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pancreas cancer
Before It Is Too Late
Developing the capability to detect pancreas cancer early
is an immediate goal at UCSF. For many types of cancers,
detecting a tumor early increases a person’s chances for
long-term survival. Few pancreas cancers are detected early,
and few pancreas cancer patients survive.
MARGARET A. TEMPE RO
c o n t e n t s
BEFORE IT i S TOO LATE
1
LOOKING FAR AFIELD FOR
PANCREAS CANCER CLUES 2
NEW DRUGS FOR SPE CIAL
DELIVERY
3
TUMORS MEET THEIR
GENETIC MATCH
4
CELLS THAT SEED TUMORS
5
GENETIC COUNSELOR HELPS
WITH TROUBLING HERITAGE
6
THE RICHARD G. KLEIN
RESEARCH FUND
7
We already know that patients with small
pancreas tumors that can be surgically
removed fare better on average than
those whose cancers have grown larger.
But early detection usually happens by
chance – when the location of the tumor
causes symptoms a patient and physician
recognize as unusual, or when imaging
undertaken for other reasons reveals an
abnormality in the pancreas.
To meet this challenge of early detection,
UCSF experts in fields ranging from basic
biology to clinical studies have made
identifying molecular and clinical clues to
pancreas cancer risk and early detection
a priority.
Current techniques for screening and
preliminary diagnosis of pancreas cancer
already can be used to detect tumors
early, sometimes even before they have
become truly cancerous.
As it stands, screening is expensive,
somewhat inconvenient and slightly
“invasive,” meaning that, very rarely, the
tests themselves can cause harm. And
ironically, without major pancreas surgery,
there are some cases in which we are not
certain whether imaging abnormalities
point to inevitable, invasive cancer. Only
about 1 percent of the general population
will ever be diagnosed with pancreas
cancer. Working first with the highest-risk
families, clinical researchers are trying
to assess what degree of risk warrants
screening.
About 10 percent of all pancreas cancers
arise in families with a pattern of inherited
cancer. Genetic counselor Amie Blanco
and other members of the Cancer Risk
Program at UCSF consult with individuals
from affected families who suspect or
know that they are at risk. (See page 6.)
Counselors refer individuals to clinical
trials when appropriate. They provide the
latest information on risk and prevention,
and can notify patients when new
research sheds light on their risk status.
For these families and for the rest of the
population, we want to better gauge
pancreas cancer risk. So far, we know
that smoking doubles risk. We know that
a family history poses an even greater
risk. Population scientists affiliated with
the Pancreas Cancer Program, including
UCSF’s Elizabeth Holly, PhD, and Paige
Bracci, PhD, are working to identify
additional pancreas cancer risks and
interactions among risk factors.
Holly’s research team has been exploring
the role of diet, and earlier identified a
gene variant that amplifies a smoker’s risk
for pancreas cancer. Holly has begun
(continued on p. 8)­­
population
ALLAN BALMAIN
sciences
Looking Far Afield for Pancreas Cancer Clues
Consider the lab mouse. The rodent is used
to model tumor growth in countless studies
of genes and cancer. About 99 percent
of mouse genes also appear in humans.
Mouse and human also are similar when
one compares the DNA code within these
genes. Mice get cancer, and they get
more cancer when genetically engineered
with human cancer-causing genes.
But Allan Balmain, PhD, has strayed from
his geneticist colleagues in his choice of
mouse. Other researchers, to help carefully control experimental variables, use
only genetically uniform laboratory strains
of the species Mus musculus. Several
years ago, Balmain began breeding
their country cousins, a Mediterranean
field mouse known as Mus spretus. Like
humans, but unlike the old lab strains,
these field mice exhibit a wealth of
genetic diversity.
Why is that important? Clearly, common
DNA variations in genes that we inherit
from our mothers and fathers affect us
in more substantial ways than simply
determining whether our eyes are blue
or brown. Some gene variations alter
disease risk, including risk for diseases
that – like cancer – arise most often later
in life.
Balmain shares with most cancer geneticists an interest in rare gene mutations
– DNA alterations – that arise within
cells over a lifetime. If a mutation hits
the wrong gene in the wrong place, it
may set the stage for cancer to develop
eventually. But Balmain also is exploring
the subtler influence of more common
variations in the genes we are born with.
Balmain uses Mus spretus, as well as
inbred lab mice, to explore how different
inherited versions of the same gene affect
cancer risk.
He can manipulate genes and interbreed
mice of both species to determine how
gene variants act in mice with different
genetic backgrounds. He can investigate
how the effects of rare mutations that
2
arise in cancer-associated genes are
influenced by the activity of other genes
and gene variants. He can apply what
he learns from human DNA to mice, and
vice versa.
The amount of raw data generated by these
experiments is tremendous. Previous
generations of biological scientists did
not have the tools to collect so much
data, nor the task of analyzing such a
complex array of information.
UCSF postdoctoral fellows in mathematics
and computational biology have developed
unique and powerful programs to visualize and quantify the degree to which the
activity of one gene affects others.
These studies have led to new discoveries of biochemical relationships among
the proteins encoded by these genes,
molecular partners in cellular crime. (See
Pancreas Cancer News 2005 online at
cancer.ucsf.edu/research/pancan2005.pdf.)
For his part, Balmain has found that the
same K-ras mutation can act differently
when it arises in different inherited forms
of the gene. Furthermore, the version of
the K-ras gene we inherit from one parent may influence and sometimes work
against the activity of the gene copy we
inherit from the other parent. (Our cells
contain 23 chromosomes from each parent – matching pairs.)
In other words, some lucky individuals
may inherit a version of K-ras that can
inhibit the activity of the mutant gene on
the other chromosome, in effect acting
as a tumor suppressor. These people
may be less likely to develop an aggressive malignant tumor.
Some gene variations alter disease risk,
including risk for diseases that – like cancer –
arise most often later in life.
some of which Balmain already has identified as being important in cancer.
While continuing these experiments,
Balmain next plans to collaborate with
pharmaceutical industry scientists to target an old foe in a new way. The nemesis
is a mutated gene that drives the growth
of almost every tumor that arises in the
ducts of the pancreas.
Mutations that rev up this same gene,
called K-ras, also appear to drive the
development of tumors in many different
organs. UCSF boasts several researchers who are seeking strategies to block
the activity of mutated K-ras and its
Balmain has begun collaborative studies
with UCSF epidemiologist Elizabeth Holly,
PhD, to evaluate how this wrinkle in K-ras
genetics affects pancreas cancer risk and
survival.
In addition, Balmain has confirmed that
there is more than one way to splice bits
of DNA together to form the complete Kras gene, and this too may be important
in cancer and its treatment.
Allan Balmain’s research is funded in
part by a generous donation from the
Schwartz Foundation.
Kathleen Giacomini
basic research
Giacomini is engaging in a kind of pharmaceutical
jujitsu – using a cancer cell’s strength against it, and
turning that strength into vulnerability.
New Drugs for Special Delivery
There is an urgent need for new ideas for cancer drugs –
especially pancreas cancer drugs. Kathleen Giacomini, PhD,
of the UCSF School of Pharmacy has a new strategy that
could lead to many new drugs for pancreas cancer and other
cancers. Although she is not reinventing the wheel, before
she is through, drugs may be rolling over cancer cells much
more easily than before.
Funded through a UC Discovery Grant and working with collaborators, Giacomini is doing some well-informed tweaking
of standard chemotherapy drugs to make them more potent.
The strategy is to get more of the drug dose into cancer cells.
Giacomini is engaging in a kind of pharmaceutical jujitsu
– using a cancer cell’s strength against it, and turning that
strength into vulnerability.
Cancer cells divide rapidly. Because they grow so fast, they
have a great need for chemical fuel and nutrients. Nutrients
and other molecular cargo enter all cells through channels
called membrane transporters. Different membrane transporters traffic in different molecules.
Cancer cells often make and use an abnormally large number
of certain transporters, including the transporters that bring
in nutrients. That’s an advantage, but Giacomini aims to turn
this characteristic into a weakness by more efficiently delivering cancer-fighting drugs into tumor cells through these same
abundant transporters.
Giacomini is one of the world’s leading experts on these cellmembrane transporters. She is well versed in the ways in
which these proteins enable or restrict the movement of molecules into and out of cells, including cancer cells. Giacomini
has studied the molecular structures, biochemical functions
and genetic code of a large number of these proteins, which
act like gatekeepers within cells’ outer membranes.
enter or leave a cell. These studies provide clues about how
to change the drug’s structure, so that it can more efficiently
pass through a nutrient transporter, for instance.
“We have made several different chemical entities, modified
from standard drugs,” Giacomini says. She has been testing
the new chemicals to see how well they kill various strains
of cancer cells grown in the lab. The best candidates will be
tested later in mice.
One of the transporters that often appears in abnormal abundance on cancer cells is a vitamin transporter. Giacomini has
modified methotrexate, an anti-cancer drug, and is testing
it for efficacy in various cancers that have high levels of this
transporter.
Giacomini has made pancreas cancer a priority. She has
modified chemotherapies and made them more potent
against different varieties of lab-grown pancreas tumor cells.
“We would like a chemical that is about 10 times more potent
than what we have now before we would begin to evaluate it
as a drug candidate,” she says.
Giacomini also is an expert in pharmacogenetics. That means
she studies how drugs act differently in different individuals
because of genetic differences. She is investigating variant
forms of genes for transporters in cancer patients and in a
cross-section of the Bay Area population to identify variations
that affect responses to chemotherapies and to the newer
chemicals her research team is developing. Some common
transporter variants might even merit their own targeted drug
development efforts, but it’s too soon to tell, Giacomini says.
Kathleen Giacomini’s research is funded in part by generous donations to the David J. Hasbun Pancreatic Cancer
Research Fund.
Before Giacomini starts changing the blueprint of a chemotherapy drug, she probes the molecular interactions between
molecules of the drug and the molecular parts of the transporter protein through which the drug molecules must pass to
3
clinical research
Joe Gray
Tumors Meet Their Genetic Match
Even when tumors look the same, more
often than not, they are genetically different from one another. Scientists are
discovering that the likelihood of patient
death or survival is associated with particular genetic abnormalities, or with telltale patterns of genetic abnormalities.
In normal cells, there are controls that
limit cell division and cause the death of
cells that become abnormal. All tumors
escape these normal controls. However,
the varying patterns of genetic abnormalities within cancers often represent
slightly different ways of doing so. These
different routes of escape may best be
blocked with different drugs.
In recent years, targeted therapies have
been developed against specific genetic
abnormalities that frequently arise within
cancer cells to foster their continued
growth and survival. In breast cancer, for
instance, the drug Herceptin is targeted
against the many breast tumors in which
abnormal production of a protein called
HER2 drives the tumor’s growth.
In recent years,
targeted therapies
have been developed
against specific genetic
abnormalities that
frequently arise within
cancer cells to foster
their continued growth
and survival.
Unfortunately, in practice, Herceptin is
effective against only a minority of breast
cancers with this abnormality, despite
the targeting.
Indeed, researchers are discovering that
the effectiveness of specific cancer
treatments may vary with the genetic
fingerprints of tumors in ways that are
not easily predicted.
Many drugs have been rejected as treatments for certain types of cancer, based
on unimpressive overall results in treating
patients – even when individual patients
appear to benefit. Among available treatments, many potentially useful drugs or
combinations of treatments have never
been evaluated in common genetic
subsets of tumors, says Joe Gray, PhD,
director of the Life Sciences Division
at the Lawrence Berkeley National
Laboratory (LBL), head of the UCSF
Breast Oncology Program and one of the
world’s leading cancer genetics researchers. As a consequence, it may be that
good cancer treatments are being overlooked, Gray says.
Gray is working with a team of scientists
and clinical investigators from LBL and
UCSF to correct this oversight. His team
already has identified potentially useful
treatment combinations and new experimental therapies that might prove effective in treating breast tumors for which
genetic profiling shows a poor prognosis
with standard treatment. Now, working
with UCSF oncologist Eric Collisson, MD,
Gray also is exploring genetics and drug
response in pancreas cancer.
Unfortunately, in pancreas cancer, virtually every patient faces a poor prognosis.
Only 5 percent of patients survive for five
years after a diagnosis. But that does
not mean pancreas tumors are all the
same genetically. Collisson already has
evidence to suggest that there is genetic
variability among them, and that these
differences matter.
Collisson examined tumor tissue from 29
patients with cancers that were confined
to a small region of the pancreas at the
time of diagnosis – thus permitting surgical removal. Historically, even among
these patients that undergo surgery, only
about one in five has no recurrence of
cancer within three years. Collisson and
collaborators identified a genetic pattern
that predicts even worse-than-average
outcomes following surgery.
Collisson seeks to build on this proof
of principle – that genetic differences in
pancreas cancer exist and do indeed
matter. The goal is to use a tumor’s
genetic fingerprints to guide patients to
better treatments and better chances
for survival.
“A lot of approved chemotherapies
have been tried in pancreas cancer and
failed,” Collisson says. “We want to
revisit them to determine if there are
genetically defined subsets of pancreas
tumors that actually do respond to some
of these drugs.”
To expand efforts to match tumor to
treatment, Collisson and colleagues are
working with 30 diverse varieties of
pancreas cancer cells that can be grown
in the lab. The researchers are collaborating with UCSF pathologist Grace Kim,
MD, to obtain additional tumor tissue
for analysis.
Gray and Collisson also are using the
same strategy to test new, experimental
treatments targeted against specific
biochemical pathways that are altered
in cancer. They want to identify genetic
characteristics that may make some
tumors particularly vulnerable to these
new drugs. Combined with preclinical
animal studies, such an approach may
lead to better patient selection for clinical
trials – enriching participation among
those patients who may be most likely
to benefit.
Joe Gray and Eric Collisson’s research is
supported in part by generous donations
to the Noren Pancreatic Cancer Research
Fund.
Kim McD ermott
young
investigator
One goal is to identify
Cells That Seed Tumors
The long hours Kim McDermott spent as a graduate student examining the world
of cancer at a molecular and cellular level in a lab at University of Nebraska Eppley
Cancer Center never blinded her to the human cost of the disease she was studying
– a fellow scientist there had been diagnosed with and succumbed to pancreas
cancer at an unusually early age.
After completing her doctoral degree, McDermott, PhD, came to UCSF to investigate
the cellular origins of breast cancer. Now, as part of a team led by Thea Tlsty, PhD,
a UCSF expert on the cellular biology of tumors, McDermott is investigating whether
the Tlsty lab’s recent success in identifying markers of early breast cancer can be
repeated in pancreas cancer.
One goal is to identify early markers of pancreas cancer that can be detected reliably
in fluid secreted by the pancreas – or better yet, in blood. The difficulty of detecting
pancreas cancer early is a key reason the disease is among the deadliest cancers.
early markers of pancreas
cancer that can be
detected reliably in fluid
secreted by the pancreas –
or better yet, in blood.
The difficulty of detecting
pancreas cancer early is
a key reason the
disease is among the
deadliest cancers.
In breast tissue, the UCSF researchers believe they already have identified a
molecular signature that will serve as the basis for a lab test to predict whether
abnormal but not yet cancerous breast lumps are destined to develop into fullfledged cancer.
Tlsty has led successful efforts to identify cells in normal breast tissue – perhaps
one in 10,000 cells – that are most likely to develop later into breast cancer. A
tumor-suppressing gene called p16 is “silenced” in these cells – meaning the gene
is switched off and its encoded protein is not produced.
McDermott explains that loss of p16 contributes to mistakes in how chromosomes
are divvied up when daughter cells form during cell division. This allocation
of chromosomes is governed by structures within cells called centrosomes.
Centrosomes often form aberrantly in cells in which p16 is not functioning normally.
The result is daughter cells with one or more unpaired chromosomes. This
characteristic, called aneuploidy, may be one of the very earliest, most common
and easily tracked changes in precancerous cells of the pancreas ducts. These
ducts are where pancreas tumors most often develop.
To advance the research, painstakingly prepared, normal pancreas ductal cells
– essentially an unwanted byproduct of diabetes research – are available from the
UCSF Islet and Cellular Production Facility. In addition, UCSF pathologist Grace Kim,
MD, provides living pancreas tissue from patients with pancreas diseases, including
many with rarely identified, early-stage cancers. (See Pancreas Cancer News 2007
online at cancer.ucsf.edu/research/pancan2007.pdf.)
Kim McDermott is developing techniques
to grow human pancreas cells in the lab,
to learn more about the earliest stages
of pancreas cancer.
But it’s up to McDermott to extract from normal tissue the rare cells that have
silenced p16 and coax them to grow in the petri dish – with whatever growth serum
does the trick. She already has made significant progress.
McDermott’s early achievements and future promise have been recognized through
a rare Pathway to Independence Award from the National Institutes of Health. The
grant helps postdoctoral fellows make a smooth transition to research careers as
university faculty.
“We’ve learned a lot from the mammary system,” she says. “Now we have been able
to quickly begin to apply what we have learned about mammary cells to the study
of cells that we think may be playing a similarly important role in the development of
pancreas cancer.”
Kim McDermott’s research is funded in part by generous donations to the
David J. Hasbun Pancreatic Cancer Research Fund.
5
AMIE BLANCO
clinical care
Genetic Counselor Helps Families with Troubling Heritage
Pancreas cancer is an uncommon disease. Even so, there are
some unfortunate families in which two or more people have
been diagnosed. In many instances, the pattern of pancreas
cancer in these families may signal that an inherited gene is
largely to blame. In fact, as with breast cancer, up to 10 percent
of pancreas cancer occurs in families at an elevated genetic risk
for the disease.
In some cases, faulty genes more famous for contributing to
other types of familial cancer – such as breast, colon or skin
cancer – also increase the gene carrier’s risk for pancreas cancer.
It was not until 2006 that researchers first identified a cancer risk
gene specifically for a familial form of pancreas cancer. It is not
yet clear whether mutations in this gene, identified in a single
family, will prove to be common in other families with multiple
cases of pancreas cancer. There still is no genetic test for pancreas cancer susceptibility unrelated to other known hereditary
cancer syndromes.
at least two successive generations and types of cancer seen in
known cancer predisposition syndromes.”
Blanco counsels individual family members on genetics, diet and
lifestyle, and develops recommendations and follow-up plans.
When it’s available, Blanco and her counseling colleagues offer
genetic testing for individuals who might be affected by a faulty
gene responsible for a family’s misfortune.
Educating family members on pancreas cancer genetics and
risk can go a long way to reduce uncertainty and anxiety among
individual family members.
Blanco reminds family members that they are still unlikely to get
pancreas cancer. Having a fourfold, or even an eightfold, higherthan-average risk for a rare disease does not turn a rare occurrence into an inevitable one. Blanco advises individuals at risk
to limit exposures to known pancreas cancer risks, such
as smoking.
“We’re clinical detectives. We sort out
family histories in great detail to determine
if we suspect a hereditary cause.”
The search for inherited genes that may influence risks for both
sporadic and familial forms of pancreas cancer is ongoing at
UCSF and other academic medical centers. (See page 2.) As
members of affected families try to gain a better understanding
and to keep abreast of the latest discoveries, they often benefit
by consulting with a genetic counselor like UCSF’s Amie Blanco.
Clinical trials are now underway to determine how best to use
ultrasound and other screening methods to prevent premature
pancreas cancer death. Blanco often refers high-risk family
members to these screening clinical studies. In addition, Blanco
helps families get involved in research studies. The UCSF
Cancer Risk Program banks blood and DNA samples.
Working with UCSF gastroenterologist Jonathan Terdiman, MD,
Blanco, a genetic counselor for the UCSF Cancer Risk Program,
helps concerned families affected by a variety of cancers. Blanco
gathers information to gauge whether chance, inheritance or
unusual exposures to environmental hazards are the strongest
contributors to a family’s patterns of cancer.
Blanco offers to enroll patients in a familial pancreas cancer registry. The hope is that new scientific discoveries will lead to valuable tests for better gauging risk and possibly even better ways
to diagnose cancer early. Blanco expects in the future to have
much more to offer family members who visit her today.
“We’re clinical detectives,” she says. “We sort out family histories in great detail to determine if we suspect a hereditary cause.
Some of the things we look for are young ages at cancer diagnosis, multiple primary cancers in a single individual, cancers in
6
“Our biggest recommendation is that they keep in touch with
us,” she says.
The integral work of our cancer genetic counselors
is supported in part by generous donors, including
Dr. and Mrs. Gordon E. Moore.
The Richard G. Klein
Research Fund
W
hen Dick Klein died of pancreas cancer five years ago, Diane Klein lost a husband, Jeffrey and Jennifer Klein lost a father, and Tom Klein lost a brother. It is difficult to
glimpse a silver lining in the dark cloud of a family’s pancreas cancer diagnosis. For the
Kleins, a small consolation was that they did not have to travel far for pancreas cancer
care and treatment that ranks among the very best anywhere. After visits to UCSF, Dick
Klein and his family could cross the Bay Bridge and return home the same day.
Diane Klein was moved by the care Dick received from oncologist Margaret Tempero,
MD, nurse Elizabeth Dito and the other members of the medical team at UCSF. Her
experience with pancreas cancer motivated her to try to make a difference and to
advance understanding of ways to improve outcomes for patients.
“For me, it is a gift to be able to offer support for the cause,” Diane Klein says. “This cancer does not get a lot of attention. The mortality rate is very high because it is detected
so late. There are no easy methods to diagnose it, and the symptoms are very similar to
symptoms of common diseases. I think pancreas cancer is probably the worst cancer
that one can have – although I know that every cancer patient feels the same way about
their cancer.”
“I was shocked to learn how fatal pancreas cancer is,” says Tom Klein, a San Francisco
resident and proprietor of Rodney Strong Vineyards. He also wanted to do something
to change the fate of those with pancreas cancer. “A cancer diagnosis is never good
news, but for other cancers, there are more ways to fight the disease,” he says. “We just
want to move the ball forward – to help give families ways to fight harder and pancreas
cancer patients better chances to survive.”
Rombauer
Vineyards
Rombauer Vineyards is
once again hosting the
Joy of Wine Fundraiser.
The 2007 event was a
big success, with more
than $100,000 raised
for the UCSF Rombauer
Cancer Research Fund
for Pancreas Cancer
and for Hospice of
Napa Valley. The next
event will be held on
July 26, 2008. For more
information, contact
Sheana Rombauer at
800/622-2206.
After being introduced to UCSF developmental biologist Matthias Hebrok, PhD, and
hearing about his research studies, Diane Klein knew she had found someone whose
work the family would be pleased to support. Hebrok studies specific molecules that
communicate signals within the developing embryo. The signaling that Hebrok is focusing on guides the formation of a functioning pancreas.
These signals appear to be abnormally activated in pancreas cancer. Hebrok is exploring whether the signals can be interfered with or otherwise manipulated to prevent the
growth of pancreas tumors.
Knowledge gleaned from basic biological investigations, including Hebrok’s, often has
broad implications. Hebrok’s research is relevant not only for pancreas cancer, but also
for type 1 diabetes, in which beta cells of the pancreas are lost. Hebrok is manipulating
the same signals in an effort to generate insulin-producing cells to treat type 1 diabetes.
“I hope the research will help others diagnosed with this deadly cancer, as well as those
– like my son – who are diagnosed with type 1 diabetes,” Diane Klein says.
7
Pancreas Cancer News
Volume 3, Number 1
May 2008
how to help
Our program depends on your support. We welcome your contributions to this
special fund. Please make your check payable to UCSF Pancreatic Cancer
Research Fund, Box 0248, San Francisco, CA 94143-0248.
(continued from p. 1)
working with experimental geneticist Allan Balmain, PhD, to identify
more gene variants that affect risk. (See page 2.)
UCSF scientists are working toward a future in which early pancreas
cancer detection may be achieved by tracking certain genes – or,
more likely, the proteins produced from these genetic blueprints.
Leading cancer biologist Thea Tlsty, PhD, has teamed with talented
young postdoctoral fellow Kim McDermott, PhD (see page 5), and
pathologist Grace Kim, MD, to identify proteins that may be shed
by abnormally growing pancreas tissue into the bloodstream, before
tumors are visible.
With support from the National Institutes of Health and from donors,
we have made new strides, and have officially incorporated the
Pancreas Cancer Program as part of the UCSF Helen Diller Family
Comprehensive Cancer Center. With additional support, we aim to
bring the Pancreas Cancer Program to the next level.
Pancreas Cancer News is published
by the Pancreas Cancer Program
at the University of California, San
Francisco
Co-Leaders:
Margaret Tempero, MD
Martin McMahon, PhD
Writer/Editor: Jeffrey Norris
Designer: UCSF Public Affairs
Photography: Grace Kim, cover;
Kaz Tsuruta, cover; Chris T.
Anderson, p. 2; Majed, p. 3; Roy
Kaltschmidt, p. 4; Elisabeth Fall,
p. 5; Susan Merrell, p. 6
Cover Photo: The image shows
cells growing abnormally within an
intralobular duct of the pancreas –
an early stage in the development
of pancreas cancer.
© 2008 The Regents of the University
of California
Produced by University Publications/
Public Affairs, PR710
pancreas cancer news
UCSF Helen Diller Family
Comprehensive Cancer Center
University of California
San Francisco
Box 0248
San Francisco, CA 94143
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