But here we have

done the opposite and started

with an environment rich

with superb engineers. We

are creating a collaborative

environment without walls

between disciplines and that

will lead to new approaches

and new knowledge and will

give us the best opportunities

to develop needed advances in

diagnostics and therapeutics

for disease prevention, treat-

ment and cure.”



What is Nanomedicine?

Dr. Jamey Marth

Rudolph Virchow, the father of pathology, noted that “all

diseases are reducible to active or passive disturbances of cells.”

Unfortunately, most medical technologies are designed to func-

tion more on the macro than the cellular level. Surgery deals with

large masses of cells or entire organs. Many medicines, including

chemotherapies, are delivered through the bloodstream and affect

most of the body. Radiation, both for treatment and diagnosis, also

works on a larger scale.

On the other hand, biological research over the past 50 years

has focused on key parts of the cell, including genes and proteins.

Nanomedicine seeks to redefine treatment and diagnosis by

engineering microscopic devices with multiple functions to focus

on the cellular roots of disease. Using impossibly tiny machines

(some as small as a nanometer, one millionth of a meter),

researchers and physicians hope to diagnose and treat cancer,

diabetes and heart disease; repair tissue damaged by trauma; and

diagnose life-threatening conditions on the cellular level, long

before there are recognizable symptoms.

Greg Lucier knows biotechnology. As Chief Executive Officer of Life Technologies (the parent company of Invitrogen and Applied Biosystems), one of the world’s largest providers of systems, reagents and services to support biomedical research, Lucier under-stands what it takes to succeed in the labora-tory. In fact, you can hardly turn a corner at Burnham without seeing Life Technologies products being used to perform critical experiments.

Lucier has been a

Burnham trustee since

2005 and succeeded Malin

Burnham as board chair in

October. He chose to volun-

teer his time and effort at

Burnham for several reasons.

Naturally, the Institute

provides a great complement

to his “day job.” Lucier was

also attracted to Burnham

by the Institute’s strong

leadership.

“I have been really

impressed by Dr. Reed, Dr.

Vuori and others,” says Lucier.

“I like working with the best,

and Burnham has the best.”

But most importantly, he

is a fervent believer in the

work that Burnham accom-

plishes every day.

“Basic research

is the foundation for

future commercial

application,” says

Lucier. “A devel-

oped country like

the United States

is morally bound to

fund basic research

because of the multi-

plier effect. Whether

the multiplier is

saving lives by curing

disease, coming up

with new methods to

improve food produc-

tion or finding new

ways to make fuel

from biological mate-

rials, this is critically

important work.”

a BUsy sEasON

Lucier takes over board

leadership at a very hectic time.

One of his first duties was

helping dedicate Burnham’s

new Lake Nona facility.

“I was blown away by the

excitement at Lake Nona,”

says Lucier. “The facility looks

great, but I was really impressed

by how passionate the entire

community is. Scientists,

administrators, government

leaders, local supporters—they

were all ready to go.”

In addition to opening the

Lake Nona facility, Burnham

expanded its presence at UC

Santa Barbara and acquired

new facilities on Torrey Pines

Mesa. Lucier knows there is a

great deal to be accomplished

in the next few years, but feels

strongly that Burnham has

the right people in place for

continued success.

LOOkING FORWaRd

In the coming years, Lucier

sees Burnham playing a signifi-

cant role in redefining how

biomedical research is done.

“I believe we are going to

see new models for research,”

says Lucier. “We have the

opportunity to bring together

universities, independent

academic institutions, contract

research organizations, phar-

maceutical companies and

other organizations to advance

the science and bring us closer

to new treatments. We are

already seeing this kind of

collaboration, both in La Jolla

and Lake Nona, and it is our

job to make sure we continue

to expand those partnerships.”

Lucier notes that he and

the other members of the

board of trustees are very

excited about where Burnham

is going.

“Our role is to work with

Burnham leadership to bring

the organization to the next

level, just as previous boards

have done. We’re here to look

after the short and long-term

welfare of the institution

through advice, financial

support, moral support and

good governance. This is

an incredible moment in

Burnham’s history, and I am

very pleased to be a part of it.”


p h I l a n T h r o p y U P d a T E

Meet Greg Lucier



The Power to Cure Gala 2009

On Saturday, November 14, more than 250 people gathered at the Hyatt Regency La Jolla Aventine for The Power to Cure Gala.

The Hyatt ballroom was

draped in deep blue, floor

to ceiling fabric, and micro-

scopic images from Burnham

laboratories, printed on 8-foot

canvases, transformed the

ballroom into a science gallery.

During the live auction, the

fund-a-need raised support for

Burnham’s work in

cancer, infectious

and inflammatory

diseases, childhood

diseases, aging and

neurodegeneration.

Also, guests bid on

vacations, an intern-

ship in Dr. John

Reed’s laboratory and

dinner at the exclu-

sive French Laundry restaurant

in Napa Valley.

In all, the gala raised more

than $950,000 to support

medical research.

Many thanks to gala co-

chairs Caroline Nierenberg

and Kathryn Stephens and

presenting sponsor Life

Technologies. For information

about the Burnham Gala or

to make a donation, please

contact Chelsea Jones at

858-795-5239 or cjones@

burnham.org.Gala co-chairs Kathryn Stephens and Caroline Nierenberg

Lydia McNeil raises her bid card T. Denny Sanford Peggy and Peter Preuss

Dr. John Reed Joan and Brent Jacobs

On October 15, the Fishman Fund awarded grants to five Burnham postdoctoral fellows to recognize their commitment to biomedical science. The researchers each received $5,000 to further their education and career development. The Fishman Fund was created by philanthropists Mary Bradley and Reena Horowitz to advance science and honor Burnham founders Dr. William and Lillian Fishman.

During their postdoc-

toral fellowships, young

researchers receive training

and hands-on experience as

they launch their scientific

careers. This year’s honorees

investigate fundamental

biological processes that

may yield new insights into

cancer, heart disease, HIV

and other conditions.

dR. PIL aR cEJUdO-

MaRTIN , of the Courtneidge

laboratory, seeks to under-

stand the roles certain

proteins play in mammalian

development. This work may

also be applicable to Frank-

Ter Haar syndrome, in which

one of these proteins is

mutated and patients do not

live beyond their teens.

dR. MaRTIN dENzEL ,

of the Ranscht laboratory,

investigates how different

organs communicate with one

another. Specifically, he is

analyzing the cardiovascular

role of adiponectin, a hormone

secreted by fat tissue.

dR. FaBIaN FILIPP ,

of the Jeff Smith laboratory,

uses magnetic resonance

spectroscopy to take a “snap-

shot” of all metabolically



An Avid SupporterMore than 100 people attended the reception to honor these scientists, among them philanthropist Sascha Siegel, a Fishman Fund supporter.

“What better way to further humanity than to support the career of a young scientist entering the world of research,” says Siegel, who learned the value of giving back to her community during World War II in England. Her family home had been destroyed during a bombing raid and, at 17, she volunteered to

be an ambulance driver. Later she became a military intelligence officer in the British Army.

“All the men, including my brothers, had left home to fight for Britain,” says Siegel. “It was then I real-ized the need to give back.”

Siegel moved to the United States

in the 1940s and built a family and a career as a fashion designer and television talk show host. But she has never forgotten the lessons she learned in war-torn England.

“I thought I’d open the door a little bit wider for these bright men and women by making an estate gift to the Fishman Fund so that the fund can continue to support this excellent science.”

Sascha Siegel and Lillian Fishman

Honoring Young Scientists

active compounds in a

cell. This novel approach

identifies diagnostic

markers for clinical

use and suggests new

drug targets for cancer

therapies.

dR. L aRs PachE ,

of the Chanda laboratory,

works to understand the

biological mechanisms that help HIV and influenza. The laboratory selectively silences cellular genes to determine how these genes aid or perturb viral infection. This work may eventually

lead to new treatments for

numerous pathogens.

dR. NaI -y ING

MIchELLE yaNG , of

the Pasquale laboratory,

investigates Eph proteins

in prostate and breast

cancer. These proteins

have been shown to

promote or suppress

tumor progression under

different circumstances.

p r e s I d e n T ’ s M E s s a G E


15. JohnReedessay

John C. Reed, M.D., Ph.D.

President and CEO

Professor and Donald Bren

Presidential Chair

An Amazing Year

As the year 2009 draws to a close, we reflect on our progress and take pride in the many

accomplishments that have advanced our medical research mission, giving hope to those

suffering from disease.

By all accounts, 2009 has been a great year for Burnham. Multiple breakthroughs were

made in our efforts to reveal the fundamental causes of disease and to develop innovative

prototype therapeutics.

This year, Burnham gained the top ranking in publication quality, with more cita-

tions per publication than any other organization worldwide in the fields of Biology and

Biochemistry for the decade 1999-2009 (among all organizations publishing at least 500

papers). We owe much of this success to our commitment to collaborative, team-based

science. In 2009, we surpassed the milestone of more than 500 issued patents based on

Burnham inventions. Moreover, according to U.S. government statistics, Burnham ranks

second in the nation in capital efficiency, as defined by the number of patents generated

per grant dollars spent.

This year, we grew to more than 1,000 staff and filled several key leadership positions.

Dr. Gary Raisl joined us as Chief Administrative Officer and Chief Financial Officer. Dr.

Paul Laikind is our new Chief Business Officer. Dr. Michael Jackson was recruited as

Vice President for Drug Discovery and Development. Dr. Jamey Marth came to Burnham

to direct the UCSB-Burnham Center for Nanomedicine. Dr. Tim Osborne joined us as

director of the Metabolic Disease and Signaling program at our new facility in Lake Nona.

Dr. Steve Smith directs the Florida Hospital-Burnham Translational Research Institute.

And, Dr. Steve Gardell directs Translational Research Resources. Truly, it has been an

incredible year of team building as we position our organization for future success.

In October, Malin Burnham stepped down as Board of Trustees Chair after a very

successful two-year term, and Greg Lucier has assumed that position. He will help us

develop our strategy for the next decade, as we near the end of our current 10-year plan

and begin thinking about what’s next for Burnham.

In 2009, we almost doubled our facilities, including opening our gorgeous and environ-

mentally friendly building in Orlando, acquiring a large research building in San Diego,

expanding our footprint in Santa Barbara and committing to occupy space in the Sanford

Center for Regenerative Medicine building, soon to be under construction.

Burnham is growing and prospering, thanks to much hard work and your support. Your

generosity provides the seed capital that allows Burnham scientists and supporting profes-

sionals to excel at what they do best— great science. In turn, that science provides the

basis to win the large research grants that fuel 80 to 90 percent of our biomedical research

enterprise. With so much accomplished in 2009, and with your help, we look forward with

great anticipation to advancing our medical research mission to new heights in 2010.

p h I l a n T h r o p y

Printed on recycled paper

Dieter Wolf, M.D., has an unlikely research

partner—yeast. Yet, the S. pombe fission yeast

he studies shares many genes with humans and

provides an excellent platform to understand

cell biology. In particular, Dr. Wolf is investi-

gating proteins implicated in prostate cancer.

Burnham trustee Jeanne Herberger, Ph.D.,

knows how valuable basic scientific inquiries

like Dr. Wolf ’s are to finding new treatments

for cancer and other diseases. She and her

husband, Gary, support the biomedical

research at Burnham because they see the

long-term payoff.

Partners in Science:

Dr. Dieter Wolf and Dr. Jeanne

Herberger

Nonprofit OrganizationU.s. Postage

PaIdThe Burnham Institute

“Beyond our interest in early detection and developing targeted treatments, we want to see research lead to prevention,” says Dr. Herberger. “Burnham has earned global respect with an impressive record of high-impact research and far-reaching discoveries. We are proud to lend our support.”

6400 Sanger Road

Orlando, FL 32827

winter 2009

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