A N S C H U T Z M E D I C A L C A M P U S

C O L L A B O R A T I N G T O C O N Q U E R C A N C E R

W I N T E R 2012

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TIGHTENING THE BODY’S

12: OUTLIVING

THE ODDS

16: TOBACCO TAX

SAVES LIVES

10: Q&A WITH

SONIA OKUYAMA, MD

11: C3 MD CLAYTON SMITH

18: SUPPORTER FOCUS ON

CANCERCURE

WWW.COLORADOCANCERCENTER.ORG

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Bladder cancer patients whose tumors express

high levels of the protein CD24 have worse

prognoses than patients with lower CD24. CU

Cancer Center Director Dan Theodorescu, MD,

PhD, shows that CD24 expression may depend on

androgens—and that anti-androgen therapies like

those currently used to treat prostate cancer may

benefit bladder cancer patients.

“This is a major finding. Bladder cancer

CU CANCER CENTER RECEIVES PRESTIGIOUS DESIGNATION

The University of Colorado Cancer Center remains in distinguished company, having earned a prestigious

designation from the National Cancer Institute (NCI). This is the fourth time CU Cancer Center has been

named a comprehensive cancer center by the NCI—one of only 41 cancer centers in the U.S. to receive

the designation.

“This designation means we are among the ‘best of the best’,” says Dan Theodorescu, MD, PhD,

director of CU Cancer Center. “We are proud to bring that level of care to our community, while

continuing to research and develop clinical trials that keep our patients living longer.”

The Cancer Center is also one of only a handful of comprehensive cancer centers that have the

“consortium” designation, meaning the center includes members from multiple universities:

University of Colorado Denver, University of Colorado-Boulder and Colorado State University.

University of Colorado Health System (including University of Colorado Hospital, Poudre Valley

Hospital, Medical Center of the Rockies and Memorial Hospital), Children’s Hospital Colorado, Denver

Health, Denver VA Medical Center, National Jewish Health and Kaiser Permanente Colorado are the

consortium patient care partners.

CU Cancer Center is the only NCI-designated comprehensive cancer center in Colorado. This

recognition comes on the heels of the U.S. News and World Report rankings placing CU Cancer Center

among the top 35 cancer centers in the U.S. The NCI re-designation lasts for five years and provides a

budget of approximately $18 million over that period.

BLADDER CANCER PATIENTS MAY BENEFIT FROM ANTI-ANDROGEN THERAPY

Modern cancer therapies start in cells:

Researchers compare cancer samples

to healthy cells to discover how cancer is

genetically different and use cell lines to test

promising new drugs. However, a CU Cancer

Center study shows that due to a high rate of

contamination and misidentification in widely

available cell lines, researchers may be draw-

ing faulty conclusions.

“I’ve seen faculty and graduate students

leave my lab in tears when we discovered the

cells on the label weren’t the cells they were

actually experimenting on,” says Christopher Korch, PhD, CU Cancer Center investigator. “When you get

a cell line, you have to look that gift horse in the mouth—there’s up to a 40 percent chance it’s a Trojan

horse, not what it says it is.”

While a misidentified cell line seems likely due to a snafu on the part of a lab assistant with a faulty filing

system, there are more ways than clerical error to end up with the wrong label on a sample of cells.

“I see two people working with different cultures in the same hood, or using the same growth medium

for the same cultures with the same pipette,” Korch says.

In order to keep results from being flawed, Korch and others are putting their data online and allowing

investigators elsewhere to compare their cell lines to the group’s controls. They recommend researchers

check their cells prior to bringing them into the lab or put them in quarantine until they know what they are.

Patients with early-stage breast

cancer usually have to wait years

to receive new cancer drugs,

but new guidance from the FDA

promises to substantially reduce

the time and cost of getting

new treatments to patients. The

approach is based on a trial

design being tested in the I-SPY

2 TRIAL, an innovative phase II

breast cancer trial at CU Cancer Center.

“New cancer drugs are usually tested first in

patients with advanced stage disease and then

approved for use in early-stage cancer but only

after additional clinical trials. It can take hundreds

of thousands of dollars and several years to study

one drug,” says Anthony Elias, MD, breast cancer

program director at CU Cancer Center. “I-SPY

2 shows us that we can find the treatments that

work and get them to patients who need them

efficiently and safely.”

The new FDA recommendations, discussed

in The New England Journal of Medicine, would

speed up approval of drugs tested prior to surgi-

cal removal of tumors in certain types of high-risk

patients with localized, early stage disease.

The I-SPY 2 Trial uses specific genetic signa-

tures—biomarkers—in patients’ tumors to select

those most likely to benefit from testing using

the new approaches. The biomarkers are also

incorporated into a unique “adaptive” trial design

that allows researchers to measure the relative

benefit of treating patients with different tumor

profiles with a specific drug, and guide treatment

assignments for subsequent trial participants.

I-SPY 2 can test new treatments with signifi-

cantly fewer participants and in half the traditional

time, which will dramatically lower costs. The

trial, launched two years ago, is screening

multiple cancer drugs at 19 major cancer

research centers across the country, including

CU Cancer Center.

MISIDENTIFIED AND CONTAMINATED CELL LINES LEAD TO FAULTY CANCER SCIENCE

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development and spread to other organs depends

significantly on CD24, which in turn depends on

androgens like testosterone,” Theodorescu says.

“By taking away these androgens, we may be able

to greatly diminish the proliferative and metastatic

power of bladder cancer cells.”

Working with mouse models and human tumor

samples, Theodorescu and colleagues showed

that not only do high levels of CD24 mark more

aggressive bladder tumors, but that CD24 in fact

drives the aggressiveness of these tumors.

“We hope the results of these studies show

the rationale for clinical studies of anti-androgen

therapies with bladder cancer, especially in those

tumors that happen to test markedly high in CD24

expression,” Theodorescu says. “The next step is

moving this promising therapy to clinical trials with

human patients.”

C3: WINTER 2012

3

MILK THISTLE HITS PROSTATE CANCER TWO WAYS

STUDY SHOWS LONG-TERM EFFECTS

OF RADIATION IN PEDIATRIC

CANCER PATIENTS

DIETARY SUPPLEMENTS INCREASE CANCER RISK

For many pediatric cancer patients, total body

irradiation (TBI) is a necessary part of treatment

during bone marrow transplant and a key to

long-term survival. But lengthened survival

creates the ability to notice long-term effects

of radiation as young cancer patients age.

A CU Cancer Center study details these late

effects of radiation.

“These kids basically lie on a table and truly

do get radiation from head to toe. There is a

little blocking of the lungs, but nothing of, for

example, the brain or the kidneys,” says

Jean Mulcahy-Levy, MD, research fellow at

CU Cancer Center and the paper’s first author.

Of 15 patients who received TBI before age

3, many developed endocrine and metabolic

problems including testicular malfunction,

restrictive pulmonary disease due to high

levels of blood triglycerides, and cataracts.

Likewise, 90 percent of patients showed

abnormally low levels of growth hormone and

71 percent were considerably under height.

Additional late effects of TBI included kidney,

liver, skeletal and cardiac malfunction, and

cognitive decline.

“Fifteen doesn’t seem like a large number,

but because we have such a good pediatric

bone marrow transplant program at Children’s

Hospital Colorado and a radiation therapy

program at CU Cancer Center, we were able

to get a large enough cohort of patients to

see these overall effects,” Mulcahy-Levy says.

“It’s not so much that you want to stop

TBI, which is frequently a necessary part of

treatment, but this study shows it’s important to

know about these problems in order to address

them appropriately and proactively,” she says.

90%A B N O R M A L LY LOW

L E V E L S O F G R OW T H H O R M O N E

Tumors are gluttons. In order to fuel their

astounding growth rate, they must gorge. A CU

Cancer Center study pinpoints the compounds

derived from milk thistle that best kill cancer cells

directly and restrict tumors’ ability to grow the new

blood vessels they need to import this massive

food supply.

In his study, Gagan Deep, PhD, CU Cancer

Center investigator and research assistant pro-

fessor in the Skaggs School of Pharmacy and

Pharmaceutical Sciences, found that mice that

were orally fed Isosilybin B at 50 or 100 mg/kg

body weight had much lower tumor volumes

than untreated mice and significantly lower tumor

volumes than mice treated with the other three

isoforms of silibinin. This Isosilybin B most effec-

tively killed cancer cells directly.

But directly targeting cancer cells isn’t the only

way to restrict tumor growth. Also important is a

tumor’s ability to grow new blood vessels that import food. The body lines blood vessels with endothe-

lial cells, and “while Isosilybin B was most effective towards prostate cancer cells, it was least effective

towards endothelial cells,” Deep says. “On the other hand, Silybin A showed highest efficacy towards

endothelial cells.”

Gagan’s group plans to test a mixture of these two strongest isoforms: Silybin A and Isosilybin B.

They anticipate B will target the tumor and A will target its ability to grow new blood vessels. “We hope

to find a synergistic effect between these two promising compounds,” Deep says.

Tomorrow’s drugs may come from the plant that today grows on the side of the road.

Beta-carotene, selenium and folic acid—taken up to three times their recom-

mended daily allowance, they’re probably harmless. But taken at much higher

levels, as some supplement manufacturers suggest, they can increase the risk

of developing a host of cancers.

“It’s not that these nutrients are toxic,” says Tim Byers, MD, MPH, professor

of epidemiology at the Colorado School of Public Health and associate director

for prevention and control at CU Cancer Center. “They’re essential and we

need them, but we need them in a certain balance.”

Currently the FDA regulates dietary supplements as food, but, as Byers

and colleagues suggest, supplements, especially at high doses, are more

accurately described as inhabiting a mid-ground between food and drugs.

Like drugs, supplement ingredients are biologically active—sometimes for

better and sometimes for worse.

“We need to do a better job as a society in ensuring that the messages

people get about value versus risk is accurate for nutritional supplements,”

Byers says. “My conclusion is that taking high doses of any particular nutrient

is more likely to be a bad thing than a good thing.”

BYERS

MILK TH ISTLE

Get more CU Cancer Center

news on our blog:

www.coloradocancerblogs.org

Sign up for our bimonthly newsletter,

Colorado Cancer News. Scan to subscribe.

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At CU Cancer Center, researchers

discover how dinosaurs, diabetes,

Star Trek extras and Keith Richards

combine to keep the body cancer-free.

Interstate 70 is bad enough on a normal Monday evening, let alone when an acci-dent makes the freeway look more like long-term parking at Denver International Airport. And so it’s easy to sit there, stewing, scanning radio stations, and thinking

about what could possibly have caused the accident in front of you and why the high-way patrol can’t move the wreck to the median. I mean—sheesh—you could be home by now sitting comfortably on the couch and grumbling about Peyton Manning’s arm!

That is, if it weren’t for that darn accident. But look at it another way: most nights the freeway is packed with 4,000-pound

chunks of fire-propelled metal, hurtling across the pavement at 70 mph while their pilots shove their heads in Cheetos bags or fidget with their supposedly hands-free smart phone systems. Some of these people you wouldn’t trust with a popcorn maker let alone a Hummer. Really, it’s pretty astounding there aren’t more accidents.

The same is true of cancer. Cancer research centers tend to focus on what to do once the body is sick, once an

accident is already on the road. For example, at University of Colorado Cancer Center when a patient walks in the door the physician asks what went wrong and how to fix it.

“But maybe a better question is, for all the people we don’t see, what goes right,” says Andrew Thorburn, PhD, deputy director of CU Cancer Center.

He points out that there are about 10 to 100 trillion cells in the human body, with 50 to 60 billion cells replaced every day. That’s 50 to 60 billion chances per day that a cell can accidentally accumulate a mutation or combination of mutations that cause cancer. Like cars on a fast freeway, “You look at those odds and it’s surprising that cancer isn’t more prevalent,” Thorburn says.

Or maybe it’s not that surprising after all.

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B Y G A R T H S U N D E M

It’s no random accident—no game of Russian roulette—that keeps the body cancer free. Instead it’s a handful of precise mechanisms that Thorburn calls “prerequisites of multi-cellular life” that have evolved to ensure we stay healthy long enough to pass on our genes. Researchers at CU Cancer Center and elsewhere are broadening their focus to explore not only what goes wrong when we get cancer, but what goes right when we don’t.

PLACE ORIGINAL FACE DOWN ON GLASSFirst, “the body has an astoundingly precise copy machine,” Thorburn says. When a cell divides, it copies the full expanse of its DNA, giving away a copy to its daughter cell and keeping a copy for itself. The code of life is made up of only four bits of infor-mation, called nucleotides, which when strung together can look something like this: ATGACGGAGCTTCGG.

If you were sitting at a keyboard, could you look at this code and reproduce it? What would be your error rate? The body’s error rate is only about one mistake in every 100,000 nucleotides. That’s pretty darn good. (See “Decoding Cancer,” page 9.)

Now imagine the 30,000-ish genes included in every human cell’s DNA—the blue-prints for all the construction and workings of your body. Each gene is made up of about 3,000 nucleotide base pairs. That’s not all: functional genes make up only about 2 percent of your DNA and so in all you have around 6 billion nucleotide base pairs in each cell’s DNA. This means that despite the body’s careful copy machine, each new cell is likely to have about 120,000 mutations. Now multiply that by 50 to 60 billion cells and you get…well, you get a really big number that you certainly don’t want to see printed here.

Andrew Thorburn, PhD, with professional research assistant Josh Thompson and postdoctoral researcher Paola Maycotte.

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“MAYBE A BETTER QUESTION IS, FOR ALL

THE PEOPLE WE DON’T SEE, WHAT GOES

RIGHT? YOU LOOK AT THOSE ODDS AND

IT’S SURPRISING THAT CANCER ISN’T

MORE PREVALENT.”

—ANDREW THORBURN, PHD

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TIGHTENING THE BODY’S

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So in addition to an accurate copy machine, the body also has an accurate proof-reader. Instead of accepting these mutations, the body tries to identify and fix them.

A cell builds DNA by stacking it one nucleotide at a time. And as it stacks nucleo-tides, the cell has enzymes that crawl along the original DNA, comparing it to the copy. When an enzyme finds an error—say a G that should be an A—it pulls the mistake and inserts a correction. The cell’s proofreading mechanism catches and fixes about 99 percent of errors this way—good but not nearly good enough to keep mutations out of your genome.

The more cells you need to replace (for example, because you kill cells with a sun-burn), and the higher a cell’s mutation rate (say, because the sun’s UV rays slice and dice DNA like Dan Aykroyd’s Super Bassomatic on “Saturday Night Live”), the more mutations make their way past the copy machine and proofreader. Now the body’s job switches from fixing errors to eliminating them.

COPY CORRECTLY OR KILLAs you’d expect, one recognizer-and-killer is the immune system. But it’s tricky: cancer cells are your own cells gone bad. Your immune system is supposed to kill foreign cells like bacteria and viruses, not your own cells, and so it has difficulty turning its firepower on more domestic terrorists.

Interestingly, there’s one kind of person whose immune system does kill cancer cells and that’s people with autoimmune diseases like Type 1 diabetes, in which the immune system’s T-cells erroneously attack the pancreas’s insulin-producing cells. Patients with Type 1 diabetes almost never get pancreatic cancer. And patients with the autoimmune condition vitiligo, in which T-cells attack the skin’s pigment-producing cells, are dra-matically protected against skin cancer. It seems that an over-sensitive immune system kills cancer cells first. On the flip side, people who are immunocompromised, as are those with HIV, have higher rates of many cancers.

“When you develop a cancer, by definition soft tissue has gone haywire. And when you develop an autoimmune condition like Type 1 diabetes, by definition your T-cells have gone haywire,” says David Wagner, PhD, CU Cancer Center investigator and associate professor of medicine at the CU School of Medicine. “Perhaps we could push T-cells to just beneath this threshold of ‘haywire’ to combat the cancer cells that have already gone past this tipping point.”

It’s like your email spam filter: one form of cancer immunology seeks to dial up the sensitivity of your immune system’s spam filter in order to route cancer cells to the “kill” folder, perhaps destroying some healthy cells along the way.

Wagner is working to control T-cell sensitivity with a protein called CD40. Tweaking CD40 in one direction makes T-cells more aggressive and tweaking it in another direc-tion makes T-cells more docile. Other CU Cancer Center immunologists are working with vaccines to sensitize T-cells against cancer.

According to Jill Slansky, PhD, co-leader of the Immunology and Immunotherapy Program at CU Cancer Center and National Jewish Health, here’s one way it works: “The immune system is designed to recognize abnormal proteins and kill the cells that present these proteins. Due to mutations, cancer cells make abnormal proteins, but because cancer cells also share so much similarity with the body’s own, healthy cells, the immune response may not be very strong.

“We’re working to boost the sensitivity of T-cells to these tumor-specific antigens. Like any vaccine, if you can give T-cells a preview of these foreign proteins, you can sensitize T-cells to recognizing these proteins on actual cells,” Slansky says.

Jill Slansky, PhD, co-leader of the Immunology and Immunotherapy Program at CU Cancer Center and National Jewish Health.

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SACRIFICING CELLS FOR THE GREATER GOODIn fact, cells containing cancer-causing mutations might not even need the intervention of the immune system to end up dead.

“Cells are hardwired to kill themselves if there’s something wrong with them,” says Thorburn, whose research focuses on this programmed cell suicide called apoptosis. “If a cell’s in the wrong place or growing at the wrong time, healthy cells have this natural default to just kill themselves.”

Like an unnamed character tagging along with the “Star Trek” crew on an unex-plored planet, cells are expendable. So the body errs on the side of caution—one teeny-tiny false move in the way a cell goes about its business can show that it harbors a dangerous mutation, and the body would rather throw the cell under the bus than risk it spawning a dangerous tumor.

For example, if you’ve taken high school biology, you probably still have that dream where you’re sitting at a desk, pencil in hand, no clothes, staring at an unexpected test on the stages of the cell cycle. Messing up the steps of the cell cycle won’t help your biology grade and it doesn’t help most cancer cells, either. That’s because the body places customs agents at the boundary of each step. If a cell rushes through or tries to skip a stage of cell division, tumor suppressor genes (customs agents) recognize the cell and mark it for apoptosis.

Likewise, these regulators look for broken DNA, unnatural bulging or misarranged chromosomes—any one of these can mark a cancerous cell and any one can get a cell marked for apoptosis.

So in addition to a mutation that allows an early cancer cell to act cancerous, cancer cells also include mutations to these anti-tumor or tumor suppressor genes, making them toothless.

In fact, “Simply disabling some of those anti-cancer genes is sufficient to create cancer,” says Thorburn, “and ironically, cancer cells are often easier to push into apoptosis than healthy cells—it’s as if they were trying to kill themselves and just didn’t quite manage it.”

DINOSAURS, KE ITH R ICHARDS AND THE BODY’S CHANGING TISSUE LANDSCAPEThen in addition to accurate copying, the immune system and apoptosis, there’s the role of the tissue surrounding mutated cells.

Sure, the older you are, the higher likelihood that one of your 50 to 60 billion cell duplications per day will result in a sneaky mutation that avoids control, but Cancer Center researcher James DeGregori, PhD, shows that it’s not only the increasing chance of a mutation with time that leads to higher cancer rates in older adults.

“You put an early cancer cell in healthy tissue and that cancer cell is unlikely to survive,” says DeGregori, professor of molecular biology at the CU School of Medicine. “It’s like what happened to the dinosaurs 65 million years ago. Dinosaurs were great and they weren’t changing that fast; they were well adapted to their landscape. Until that darn meteor. Suddenly dinosaurs weren’t a good fit for the new landscape. The species didn’t have to change their mutation rate; it was the new landscape that drove speciation.

“Similarly, what primarily drives cancer rates higher as we age is the changed landscape,” he says.

Our healthy cells are optimized for the conditions of our healthy, younger tissue. In fact, they’re so perfectly optimized for young tissue that changing anything about a cell makes it less fit for its surroundings. That’s the case of cancer cells—they’re different

James DeGregori, PhD (standing), with postdoctoral researcher Curtis Henry.

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and thus less fit, and so healthy cells simply out compete them. The young body uses basic survival-of-the-fittest to keep cancer in check.

But, “when tissue is old, healthy cells are no longer a perfect fit for the landscape, and mutations might help a cancer cell adapt in ways a healthy cell can’t,” DeGregori says.

Blot out the sun with a meteor’s cloud of dust and mammals will eventually outcom-pete thunder lizards. Age or transform tissue until it’s far enough from its healthy norm and cancer cells can outcompete their healthy peers.

DeGregori’s work supports the conclusions of CU Cancer Center investigators Pepper Schedin, PhD, and Ginger Borges, MD, who work with the tissue landscapes that give rise to breast cancers.

“We see that breasts with higher rates of inflammation—as those undergoing the process of involution during which milk-producing cells are replaced by fat cells—have higher rates of both initial cancer and metastasis,” Schedin says.

Inflammation and a dramatically changing tissue landscape leave healthy cells look-ing for their footing, while cancer cells, like dandelions, take advantage of the disturbed earth. Borges and Schedin’s work explores the use of non-steroidal anti-inflammatory drugs like ibuprofen to reduce inflammation in these tissues, hopefully bringing it in line with the conditions for which healthy cells are optimized.

OBESITY AND THE CHALLENGE OF PROVING PREVENTIONThe influence of tissue on cancer is also important on a more global scale. The process of breast involution, sunburn and smoking are not the only ways to create inflamma-tion. Obesity can also create cancer risk. (Read “Battle of the Bulge” in the previous edition of C3 at www.coloradocancerblogs.org for details.)

In fact, Tim Byers, MD, MPH, professor of epidemiology at the Colorado School of Public Health and associate director for prevention and control at CU Cancer Center, believes that in many cases an intentional 10 percent weight loss after surgery for breast cancer can be as effective as adjuvant chemotherapy in preventing relapse.

Knowing these mechanisms the body uses to stay cancer free, you’d think we could design and test interventions to help the body with its work and artificially boost its defenses.

Unfortunately, “the real difficulty in exploring any of these preventative strategies is the logistical and ethical difficulty of prescribing any intervention for people who aren’t yet sick,” Thorburn says.

For example, you can’t give 1,000 women ibuprofen and compare their breast cancer rates to 1,000 women given sugar pills. Likewise, you can’t experimentally introduce cancer proteins in a vaccine to people who don’t yet have the disease. Thus, prevention strategies are tricky to prove.

But the times they are a-changing.Like CU Cancer Center, other cancer centers are starting to prioritize their depart-

ments of prevention and control. And cancer vaccines, including the drug Yervoy for metastatic melanoma and Gardasil for HPV that causes genitourinary cancers in men and women, have gone from fringe science to FDA approval.

Next time you’re stuck in an I-70 traffic jam, instead of fretting in a way that’s really not good for your blood pressure, try being thankful that accidents are rare.

In addition to being courageous as you face cancer, offering your compassion to others affected, and helping support organizations looking for tomorrow’s best fixes, take a minute to marvel at the body’s ability to get it right so often.

We are machines made to resist cancer. By understanding how these machines work, we may find ways to help them resist cancer just a little bit better.

“THE REAL DIFFICULTY IN EXPLORING

ANY OF THESE PREVENTATIVE STRATEGIES

IS THE LOGISTICAL AND ETHICAL DIFFI-

CULTY OF PRESCRIBING ANY INTERVEN-

TION FOR PEOPLE WHO AREN’T YET SICK.”

—ANDREW THORBURN, PhD

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DEC DINGCANCER

A cell builds new DNA like zipping closed

a winter coat, adding new zipper tines as the

new DNA matches itself to the pattern DNA. But

sometimes these two strands don’t stay perfectly zipped

together; sometimes they slip or wobble.

When the new strand slips, a little kink in the zipper can

result in an extra nucleotide “tine.” When the pattern strand slips,

the kink can result in a missing nucleotide.

A wobble briefly makes a nucleotide “tine” on the pattern strand

able to grab a nucleotide tine other than its proper pairing—the

wobble can insert the wrong nucleotide in the new strand. Most of

these wobbles don’t last long—a mismatched tine doesn’t attach

HOW GOOD DNA GOES BADwell to subsequent tines, and the difficulty attaching the next

building blocks sounds an alarm that signals the DNA polymerase

enzymes that do the actual stacking to quickly fix the problem.

And then even after DNA replication is finished, the new strand

is compared to the old strand and any mismatched bulges or other

abnormalities are pruned and repaired. Any errors that remain after

stacking and checking are coded into the DNA as mutations, but even

then cells with abnormal DNA aren’t likely to survive to replicate.

Cells have to pass frequent tests of normalcy—like a Tour de France

rider taking a drug test at the end of every stage—and cells that rush

through their lifecycle like a doping rider aren’t allowed to continue.

Doping cells are pruned by apoptosis—programmed cell suicide.

NEW STRAND

NEW STRAND

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PATTERNSTRAND

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MISMATCHED NUCLEOTIDE

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A CONVERSATION WITH SONIA OKUYAMA, MD

C3: How did you get interested in the

psychosocial aspects of cancer care?

Okuyama: Where I trained in Peru, we had none

of the modern medicines or technologies. The

psychosocial aspect was fundamental to patient

care—many times it was all we had—so it’s close

to my heart. I see similar challenges during my

clinical work at Denver Health, where about half our

patients are uninsured. Even with insurance it can

be very difficult to get appropriate psychological

support, since coverage is so limited. My work is to

gather evidence that can help patients access this

integral part of cancer care.

C3: So instead of treatments targeting

cancer, what’s the focus of your research?

Okuyama: I have projects looking at the psycho-

social care of cancer patients at every stage of the

disease. For example, the Dignity Therapy Project

is testing a structured videotaped interview as an

intervention to improve psychosocial outcomes in

advanced cancer patients. This allows patients to

reflect back on their lives, what they want to leave

behind and what they’re most proud of.

Assistant Professor, Medical Oncology, University of Colorado School of MedicineDirector, Cancer Information and Counseling Line (CICL), CU Cancer Center

B Y GA RT H S U N D E M

I remember one patient in particular who was

nearing the end of the medicines we could offer to

treat his colon cancer. We talked about palliative

care and end-of-life planning, but there was a wall

we couldn’t penetrate; he would shut us down.

We were worried that without a proper discussion

he would end up dying in the ICU. Then he took

part in the Dignity Therapy Project and it was such

a breakthrough. Two or three months down the

road, when the time came, the transition to

end-of-life was completely opposite to what

we feared. It was dignity.

C3: And at other stages of cancer?

Okuyama: We’re studying programs for cancer

survivors as well. For example, the C-STEPS

[Cancer Survivorship Telephone Education and

Personal Support] program is a six-session tele-

phone counseling program delivered by the CICL,

After medical school in Peru and an oncology fellowship at CU Denver, Sonia Okuyama,

MD, took a turn from the study of drugs and devices to the study of cures for the mind

as well as the body. As the new director of the Cancer Center’s Cancer Information and

Counseling Line (CICL), Dr. Okuyama develops and implements interventions that help

patients cope with the many challenges of cancer outside the traditional conception of

physical health. Here we talk with Dr. Okuyama about her work.

where survivors learn to manage and cope with

the increased distress that can be very poignant

in cancer survivors. The other component of this

counseling program is to help patients adopt healthy

lifestyles—eating more fruit and vegetables and

exercising. As you can see, my research is about

helping people through the cancer journey, not

from the medical/drug standpoint, but from the

psychosocial, whole-person standpoint.

C3: How do you think being trained as

an oncologist and not necessarily as a

psychologist affects your work?

Okuyama: We have phenomenal psychologists

as part of our research team, but I do think it helps

in many ways to have an oncologist bridge the gap

between these worlds to ensure a collaborative

effort—and I’m happy to be such person. As any

oncologist will tell you, every day we deal firsthand

with highly distressed patients who seek not only

the best medical treatments, but also a more holistic

understanding of the cancer experience. Cancer

care is definitely moving in that direction. I hope I can

help the University of Colorado Cancer Center offer

the most outstanding care, in the broadest definition

of the word.

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The Cancer Information and Counseling Line helps patients cope with the many challenges of cancer.

Learn more about the free Cancer

Information & Counseling Line at

www.thecancerline.org

or call 800-525-3777.

C3: WINTER 2012

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MD C L I N I C A L C A R E

Lured by Great Science, CollaborationNEW TO COLORADO, CLAYTON SMITH IS ADVANCING BLOOD CANCER TREATMENT AND CARE AT CU

Great science is the main reason Clayton Smith

came to Colorado. Easy access to beautiful

mountains, strong research collaborators and the

opportunity to lead University of Colorado Cancer

Center’s Bone Marrow Transplant Program are

additional perks.

“I visited Colorado over the years for scientific

conferences and I loved it,” Smith says. “You’ve got

to love the mountains and the sunshine. Believe

me, after the gloomy, rainy weather in Vancouver,

B.C., the sunshine is a big deal.”

Prior to coming to CU Cancer Center in

July 2012, Smith spent years fostering a long-

distance collaboration with a member of University

of Colorado Skaggs School of Pharmacy and

Pharma ceutical Sciences faculty—Vasilis Vasiliou,

PhD. For 25 years, Vasiliou’s laboratory has studied

aldehyde dehydrogenases (ALDHs) focusing on

their role in metabolism, cellular responses to

stress, metabolic diseases, cancer and cancer

stem cells. Smith and Vasiliou research the role of

ALDHs in controlling the growth of normal stem

cells and leukemia stem cells.

“Vasilis is the leading expert in the world on the

ALDH gene family,” says Smith. “I read his papers,

followed his research, and then had the good

fortune to meet him in San Francisco. We were

attending different conferences at the same time,

but we sat down to a crab dinner and talked

about science.”

Today, instead of multiple phone calls and

emails or meetings in other cities, Smith walks

across campus.

“It is particularly nice on the University of

Colorado Anschutz Medical Campus to have a

superb group of researchers all within easy walking

distance of each other—this really fosters collabo-

ration and interaction,” Smith says.

“I have a fruitful collaboration with Clay. It’s

wonderful having him closer,” Vasiliou says. “Easy

access provides opportunities for a more produc-

tive collaboration and spontaneous genius—both of

which have the potential to lead to a breakthrough.

That’s exciting.”

Smith’s research involves manipulating ALDH

genes to grow more normal stem cells, which in

turn compete against and eliminate leukemia stem

cells. Additionally, by learning to manipulate stem

cells, he may help unlock the mystery of how

ALDH genes turn on cancer.

“If we can identify how blood stem cells

become cancerous, the next step will be research-

ing whether we can interrupt that process,” Smith

says. “Learning how these cells operate may also

help us identify existing targeted therapies or even

develop new drugs to treat blood cancer.” One

day Smith, Vasiliou and other researchers could

discover how to prevent leukemia from developing

in the first place.

Turning lab findings into targeted therapies

isn’t only a huge success for Smith and other

researchers; it’s also a success for patients around

the world living with leukemia and a success for

Smith’s patients at CU Cancer Center.

“When I was an intern at Parkland Hospital in

Dallas, Texas, one of my patients had acute leuke-

mia and I could look under a microscope and see

his disease,” says Smith. “Patients like him have to

fight hard to beat leukemia and I want to find them

hope and extend their lives.”

Smith credits his enthusiasm to people—

to these patients and to his colleagues. “My

collaborators at CU Cancer Center are the most

dedicated and passionate people in medicine,”

Smith says—and he should know, having trained

with leading experts from institutions including

Memorial Sloan-Kettering Cancer Center, Moffitt

Cancer Center, Duke University Medical Center and

Stanford University Medical Center. That was before

becoming the director of the BC Cancer Agency’s

Leukemia/BMT Program in Vancouver.

“Science and technology are constantly

changing and there have been spectacular

advances in treating leukemia in my lifetime,”

Smith says. “Being part of that change offers

the opportunity to use what I see in the lab

when I’m seeing my patients.”

ABOUT CLAYTON SMITH, MD

Director, Bone Marrow Transplant Program, University of Colorado Cancer Center

Professor of Medicine, University of Colorado School of Medicine

B Y E R I K A M A T I C H

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“It is particularly nice on the University of Colorado Anschutz Medical Campus to have a superb

group of researchers all within easy walking distance of each

other—this really fosters collaboration and interaction”

—clayton smith, md

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Outliving the OddsIN 20 YEARS, HARRY PETERSON EXHAUSTS HIS DOCTOR’S “BAG OF TRICKS,” FINDS HOPE IN A CLINICAL TRIAL

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When Harry Peterson, a retired engineering professor, had his first prostate cancer scare, Bill Clinton was in his first

term as president of the United States. More than 20 years have passed since President Clinton was

elected and two more presidents have served, yet Harry, now 81, continues to fight prostate cancer—despite exhausting two doctors’ “bags of tricks.”

“I was beyond what my urologist and oncologist Dr. David Link could offer,” Harry explains. “I was at the end of the road. I’d had such good luck with previous treatments—and then to live for 15-plus years, it was a big surprise to see everything go to pot.”

Today, Harry’s not giving up hope. He’s turned to urologic medical oncologist Thomas Flaig, MD, and a clinical trial at the University of Colorado Cancer Center.

“This clinical trial is a unique treatment option not available at other places in Colorado,” says Flaig. “Patients like Harry have the opportunity to participate in trials that determine the effectiveness of a new a hormonal agent for prostate cancer.”

By choosing the clinical trial of a genetically targeted treat-ment, Harry anticipates he’ll avoid chemotherapy’s harsh side effects and outlive his latest prognosis.

WATCHFUL BUT WAITINGThis year nearly 242,000 American men will be diagnosed with prostate cancer, the most common cancer in men. Of those diag-nosed, nearly two thirds are 65 or older. Very few cases are diag-nosed prior to age 40. Although most men die with and not from prostate cancer, still, nearly 30,000 lose their lives every year.

At 65, Harry’s first warning signs were an elevated prostate-specific antigen (PSA) and a small growth on his prostate. After a sonogram and biopsy, the growth was found to be benign. A number of benign prostate conditions can cause an elevated PSA so Harry and his physician weren’t too concerned.

“Back in the day they didn’t take a lot of specimens,” Harry recalls. “At first, my prostate cancer didn’t develop a lot of PSA; it wasn’t as elevated as the doctors were looking for.”

Harry and his physician decided it was best to continue to monitor his PSA, a strategy called “watchful waiting,” to see if levels stabilized.

While Harry waited, his brother-in-law was also diagnosed with prostate cancer. Unlike Harry, his PSA climbed drastically in a short period of time. He opted for brachytherapy, a type of treatment where tiny radioactive pellets are implanted in the prostate to kill the tumor.

Harry had a feeling it was time for him to go back to his doctor. Could his PSA also be rising?

By now it was 1996. Four years had passed since the watch-ful waiting began, but his PSA graphs were inconclusive. He decided it was time to have another sonogram and a set of biop-sies. They were conclusive: Harry had cancer.

Rather than undergo brachytherapy like his brother-in-law, Harry opted for a radical prostatectomy in early 1997. He hoped by removing the cancerous prostate he’d be cancer free. He wasn’t so lucky.

“It turned out that the cancer was everywhere and it wasn’t slow-growing,” Harry says. “It was a seven on the Gleason scale.”

The Gleason scale is the most common system used to grade prostate cancer. Scores range from two to 10. In order to come up with the Gleason score, a pathologist looks at the patterns of cells in the prostate tissue samples. The most common pattern of cells is given a grade of one to five. Five is the most abnormal. An additional score is given to a second common pattern of one to five and these two scores are added together to get the Gleason sum score.

With a Gleason score of seven, Harry’s life expectancy was five years at best, he was told. Despite the odds, he wanted to face cancer the same way he faced work and life—with perfection.

NEVER FIN ISHEDHarry has had to get through good times and bad for more than 60 years—thankfully, he’s had his wife right by his side all those years. As a 19-year-old college sophomore at Colorado A&M, now Colorado State University, Harry married Delores, “Dee,” his high school sweetheart.

“We didn’t know any better when we got married,” Harry says. “Our moms were a little upset. They didn’t think we’d make it through school.”

Determined to beat the odds, Harry finished his bachelor’s. Subsequently, he was accepted into the engineering mechanics PhD program at Cornell University and was offered a teaching

Opposite: Harry Peterson with Dee and his prized 1962 Morgan Drophead Coupe.Above: Xiaoping Yang, PhD (left), Thomas Flaig, MD, and Lih-Jen Su, MS, focus on genitourinary cancer translational research in Flaig’s lab at CU Cancer Center.

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14WWW.COLORADOCANCERCENTER.ORG

position. This was the start of his career as an engineering pro-fessor, eventually leading him to the Martin Marietta Corporation (now Lockheed Martin), University of Denver and Colorado School of Mines.

In the late 1960’s, Harry began researching motorcycle acci-dents and rider injuries through computer simulation with the U.S. Department of Transportation and a British testing lab. His research concluded the need for leg protectors and redesigned fuel systems.

“Back then guys were basically riding around with tin cans between their legs that could easily catch on fire,” Harry explains. “We researched ways to prevent severe leg burns and injuries.”

By 1973, Harry was an expert witness in motorcycle accidents around the country. That work, plus teaching, kept him busy up until 1995, when he retired.

“I was never able to put my work aside,” says Harry. “I couldn’t stop working until it was complete. Some people call it perfectionism; it was my life.”

ANOTHER FIVE, 10 YEARSWith determination, Harry survived the first five years post prostatectomy, despite rising and falling PSA’s. Six months of radiation helped his PSA drop, but it escalated once treatment was complete.

“When he first started treatment, Harry’s urologist said if he could keep him alive for five years there would probably be better drugs available for someone like him,” Dee says.

“Well, that was years ago,” Harry chimes in. “The good Lord must have been looking out for me because those five years are long gone.”

In 1999, Harry started leuprolide (Lupron) injections every four months to help decrease testosterone, prostate cancer’s fuel. Harry’s PSA started to drop and stabilize.

Another 10 years flew by. By late 2010, Harry’s PSA was going wild.

Leuprolide was failing. Hoping to again control the testosterone, his urologist introduced bicalutamide (Casodex) into his treatment regimen. Bicalutamide is another hormonal therapy that works to block the effects of testosterone in conjunction with leuprolide.

The combination therapy didn’t work. The only option his oncologist had left was chemotherapy; life expectancy at that point wasn’t great—three months to three years. His oncologist’s “bag of tricks” was empty. “There were very few options left,” Dee says. “He was at the end.”

A LESS TOXIC CHOICEWith only chemotherapy left, Harry’s oncologist contacted Dr. Flaig, who’s also the medical director of the Clinical Investigations Shared Resource at CU Cancer Center, to ask if any clinical trials were open for advanced prostate cancer patients.

Harry was in luck.

The PREVAIL study, a global Phase III clinical trial of an investigational drug, was enrolling patients with advanced pros-tate cancer. Harry qualified and enrolled in 2011. At this point, his PSA was doubling every two months.

“I was certainly praying I could get on the clinical trial,” says Harry, “but I worried it was a double-blind study. I could poten-tially get the placebo.”

The randomized, double-blind, placebo-controlled, multi-national PREVAIL trial enrolled 1,680 patients with metastatic prostate cancer who had progressed despite treatment with androgen deprivation therapy, like leuprolide or bicalutamide. In addition to standard-of-care treatments (Harry stayed on leupro-lide), half of the participants get a placebo and the other half get the drug enzalutamide.

“We’re looking to see if we can use a less toxic hormonal pill to treat advanced prostate cancer cases where we’d traditionally use chemotherapy,” says Flaig. “Enzalutamide has already been proven to help patients live longer in more advanced settings in which the patient has already received chemotherapy. Now we want to see if it works as well if used before chemotherapy.”

In the year and a half Harry’s been on the clinical trial, he’s already started to feel better and he hasn’t had to endure the harsh side effects of chemotherapy.

“The difference between the side effects of taking this pill versus undergoing chemotherapy is night and day for most patients,” Flaig explains. “The pill makes sense and we need to see if we can use it earlier in the process and delay the need for chemotherapy.”

With time Harry has seen his PSA drop. More time will tell if it stabilizes. Right now, he doesn’t know if he’s taking the placebo or enzalutamide.

“I really owe Dr. Flaig a debt. He’s kept me alive a lot longer than was expected,” Harry says. “I don’t think I was supposed to survive this long.”

“It’s gratifying to see patients respond well to new treatments,” says Flaig. “We’ll be excited to see the results of this clinical trial in the months to come.”

While it’s been a long 20 years, another year or two of waiting is just a drop in Harry’s bucket. Flaig hopes the trial’s results will be published in 2013.

Until then, Harry continues to simply live.

LIVING LIFEDespite diabetes, arthritis and old age, Harry says, life’s been good. He hasn’t needed a support group. “I don’t know what I’d complain about,” he says. “For better or worse, it’s something that’s there, but it hasn’t made a big difference in our life.”

When Harry’s arthritis isn’t getting the best of him, you’ll find him and a buddy tinkering with his English car collection. Today, he’s probably out working on his 1962 Morgan Drophead Coupe, a car “that outshines them all,” he says.

He, too, is outshining prostate cancer.

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Do you have an inspirational story? Tell your story at

http://story.coloradocancercenter.org.

C3: WINTER 2012

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ST RYINSIDE

To learn more about prostate cancer treatments at

CU Cancer Center, visit

www.uch.edu/conditions/cancer/prostate-cancer/

To search for a cancer clinical trial, visit

www.uch.edu/conditions/cancer/research/

research_trials/

Like Harry Peterson (page 12), patients with advanced prostate cancer are directly benefiting from the develop-

ment of new androgen-blocking drugs and immunotherapies. Recently, three new drugs have improved survival

outcomes by curbing testosterone or training the body’s immune system to attack prostate cancer cells.

ENZALUTAMIDE ADDS MONTHS TO SURVIVALProstate cancer cells need androgens, like the male hormone tes-tosterone, to grow. For prostate cancer patients with cancer that has spread beyond the prostate, hormonal therapy or androgen deprivation therapy can help prevent further tumor growth and improve quality of life.

Recently, enzalutamide (Xtandi®, MDV3100) came on the market with the best survival data ever seen in prostate cancer. It lowered PSA levels, shrunk tumors and extended survival of advanced prostate cancer patients who had undergone chemo-therapy by five months.

“This is a major advance. Not only do we see more survival benefit than from traditional chemotherapy, but the side effects of enzalutamide are much lower,” says Thomas Flaig, MD, medi-cal director of the CU Cancer Center Clinical Investigations Shared Resource and co-author of the study. “It provides both more benefit and less harm—you get the quantification of more life, but also see quality of life improvements.”

To the body, enzalutamide looks a little like testosterone—the same pieces of cell machinery that grab testosterone grab enzalu-tamide instead; but unlike testosterone, enzalutamide molecules don’t tell prostate cancer cells to grow. Other therapies make the body produce less testosterone: enzalutamide ensures the body can’t use the little testosterone it continues to produce.

The FDA has approved the drug for treatment of advanced castrate-resistant prostate cancer in patients who have already been treated with the chemotherapy drug docetaxel (Taxoterne). Now researchers are studying whether it can improve survival outcomes for patients, like Harry, who haven’t been treated with chemotherapy.

“Enzalutamide is a key member of a half dozen new and emerging drugs and the challenge of the next five years is to discover how to best time and potentially combine these new agents. But even at this early stage, enzalutamide is a game changer,” Flaig says.

AB IRATERONE: ANOTHER TESTOSTERONE INHIB ITORApproved in 2011, abiraterone (Zytiga) has been shown to boost survival by more than three months for men whose cancer has progressed after chemotherapy with docetaxel.

Abiraterone is a hormonal therapy that targets a protein called cytochrome P450 17A1—a key player in producing testosterone. The drug works in combination with prednisone to decrease the production of testosterone in the testes, adrenals and in the cancer itself.

This class of drugs is called androgen biosynthesis inhibitors, and abiraterone was the first of its type approved by the FDA. Unlike chemotherapy, these new drugs kill fewer healthy cells along with the cancerous cells and so have fewer side effects.

“Targeting cells’ androgen receptors is a new and exciting development in the field of prostate cancer therapy,” says E. David Crawford, MD, head of urologic oncology at CU Cancer Center. “As these new drugs make their way from the lab to clinic, we expect the ability to offer androgen antagonists to patients whose cancers have resisted other treatments.”

PROSTATE CANCER’S FIRST IMMUNOTHERAPYFor men who have advanced prostate cancer that is not respond-ing to hormonal therapies, researchers are advancing the use of a new class of drugs known as immunotherapies, including the drug Provenge®.

Provenge trains the body’s immune system to attack prostate cancer cells. The treatment involves removing the patient’s own white blood cells, mixing the cells with a drug designed to target prostate cancer cells, and then re-infusing the treated blood into the patient. The treatment is repeated three times over the course of a month.

In 2010, data from the IMPACT trial showed patients who received Provenge lived on average more than four months longer than men who received the placebo treatment.

While Provenge, Abiraterone and Enzalutamide are not cures, they offer hope to patients who previously exhausted all treat-ment options.

“Even without the addition of any more drugs, we may now have the tools that in combination will allow us to extend the survival prognosis of a prostate cancer patient long enough to make prostate cancer a disease a patient is more likely to die with than from,” Crawford says.

—Kim Chriscaden and Garth Sundem

New drugs changing prostate cancer treatment

16WWW.COLORADOCANCERCENTER.ORG

From 2004 to 2008, money from the Amendment 35 tobacco tax funded chronic disease prevention programs. Then the recession hit and the state redirected this

money to other urgent needs. Now, with the economy’s slow climb from the doldrums,

millions of dollars from Colorado’s tobacco tax are once again flowing. Researchers in cancer prevention programs at the University of Colorado Cancer Center are hopeful the money will impact the state’s cancer rates—and save both lives and health care costs in the long run.

“The good news is programs to prevent cancer are being funded again,” says Tim Byers, MD, MPH, associate director of cancer prevention and control at CU Cancer Center and associate dean of public health practice at the Colorado School of Public Health.

For example, CU Cancer Center projects that screen uninsured individuals for colon cancer, help smokers quit, and identify patients at risk for hereditary breast and colorectal cancer are rediscovering their footing due to returned Amendment 35 funding.

“The competitive grants given because of Amendment 35 mean the best of the best evidence-based programs can once again compete for funding,” Byers says. “As a result, hundreds of people won’t get cancer and the health care system won’t have to bear those costs.”

BALANCING THE SMOKING BURDENSmokers tend to tax the health care system, so the system should in turn tax smokers. That was the gist of the thinking in 2004, when 61 percent of Colorado voters approved Amendment 35 to increase taxes on cigarettes and other tobacco products.

The thinking was right: Annual health care costs in the United States directly related to smoking are more than $1 billion. Approximately $425 million in income and produc-tivity is lost every year due to premature death caused by smoking. And tobacco-related illnesses are the leading cause of preventable death in Colorado.

Tax revenue went to programs that sought to balance these numbers—to prevent these preventable deaths and save the health care system the money it would eventually spend taking care of these smokers.

For example, the statute requires 16 percent of tobacco tax revenues to be used for school funding of tobacco education programs aimed at keeping youth from smoking, smoking cessa-tion programs and programs to reduce exposure to secondhand smoke. Another 16 percent goes to prevention, early detection and treatment of cancer, cardiovascular disease and chronic pulmonary disease.

CU Cancer Center got a slice of each of these funds—and came to depend on these monies to keep the lights on in many of the Center’s prevention and control programs.

When the economy went south, Colorado legislators declared a fiscal emergency. From 2009 to 2011 Amendment 35 funds were down in general—fewer people could afford to smoke. And these reduced funds were redirected to cover expanding Medicaid costs. Cancer prevention programs like CU Cancer Center’s Colorado Colorectal Screening Program saw their bud-gets slashed—free screenings were reduced and research projects went into maintenance mode.

CANCER SCREENING INFORMATION

Colorado Colorectal Screening Program participating clinics 866-227-7914, www.colonscreen.coloradocancercenter.org

Women’s Wellness Connection 866-951-WELL (9355)

Metro Community Provider Network 303-360-MCPN (6276)

TOBACCO TAX SPENDS MONEY TO SAVE MONEY …AND LIVES

W I T H E C O N O M Y ’ S C L I M B ,

AMENDMENT

35 A G A I N F U N D S P R E V E N T I O N

P R O G R A M S

B Y E R I K A M A T I C H

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At the same time, Byers and Cancer Center colleague Paul Bunn, MD, joined the American Cancer Society’s effort to encourage state legislatures to preserve Amendment 35 money. Their efforts worked.

Today, Colorado’s economy is recovering and Amendment 35 funding is being restored. In fiscal year 2012-2013, the state of Colorado predicts it will receive approximately $140 million in tax revenue from Amendment 35—about $46 million of which will be available to agencies working to prevent cancer—agencies like CU Cancer Center.

OUT OF HIBERNATIONThe economy goes up, tax revenues go up, prevention and con trol programs go up. Hopefully speaking, smoking and cancer rates will go down. With the first now gaining traction, CU Cancer Center researchers are starting to see the other three fall in line.

Arnold Levinson, PhD, MJ, a tobacco control expert at the CU Cancer Center, is the scientific director on a new three-year, $600,000 grant to design, implement and evaluate smoking cessation treatment programs for tobacco-using patients in the University of Colorado Health system.

The project—a collaboration between CU Cancer Center and University of Colorado Hospital (UCH)—brings together the academic expertise of Levinson’s research group with system-wide access to patients in three University of Colorado Health hospitals: UCH, Poudre Valley Hospital and Medical Center of the Rockies.

“We hope our initiative will serve as a model for other hospitals,” Levinson says.

Byers hopes the program will directly result in quitting. “About 17 percent of the population in Colorado smokes,” he says. “There is really no reason we can’t continue to drive down that number.”

BEYOND TOBACCOIn addition to funding tobacco cessation and education programs, Amendment 35 sets aside money for research and treatment grants.

Jan Lowery, PhD, MPH, CU Cancer Center investigator and assistant professor of epidemiology at the Colorado School of Public Health, is benefitting from one of these grants—and her work could soon benefit all Colorado residents. Lowery’s project, called “Colorado Generations” (for which she teamed up with Metro Community Provider Network and Plains Medical Center), is all about maximizing thin resources. Who should undergo costly advanced cancer screening? Well, the people who are at the greatest risk of developing the diseases.

“It’s critical that we identify people who are at risk for her e-ditary cancer because their risk for developing cancer may be as high as 80 percent,” Lowery says. “This project will help clinics identify their patients that, due to their family history, are at increased risk for cancer and in need of cancer screening.”

“Hopefully, by identifying high-risk patients, clinics can prioritize their already limited resources for subsidized screen-ings,” she explains.

Colorado Generations matches medi-cally underserved Coloradans with genetic counselors who can help assess cancer risk, coordinate testing and make screening recommendations for those at especially high risk for hereditary cancers.

“The goal is to increase awareness about family history and hereditary cancer risk among patients and their providers,” Lowery says. “We want them to know what it is and whether it may affect them so that they can get appropriate care and make informed, pro-active decisions about their health.”

Colorado Generations refers patients to Women’s Wellness Connection for free breast cancer and cervical cancer screen-ings. It also refers patients to the Colorado Colorectal Screening Program (CCSP)—another Amendment 35-funded project at CU Cancer Center, which through June 2011 had screened more than 13,000 Coloradans at 65 community health clinics and detected 112 cancers.

“The program saves millions in medical costs by preventing colorectal cancer,” says Andrea Dwyer, CCSP Program Manager. “And you can’t put a price tag on the lives saved by those whose cancers were caught early or completely prevented.”

With the loss of Amendment 35 money, the CCSP had to cut way back. Now the money has returned.

“We were awarded nearly $3 million dollars this year in the state’s competitive grants program to rebuild the program infrastructure and screen several thousand people.”

Amendment 35 money goes up, cancer goes down. Byers, Bunn, Levinson, Lowery, Dwyer and their CU Cancer Center colleagues hope that 2012 and 2013 are only the start.

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The Colorado Colorectal Screening Program at CU Cancer Center has screened more than 13,000 Coloradans at 65 sites across the state.

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S U P P O R T E R F CUS

Midge Wallace, Carolyn Fancher and Nina Ahbe

are more than friends and neighbors. They’re also

breast cancer survivors committed to funding cancer

research and spurring others to do the same.

Affected by breast cancer in the 1990’s, Midge

and Carolyn know firsthand the impact the disease

has on patients and families. In 1996, not wanting

their children or grandchildren to have to go through

the same experience, Midge and Carolyn founded

CancerCure, a membership group for donors inter-

ested in supporting cancer research at University

of Colorado Cancer Center.

“Our mission is really to spread the word about

the CU Cancer Center, what a National Cancer

Institute-designated cancer center is, and how

important it is to have this high level care and

research here in Colorado,” Midge says.

When they founded CancerCure, Midge was

only interested in funding breast cancer research;

however, she quickly learned that a rising tide floats

all boats—discoveries in one cancer are frequently

relevant to others.

“At first I only wanted to focus on breast

cancer since my mother, sister and I have had the

disease,” says Midge. “After meeting and spending

time with researchers, I realized there are so many

crossovers to multiple cancers.”

Another Survivor

Ten years ago, Nina Ahbe and her family moved

to Colorado and bought a house in the same

neighborhood as Carolyn and Midge. She was

diagnosed with breast cancer shortly after, having

not met either of the women.

A fluke phone call from their daughters at

Miami University in Ohio brought Carolyn and Nina

together. It turned out that both Carolyn’s and

Nina’s daughters were starting their freshman year

and living in the same dorm. It wasn’t long after

that Nina and Carolyn became friends—and Nina

became a breast cancer survivor.

After Nina’s treatment was completed she and

her husband joined CancerCure. Two years ago,

she became CancerCure’s co-chair with Midge.

“When you’ve been touched by cancer, like

Midge, Carolyn and I have, you want there to be

more research so that new discoveries are made,

potentially impacting future generations,” Nina says.

Now 16 years later, Midge, Nina, Carolyn and

other CancerCure members have raised nearly

$1.5 million through individual gifts. The members

have funded seed pilot grants for young research-

ers, summer student cancer fellowships, critical

research equipment and a melanoma research

group, among others.

One hundred percent of their funding goes

towards cancer research in Colorado and is used at

the discretion of the CU Cancer Center director.

Shifting Focus

Last fall, CU Cancer Center Director Dan

Theodorescu, MD, PhD, challenged CancerCure

to undertake a larger fundraising initiative: establish

a premier prevention and control program, headed

by an endowed chair—a five-year, $1.5 million

commitment.

“This is the first time the director came to us

ahead of time,” Midge says. “Dr. Theodorescu felt

the endowed chair for cancer prevention and con-

trol was one of the Cancer Center’s greatest needs.

We decided to accept his request and commit to

raising $750,000 over the next five years.”

AMC Cancer Fund, the CU Cancer Center’s fun-

draising partner, is collaborating with CancerCure

to raise the additional $750,000 needed to fund the

CancerCure/AMC Cancer Fund Endowed Chair for

Cancer Prevention and Control. In May 2012, Nina

and Midge presented an initial $250,000 check to

the Cancer Center on behalf of CancerCure.

“AMC Cancer Fund is honored to partner with

CancerCure to establish an endowed chair,” says

Nancy Stewart, vice president of community

relations at AMC Cancer Fund. “Historically,

the investigators of what was the AMC Cancer

Research Center were at the forefront in this area

of cancer research. We believe the endowment

is a wonderful way to honor our legacy.”

Because the majority of research funding goes

to science aimed at treating cancer rather than pre-

venting it, CancerCure and AMC Cancer Fund will

fund projects aimed at reducing cancer incidence,

morbidity and mortality, as well as improving the

quality of life for cancer patients. These projects

will be funded using investment income from the

endowed chair.

“In our world today we don’t allow for

enough great research to happen,” Midge says.

“Because we have an NCI-designated compre-

hensive cancer center in Colorado, I’m excited to

support the research CU Cancer Center does so

that we can eradicate cancer from our and our

children’s lives.”

CancerCure welcomes new members throughout

the year and hosts two annual events for its general

and patron members. General memberships are

$100 and patron level memberships are $750

annually. Learn more about membership levels at

www.wearecancercure.org or contact Nina Ahbe

or Midge Wallace at wearecancercure@gmail.com.

Neighborly CommitmentCANCER SURVIVORS, NEIGHBORS “ALLOW GREAT RESEARCH TO HAPPEN” FOR 16 YEARS

Nina and Midge with one of CancerCure’s founding members, Mary Lee Beauregard at the check presentation in May 2012.

Nina Ahbe and Midge Wallace present an initial $250,000 check to the CU Cancer Center on behalf of CancerCure.

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C O M M U N I T Y N E W S

RESEARCHER LEADS TWO-DAY FRONT RANGE RIDE FOR CANCER RESEARCH

FIRST YEAR RIDE HOSTS 35 RIDERS, RAISES $10,000

NEW “PINK LIFE SAVER” HITS THE STREETS, PROVIDES BREAST CANCER SCREENINGS

When Scott Cramer, PhD, professor of pharmacology, prostate cancer researcher and co-director of the

Hormone Related Malignancies Program at the University of Colorado Cancer Center, moved to Colorado

a year ago, he instantly organized his life around cycling.

Besides commuting 16 miles to work every day, Cramer started planning the Cancer Center’s first

group bike ride to support cancer research—an event he assumed already existed.

“When I first moved to Colorado I was surprised there wasn’t an organized ride for the University of

Colorado Cancer Center,” Cramer says. “I figured there would be with how big cycling is in Colorado.”

That didn’t stop Cramer from starting his own. In September, Cramer and more than 30 other riders

piloted the Cancer Center’s first Front Range Ride taking riders 110 miles from the CSU Animal Cancer

Center to CU-Boulder and then on to the CU Anschutz Medical Campus. The riders raised nearly $10,000

for cancer research.

“The goal is to eventually make this a fundraising event that would be the signature event for the Cancer

Center, while highlighting our unique consortium,” he says.

The ride linked four of the Cancer Center’s nine consortium members: Children’s Hospital Colorado,

University of Colorado Hospital, CSU Animal Cancer Center and CU-Boulder. The Cancer Center consor-

tium unites Colorado’s basic, translational and clinical cancer research at three universities, five medical

centers and one health maintenance organization.

The top two reasons women don’t get annual mammograms are time and convenience. In an effort to

overcome those excuses, University of Colorado Hospital, CU Cancer Center’s patient care partner, has

created a mobile mammography coach named “The Pink Life Saver.”

The Pink Life Saver was unveiled to the public for the first time on October 16 at the annual Men for the

Cure event. Funds raised by Men for the Cure, along with money donated by King Soopers, paid for the

unit, which is fully equipped to provide breast cancer screenings to women around the metro Denver area.

Patients are able to schedule appointments for screenings in The Pink Life Saver, as the unit travels to

UCH clinics and The Little Clinic at select King Soopers stores, one day a week. If the service is successful,

the hospital plans to expand it to corporate clients.

To find out where The Pink Life Saver is going to be or to schedule an appointment, call 720-848-1030.

Dinner in White pops up in

downtown Denver

Downtown Denver was blanketed in a sea of

white as the 3rd annual Dinner in White, hosted

by AMC Cancer Fund, popped up near Denver

Union Station. The annual event hosted 350

guests and brought in more than $38,000 for

cancer research at CU Cancer Center.

Make your appointment at

UCH.EDU/MAMMOGRAMor call 720.848.1030

University of Colorado Hospital Mobile Mammography

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New joint fundraising team, location

and name in 2013

In January, the AMC Cancer Fund will be

changing its name to the University of Colorado

Cancer Center Fund. Partnering with CU

Foundation fundraisers dedicated to the

Cancer Center, CU Cancer Center Fund will be

located on the University of Colorado Anschutz

Medical Campus. Their new address is

13001 E. 17th Place, MS F500, Aurora, CO,

80045. Stay tuned for a new website, brand

and logo.

MARCH 7 – COCKTAILS FOR A CURE

Join AMC Cancer Fund on March 7, 2013 for the

4th annual Cocktails for A Cure Women’s Event

benefiting CU Cancer Center. Bring a girlfriend

and sip on a signature cocktail, peruse the silent

auction or take a chance at the wall of wine.

Most importantly, enjoy an enlivening experience

celebrating Colorado women and supporting the

research and treatment of women’s cancers

at CU Cancer Center.

S A V E T H E D A T E

20WWW.COLORADOCANCERCENTER.ORG

W I N T E R 2 0 1 2

www.coloradocancercenter.org

C3: Collaborating to Conquer CancerPublished twice a year by University of Colorado Denver for friends, members and the community of the University of Colorado Cancer Center. (No research money has been used for this publication.)

Editor: Kim Chriscaden | 303-724-0114 | Kimberly.Chriscaden@ucdenver.eduContributing Writers: Garth Sundem, Erika MatichPhotos: Glenn Asakawa, Casey Cass, Lynn Clark, Dana McGrath, Steve Z. Photography

The CU Cancer Center Consortium MembersUNIVERSITIESColorado State UniversityUniversity of Colorado BoulderUniversity of Colorado DenverINSTITUTIONSUniversity of Colorado HospitalChildren’s Hospital ColoradoNational Jewish HealthDenver Health Medical CenterDenver Veterans Affairs Medical CenterKaiser Permanente Colorado

Visit us on the web: www.coloradocancercenter.orgThe CU Cancer Center is dedicated to equal opportunityand access in all aspects of employment and patient care.

UNIVERSITY OF COLORADO DENVER

13001 EAST 17TH PLACE, MSF434

AURORA, CO 80045-0511

R E T U R N S E R V I C E R E Q U E S T E D

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The accelerating pace of cancer discovery makes the next six months a critical, exciting and hopeful time in our fight against the disease

T H E M E S S A G E

FROM THE DIRECTOR DAN THEODORESCU,

MD, PhD

Six months ago when we sent the previous issue of this

magazine, we didn’t know the spread of bladder cancer

is dependent on androgens like testosterone. As you’ll

read in this issue of Collaborating to Conquer Cancer, we now

hope to eventually target bladder cancer with anti-androgens

like those used to treat prostate cancer. Six months ago, the

drug enzalutamide was still investigational. Now due in part to

clinical trials at the CU Cancer Center, the drug has earned FDA

approval and is being used to extend the lives of patients with

advanced prostate cancer. We were recently

instrumental in discovering melanoma stem

cells and at the Charles C. Gates Center for

Regenerative Medicine and Stem Cell Biology,

we just opened a clinical trial of a drug targeting

cancer stem cells.

In the past six months, we cut the ribbon

on a major expansion of the Anschutz Cancer

Pavilion at our clinical care partner, University of

Colorado Hospital, opening 42,000 square feet

of new space and dozens of new exam and treatment rooms.

On the heels of our partnership with Poudre Valley Health, we’ve

forged a new alliance with Memorial Health System, expanding

the reach of our care from Fort Collins to Colorado Springs and

beyond. And in the last six months, the National Cancer Institute

renewed our prestigious designation as a comprehensive cancer

center, recognizing our excellence in all aspects of the search for

cures, from basic lab research to patient care.

It’s been a big six months.

With the involvement and support of our community, the

University of Colorado Cancer Center looks forward to an even

bigger six months ahead. In partnership with MD Anderson, we

have a new grant to develop drugs for bladder cancer. Our lead-

ing work in targeted lung cancer treatments continues. Our clini-

cal trials program continues to offer tomorrow’s drugs to today’s

patients. And we are taking major steps in our understanding

of cancer as many individual but related diseases, defining the

genetic signature of a patient’s tumor and using

that signature to match patients with the most

effective treatments.

The Cancer Center represents the conflu-

ence of expertise, technology, experience

and compassion from our consortium sites

that encompass nearly all federally-funded

cancer researchers in the state of Colorado.

Investigators’ home sites include CU Denver,

CU-Boulder, Colorado State University,

University of Colorado Health, Children’s Hospital Colorado,

Denver Health, Denver VA Medical Center, National Jewish Health

and Kaiser Permanente Colorado. Members at these institutions

create a critical mass—with your help, we can not only continue

the trajectory of cancer discovery but accelerate that pace.

Here’s to the next six months.

“The Cancer Center represents the

confluence of expertise, technology, experience

and compassion...”