University of Colorado Cancer Center's Spring 2016 C3 Magazine

C O L L A B O R AT I N G

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C O N Q U E R

C A N C E R

SPRI NG 2016

Harnessing

EVOLUTION to Cure Cancer

WHY DID THE DINOSAURS LOSE?

12: ALL HANDS ON DECK 16: THE ELEPHANT IN THE ROOM 10: Q&A WITH SANA KARAM, MD, PhD 11: C3 MD ANA GLEISNER 18: SUPPORTER FOCUS ON THE FINLONS ANSCHUTZ MEDICAL CAMPUS

FLIC KR/C LIMAT E STAT E

N3WS HALF O F E LD E R LY C O LO R E CTAL CAN C E R PATI E NTS R E C E IVE VALU E LE S S TR EATM E NT A CU Cancer Center study shows that 53 percent of metastatic colorectal cancer patients older than age 75 received three or more treatments at a total 1-year treatment cost of $2.2 billion.

However, median survival for these patients increased by only one month over less invasive, less costly treatments.

BRADLEY

“These patients may get sicker and it costs them a lot of money with almost no survival benefit,” says first author Cathy J. Bradley, UNPACKING SPACE RADIATION KEY TO CONTROLLING ASTRONAUT AND

PhD, associate director for Population Science

POTENTIALLY EARTHBOUND CANCER RISK

Research at CU Cancer Center and professor

“I have become a bit of a space aficionado, but I suspect the major impact of what we do is going to

in the Colorado School of Public Health.

be for cancer patients,” says Michael Weil, PhD, professor in the Colorado State University Department

“No one wants to give up. It’s hard for anyone

of Environmental & Radiological Health Sciences. This is because high-energy ions similar to the radia-

to say they’ve had enough,” Bradley says.

tion experienced in space is being increasingly used in cancer treatments. Carbon ions are in use to treat

“However, in these situations palliative care may

cancer patients in Japan and Germany, and similar treatment facilities are in the planning stages in the

be a good option.”

The study closes by stating rather bluntly,

United States.

“The way carbon ions deposit energy is very suitable for hitting tumors while missing healthy tissue,”

“Taken together, multiagent regimens may not

Weil says. However, the same radiation used in cancer treatments presents a risk for the future develop-

be of high value in terms of costs and survival

ment of new tumors. How much risk is a question being answered by NASA.

for older mCRC patients.”

“NASA is most concerned about galactic cosmic radiation and the worst component is HZE ions,” Weil says. These ions, composed of atomic nuclei stripped of their electrons and moving through space at near light speed “can punch right through a couple meters of aluminum or right through an astronaut, leaving ionization tracks,” Weil says.

Get more CU Cancer Center

To study the effects of HZE ions on cancer risk, Weil uses a particle accelerator to fire ions at samples of human cells. The eventual goal of this work is to understand how, when and with what outcomes

news on our blog: www.coloradocancerblogs.org

HZE ions cause cancer. In addition to allowing human beings to travel to Mars, solving these questions

FLI CKR/ RD_ELSI E

may make us healthier here at home.

MAN’S BEST FRIEND HELPS FIGHT CANCER The University of Colorado Cancer Center and

animals are indistinguishable under the microscope

Colorado State University’s Flint Animal Cancer

or by genetic analysis.

Center (FACC) work together to advance the dis-

“That gives us an opportunity when there is a

covery of cancer therapies in humans and compan-

tenfold increase to expedite the drug discovery

ion animals. One way to make those advances is

process,” says Rod Page, DVM, FACC director.

to offer compassionate cancer care to companion

It goes both ways: People with cancer also are

animals and apply the knowledge to the treatment

advancing treatment in dogs. Dan Theodorescu,

of human cancer patients and vice versa.

MD, PhD, director of the CU Cancer Center, has

For example, FACC specializes in the treat-

pioneered work in predicting which cancerous

ment of osteosarcoma, commonly known as

tumors will respond to which kinds of chemotherapy

bone cancer, which occurs 10 times more often

agents. Recently scientists at FACC found those

“As the owner of two dogs, I’m really happy

in dogs than in people. Cancer also accounts for

predictions to be accurate across species, mean-

our work could contribute to help our best friends,”

50 percent of deaths in dogs above the age of 10.

ing that pet dogs treated at CSU may benefit from

says Theodorescu.

Osteosarcoma in people and tumors in companion

the discoveries made with human patients at the Anschutz Medical Campus.

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“This is a win-win situation for people and for my four-legged patients,” Page says.

CRC

INCREASES IN UNDER 50s

LUNG CANCER SURVIVORS WIN FUNDRAISING CHALLENGE Kim Ringen and Kathy Weber have a lot in common. Both live in Colorado, they are both fans of the Denver Broncos and both received treatment for lung cancer at CU Cancer Center. Kim and Kathy also took part in the 2016 Lung Cancer Survivors Super Bowl Challenge sponsored by Team Draft, an initiative of The Chris Draft Family Foundation.

Former NFL linebacker Chris Draft and his wife launched Team Draft at their wedding. Keasha Draft

STUDY SHOWS DIFFERENT GENETIC

passed away in December 2011 about a year after her stage IV lung cancer diagnosis. The Super Bowl

DRIVERS OF COLORECTAL CANCER

Challenge recruits lung cancer survivors to raise funds to find new ways to combat the disease.

E RIKA MAT IC H

IN OLDER AND YOUNGER PATIENTS A CU Cancer Center study shows genetic differences between colorectal cancer (CRC) in young and old patients, possibly pointing toward different treatments and strategies in combating the young form of the disease. Comparing 9 tumors from younger patients (median age 31) with 9 tumors from older patients (median age 73), showed “distinct genetic differences between younger and older patients with colorectal cancer,” says Christopher Lieu, MD, assistant professor of medical oncology at the CU School of Medicine.

While the overall rate of colorectal cancer (CRC)

WEBER, DRAFT, AND RINGEN PROMOTE TEAM DRAFT’S FUNDRAISER FOR LUNG CANCER RESEARCH Kim Ringen, DVM, of Denver, won the challenge raising more than $23,000. She was diagnosed with metastatic non-small cell lung cancer in May 2013. Ringen, a never-smoker also is quick to point out that

is declining, CRC specifically among young patients

anyone “with lungs can get lung cancer.” With her win, Ringen earned a spot in the stands to watch the

is increasing. Previous studies have shown that CRC

Broncos beat the Panthers at Levi’s Stadium in Santa Clara, CA!

in patients younger than 50 years old tends to be more aggressive than CRC in older patients.

Lung cancer survivor Kathy Weber, of Kiowa, raised more than $8,000 to take second place in the Super Bowl Challenge, earning Kathy and her family a trip to the Pro Bowl in Hawaii.

“If I were to shoot for the stars, I would say that

Weber had been training for figure body building competitions when she noticed pushups becoming

our end goal is to be able to offer better treatments

more difficult, but only on one side. The cause was a tumor in the upper lobe of one of her lungs, which

for this population of young colorectal cancer

was removed by CU Cancer Center thoracic surgeon Michael Weyant, MD.

patients that seems to be at higher risk from the

“Kathy’s case is another illustration that anyone can get lung cancer, even non-smokers,” says Weyant.

disease,” Lieu says.

“I am very happy to tell you that I am now a lung cancer survivor,” says Weber.

When Stephen Estrada started having unusual abdominal pain in 2013 he didn’t think much of it.

Stephen start a phase I immunotherapy clinical trial.

“I was scared to sign up at first,” says Stephen.

“Stomach problems are so common these days

“But Dr. Messersmith reached out to me and said

that I was not too worried,” he explains. “I started

that if he were in my shoes participating in the trial is

changing parts of my diet and exercising more to

exactly what he would do. That was enough for me.”

try and stop the pain. At the time I thought I might have celiac disease or something.”

However, after many trips to emergency rooms

Stephen started the trial and the results were astounding. “Almost immediately I started gaining weight, my hair came back thicker and faster, and

Stephen eventually went to his primary care doctor

I felt good every day,” he says. “The treatments are

to see if she could do anything. The lymph nodes

also a breeze compared to chemotherapy.”

in his back were the size of peaches. Stephen had stage IV colon cancer.

Genetic testing showed a mutation in Stephen’s

On the trial Stephen experienced initial shrinkage of the tumor and is now considered stable. Now Stephen is not only a patient but he and his partner,

MLHI gene, indicating Lynch syndrome, which is

Kenley, are also highly involved in the colon cancer

passed down through families. His mother was

support community; both are members of the sup-

tested and came back positive for stage II colon

port group Colontown.

cancer – an early, treatable stage.

“They were able to treat her cancer and we think about it as me saving her life now,” Stephen says.

After surgery and chemotherapy, his cancer was

S TEPHE N ESTRADA

IMMUNOTHERAPY TRIAL GIVES YOUNG COLON CANCER PATIENT BACK HIS LIFE

“Joining Colontown has been so helpful to both of us as a patient and caregiver,” says Kenley.

“I am able to talk with other caregivers about their

STEPHEN (RIGHT) TAKES A SELFIE WITH KENLEY AT THE LINCOLN MEMORIAL

experiences and that helps me continue my support “Don’t think that a clinical trial is the last option,”

still growing. That’s when he made an appointment

of Stephen. If there is one piece of advice I can give

with Wells Messersmith, MD, CU Cancer Center

people that are going through a similar experience it

Stephen says. “Educating yourself about your

investigator. Messersmith recommended that

would be to find a good support group.”

cancer is so important.”

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D oes

EVOLUTION hold the key

TO CREATING, CURING AND PREVENTING CANCER?

WHY NATURAL SELECTION AND NOT JUST MUTATIONS CAUSES CANCER ... AND HOW CU DOCTORS ARE HARNESSING EVOLUTION TO STOP IT.

DEPOSIT PHOTOS

By Garth Sundem

HEALTHY CELLS OUT-COMPETE CANCER CELLS FOR THE BODY’S RESOURCES AND THUS KEEP CANCER IN CHECK. AS WE AGE, THOUGHT, THE TISSUE ECOSYSTEM CHANGES. —JAMES DEGREGORI, PHD

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T

he other day, I was chaperoning a 2nd grade field trip to the Denver Museum of Nature and Science when the conversation turned, as it usually does, to the question of whether animal X would beat animal Y in a fight. The combat in question was that of Daeodon, a giant, carnivorous pig native to North America, Eurasia and Africa during the Miocene period, versus the tyrant lizard, T-Rex. If you’ve been to the museum, you know that the monster pig is the stuff of nightmares. But the answer was pretty obvious: T-Rex would totally win. Hands down.

The kids were pretty quick to the conclusion that not only would T-Rex make a quick snack out of Daeodon, but the tyrant lizard would easily munch on the short-faced bear too, largest of the Ice Age carnivores. In fact, when you look across the whole potential spectrum of theoretical mammal-versus-dinosaur duels – from the tiniest little protomammal versus its chicken-sized dinosaur ancestor, to packs of wolves versus packs of velociraptors – it’s pretty obvious that the dinosaurs would win every time.

Which brings up an important question: Why did the dinosaurs lose?

The reason, as you know, is that 65.5 million years ago a six-mile diameter space rock smashed into present-day Chicxulub, Mexico, detonating with the force of 100 teratonnes of TNT. The landscape changed overnight. In fact, the landscape became night. A dust cloud blocked the sun for a year and the Earth was plunged into winter.

The dinosaurs took this badly (they just would, wouldn’t they?).

But it was great for furry little creatures like the marmot-sized alphadon. Sure, alphadon existed in the Cretaceous – one of a few proto-mammals to eke out a tenuous existence – but its population was kept in check by its more toothsome and scaly dinosaur cousins. That is, until the asteroid kicked the earth into the Cenozoic.

With the asteroid, warm blood and thick fur made alphadon suited to the new normal. Picture it: Sixty-six million years ago, the marmot revolution became reality.

According to University of Colorado Cancer Center Associate Director for Basic Research, James DeGregori, PhD, the mammals’ meteoric takeover models the way cancer claims the human body.

“Healthy cells are perfectly optimized for a healthy tissue ecosystem. They are the most fit. In fact, they are so optimized, that most any mutation makes them less fit. In this tissue ecosystem, healthy cells out-compete cancer cells for the body’s resources and thus keep cancer in check. As we age, though, the tissue ecosystem changes. Now healthy cells may no longer be optimized to these new surroundings. Now cancer cells, with their ability to mutate and adapt, may be able to generate cells with a better fit.

It is this changing tissue ecosystem and not just the occurrence of ‘new’ mutated cancer cells that lets the disease develop,” DeGregori says.

This line of thinking challenges the more basic model of oncogenesis that has dominated the field of cancer research for 50 years. In the traditional model, the longer you are alive, the more time you have for a chance set of mutations to cause cancer.

Think about it like playing dice: The more times you roll, the more chance you have of shooting a double six. This line of reasoning makes intuitive sense: We all know that mutations cause cancer cells and the older you are, the higher your chance of developing the disease. Scientists refer to this as the “mutation accumulation” model.

Only, scientists have struggled with some pretty significant holes in this line of reasoning – actually, the holes are more like tunnels big enough to drive a truck through.

Another hole is the fact that cancer risk doesn’t increase at a constant rate over time – it’s not just rolling dice. For example, there is a leukemia spike in very young children, then rates stay low through middle age before increasing exponentially in older adults.

Instead of the progressively increasing risk predicted by the accumulation of mutations model, leukemia rates go up and down and up again like a roller coaster.

Working with postdoctoral researcher Andrii Rozhok, PhD, DeGregori blames the leukemia spike in young children on another evolutionary force, called “genetic drift.”

Genetic drift is the role of chance – the possibility that despite being less fit, a lucky organism happens to survive to reproduce and eventually shift the genetic makeup of the population. Importantly, the influence of drift is greater in small populations.

“Imagine if you flip a coin 10 times. You would not be too surprised if seven of 10 flips gave you heads. In fact, the odds are about one-in-six. But if you flipped the same coin 1,000 times, the odds of getting 700 heads would be much smaller – less than one in a million,” DeGregori says. “Basically, the more trials we do, the less chance plays a role.”

Now replace these coin flips with a population of cells. A young child has relatively few blood stem cells – with only a few “coin flips” a less fit cancer cell can get lucky. An adult has far more blood stem cells – this blunts the influence of drift and means that to cause cancer in a healthy adult, a less fit cancer stem cell would have to be really, really lucky.

Again, seeing cancer through the lens of evolution explains a gap in the accumulation of mutations model: The spike in cancers among very young patients is likely in part driven by genetic drift in which less fit cancer cells have a better chance of getting lucky in a smaller population.

Now that we’ve seen how evolution drives the development of cancer, let’s look at how doctors are exploiting the same forces to kill it.

DIFFERENT SIZES AND LIFESPANS ALL SEEM TO DEVELOP CANCER MOSTLY LATE IN LIFE?

CU Cancer Center researchers Curtis Henry, PhD, (left) and James DeGregori, PhD

THE SPIKE IN CANCERS AMONG VERY YOUNG PATIENTS IS LIKELY IN PART DRIVEN BY GENETIC DRIFT.

D EP OSIT PHOTOS

CAN CER R ISK IS N’T L INE A R

WHY DO MAMMALS OF VASTLY

CASEY CASS

One of these holes is big enough to have a nifty name – it’s called Peto’s Paradox.

Basically, the paradox says that if cancer is due to random activating mutation, larger animals with more cells should be at greater risk of developing the disease earlier in their lives. Why then do mammals of vastly different sizes and lifespans all seem to develop cancer mostly late in life?

“Blue whales have more than a million times more cells and live about 50 times longer than a mouse, but the whale probably has no more risk than a mouse of developing cancer over its lifespan,” DeGregori says. (Although admittedly, it would be hard to prove this in the laboratory, unless it was a very, very big laboratory.)

It’s as if the whale’s many cells are rolling more genetic dice – meaning more chance for it to roll the “double six” of a cancerous super cell. But working with CU Cancer Center research instructor Curtis Henry, PhD, DeGregori shows that cancer cells aren’t “super” at all. Again, healthy cells are optimized for healthy tissue – the genetic changes that cause cancer actually make these cancer cells less fit for their surroundings. That is, unless the surroundings are adjusted.

Here’s an example: The DeGregori lab shows that inflammation in the bone marrow provides conditions in which cancerous blood stem cells are more fit and thus can out-compete healthy blood stem cells. Here’s the important part: chronic bone marrow inflammation is associated with age. When DeGregori and Henry removed the ability of mice to create inflammation, even old mice stayed free of leukemia. It was not just mutation and not just age that was most associated with cancer – it was inflammation.

This provides a solution to Peto’s Paradox: The whale’s cells may roll more double sixes, but in healthy tissue, the cancer cells they create naturally die out. It is only a disturbed tissue landscape in both whale and mouse in which cancer cells can out-compete healthy cells. And disturbed tissue landscape occurs late in life.

And Peto’s Paradox isn’t the only hole in the accumulation of mutations model.

DE POSIT PH OT OS

PETO’ S PA R A D O X

5 C3: SPRING 2016

DEPOSIT PHOTOS

CA N C ER EVO LU TI O N I N TH E C LI N I C

THE REALIZATION THAT A TUMOR MAY CONTAIN A COUPLE OR EVEN MANY TYPES OF COMPETING CANCER CELLS HAS VERY REAL

CA SEY CASS

TREATMENT IMPLICATIONS.

CU School of Medicine associate professor Robert C. Doebele, MD, PhD

Aging-associated inflammation isn’t the only thing that affects our tissue ecosystem.

On the downside, things like smoking, radiation exposure, obesity and alcohol damage tissues ... and cancer rates rise accordingly. On the upside, doctors can affect the tissue landscape, too. In a roundabout way, this is a strategy of cancer therapy: Doctors can introduce drugs that make the body’s ecosystem more hostile to cancer cells than to healthy cells. But then why, after a period of control, do these cancers so often restart their growth even in this ecosystem that selects against them? Again, the answer lies in evolution.

“Diversity exists in cancers and is generated every time the cancer cells replicate. That diversity sets the stage for evolution in the environment of any active drug,” says D. Ross Camidge, MD, PhD, Joyce Zeff Chair in Lung Cancer Research at CU Cancer Center and director of thoracic oncology at University of Colorado Hospital.

What Camidge means is that in many cancers, evolution may be more than a fight between healthy cells and cancer cells. For example, some cells in a lung cancer that we call ALK-positive may have a dominant cancer-driving abnormality in a gene called ALK. But other cancer cells living right next to them may have ALK and some additional genetic changes capable of driving the cell. At diagnosis, these other cells have no specific advantage – you don’t need two steering wheels in a car. However, when doctors use the drug crizotinib to “select against” ALK-positive cells, this may clear the path for the other kind of cancer cells to make use of their extra potential to keep driving, and so the new “double driver” cells become dominant in the tumor.

Thus the competition is not just between healthy cells and cancer cells, but between all the cell types – healthy cells, ALK-positive cancer cells, and all the other populations of cancer cells fighting for resources and survival in the diverse ecosystem of the body.

The realization that a tumor may contain a couple or even many types of competing cancer cells has very real treatment implications. As Camidge explains, “This suggests the use of rebiopsies to sample growing lesions to discover the weaknesses of the newly dominant cell population so that we can use or develop new drugs or drug combinations to target these emerging populations.”

And second, Camidge describes a creative new strategy that uses evolution to pit types of cancer cells against each other: “When targeted therapy controls the dominant cancer, a subtype that is less fit but is resistant to the drug may supplant the original cancer. But when you stop the targeted therapy and, for example use a less selective therapy like chemotherapy, you reinstitute the landscape that favored the first cancer. Now if the cancer grows during treatment with nonselective chemo, the original cancer may once again be the form that out-competes and controls the drug-resistant subtype. At that point, after a targeted therapy holiday, you can re-challenge a tumor with the first, targeted therapy and gain a second response – a second honeymoon with the original drug,” Camidge says.

This innovative and promising strategy is in use now in the clinics of CU Health.

Equally exciting is new thinking that is trying to push active interventions even earlier in the cancer’s evolutionary path.

S TAY I N G A STEP AH EAD O F EVO LU TI O N “When you perturb a cancer cell in the lab, you see the cell adapt very rapidly, in minutes,” says Robert C. Doebele, MD, PhD, associate professor of Medical Oncology at the CU School of Medicine. In other words, when doctors make a hostile ecosystem, cancer cells adapt to the change – think of it like dinosaurs sprouting fur. “A subset of the cells rapidly turn on other programs that allows them to survive, even if they aren’t immediately ready to grow,” Doebele says.

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DE POSIT PH OT OS

WHEN YOU PERTURB A CANCER CELL IN THE LAB, YOU SEE THE CELL ADAPT VERY RAPIDLY, IN MINUTES. —ROBERT C. DOEBELE, MD, PHD

CAS EY CASS

The thing is, some cancer cells do this better than others. This is one reason we see varying results from targeted therapies. Some patients have cancers that are slow to evolve and these patients see strong, long-lasting responses to therapies that select against a cancer cell’s genetic needs. Other patients, with seemingly the same cancer, treated with the same drug, happen to have cancers that are quicker to evolve and these patients manifest more modest tumor responses.

“People have been so impressed by the responses to targeted therapies that we overlooked the fact that we aren’t getting 100 percent response in all patients. We’ve had this success, but now it’s time to go back and ask how we take it to the next level. Maybe we can move the science beyond treating with one drug and waiting until the tumor evolves and progresses before trying to figure out what makes it resistant,” Doebele says.

For example, Doebele’s lab has now shown that one particular pathway, the Epidermal Growth Factor Receptor (EGFR) pathway, is commonly used by lung cancers to turn on an immediate survival signal in the face of an active targeted therapy.

“For several years we’ve known that nearly 90 percent of lung cancers express high levels of the EGFR protein, but that most lung cancers are not sensitive to inhibiting just that one pathway. If it’s not functioning as a driving pathway, but, rather, an immediate survival pathway to shield a subset of cancer cells from active treatments, its high frequency starts to make a lot more sense.” To explore this in the clinic, Doebele is now leading a clinical trial looking at combining an ALK inhibitor with a short course of an EGFR inhibitor.

DeGregori says it this way: “Humans have one advantage over cancer. We have some ability to predict the future. Cancer does not.” The crystal ball is still under construction.

But with work, we may be able to take one very important step ahead of cancer’s evolution, treating not only the cancer that exists, but the cancer that we predict will exist.

PO P ULATION R E S E RV O IRS

CU School of Medicine associate professor Carol Sartorius, PhD

CANCER STEM CELLS ACT AS A RESERVOIR THAT CAN RESEED THE DISEASE ONCE THERAPY ENDS. D EPO SIT P HOTOS

When evolution isn’t enough, cancer is willing to wait. Here’s how: Scientists studying infectious diseases talk about “reservoirs” – species that harbor a disease and can periodically reintroduce it into a population. For example, the reservoir for Ebola may be fruit bats. Doctors, patients and aid workers may select against an Ebola outbreak ... but the bats carry the virus and can restart the disease months or years later.

Carol Sartorius, PhD, associate professor in the Department of Pathology at the CU School of Medicine shows that reservoirs are an important evolutionary strategy for cancer, too. For example, as you know, the cells of many breast cancers depend on estrogen. These cancers are called estrogen-receptor-positive, or ER+, and we have very successful medicines to kill cells with this dependence. However, “The interesting thing is that long after therapy has killed ER+ cells, in many cases we can see the resurgence of this population that leads to recurrence of the cancer even five or ten years after treatment ends. Why is that?”

Does the medicine not reach all cells? Is the medicine against ER+ cells not universally lethal? Are some cells not ER+ after all? Do these ER+ cells evolve ways to resist the medicine? Sartorius offers another explanation, namely that, “Cancer stem cells, the cells that can really repopulate a tumor, can become dormant. Maybe there were a couple stem cells sitting there that, long after treatment ends, restart the growth of the tumor.”

These cancer stem cells are the fruit bats of ER+ breast cancer, acting as a reservoir that can reseed the disease once therapy ends. To do so, cancer stem cells may employ yet another evolutionary strategy: symbiosis.

7 C3: SPRING 2016

DE POSIT PH OT OS

A S I F I T WER EN ’ T H AR D EN O U G H TO KI LL C O M P E T IN G C AN C ER C ELLS

THE FORD LAB STUDIES CANCER CELLS THAT REACTIVATE OLD DEVELOPMENTAL PROGRAMS BURIED IN THE DEPTHS OF THEIR DNA TO ACT MORE LIKE EMBRYONIC CELLS.

Symbiosis classically refers to different species working together for mutual gain. For example, clownfish receive protection from anemones and in return the clownfish protect anemones from butterfly fish. Now, it seems that cancer cells can also cooperate to survive threats. Just ask Heide Ford, PhD, professor in the CU School of Medicine Department of Pharmacology.

The Ford lab studies cancer cells that reactivate old developmental programs buried in the depths of their DNA to act more like embryonic cells. One developmental program reactivated by cancer cells is referred to as epithelial-to-mesenchymal transition, or EMT. There is significant benefit to EMT: “Most tumors have to stay attached to their ‘home’ tissue – if they become detached, they die. But undergoing this transition makes them more motile and aggressive, as well as better able to survive detachment so that they can travel away from the primary tumor and through the body to seed tumor sites elsewhere,” Ford says.

However, these cells that have undergone EMT aren’t especially good at growing the bulk of a tumor and are thus unable to form large metastases at secondary sites. One theory is that cells may undergo EMT to travel and then reverse the process once they arrive. But Ford’s lab has found this reversion may not be necessary – instead, these EMT cells cooperate with cells that have not undergone EMT; they shepherd the ability of these other cells to survive travel through the body, temporarily gifting these cells with the capacity to endure detachment. In return, these enhanced “regular” cancer cells may allow a few rare EMT cells to survive at the secondary site alongside them.

CASEY CASS

U SI N G EVO LU TI O N TO PR EVEN T C AN C ER

CU School of Medicine professor Heide Ford, PhD

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We’ve seen how evolution drives cancer, helps it survive therapy, and how doctors are using strategies based on evolution to combat cancer. But perhaps the most powerful tool stemming from an evolutionary perspective on cancer is the ability to prevent the disease in the first place.

Let’s go back to our dinosaurs. What would the world be like if the asteroid hadn’t hit? Of course, we can’t know for sure, but it’s likely that for at least a few more million years, giant lizards would have ruled the earth. In other words, if the ecosystem had stayed the same, “healthy” dinosaurs would have continued as the dominant population. There would have been no marmot revolution.

“We’ve been trying to make drugs that target the products of mutated genes in cancer cells. But if it’s the ecosystem of the body and not only cancer-causing mutations that allows the growth of cancer, we should also be prioritizing interventions and lifestyle choices that promote the fitness of healthy cells in order to suppress the emergence of cancer,” says James DeGregori.

You can avoid smoking. You may be able to avoid radiation. You can’t avoid aging.

But you may be able to avoid some of the cancer-causing effects of aging. For example, do you remember the work of the DeGregori lab showing that cancers are poised to take advantage of age-associated inflammation? Knowing this, the cancer-protective effects of anti-inflammatory drugs, such as aspirin, start to make sense. What else can we do to maintain a healthy environment in order to keep our healthy cells at the top of the body’s food chain? Exercise? Diet? Other Medications? All of this will need to be studied and understood in the light of our increased understanding of the underlying biology of cancer risk.

If cancer is caused by changes to the body’s evolutionary ecosystem, the best way to combat cancer may be to take care of your ecosystem. Rather than playing whacka-mole with the mammals that sprang up in the wake of the asteroid, a better strategy may be to prevent the impact in the first place.

DEC DINGCANCER

The ECOSYSTEM of Cancer

AN EVOLUTIONARY VIEW

James DeGregori, PhD, and CU Cancer Center colleagues are leading a shift in how science sees the development of cancer – what if, instead of blaming cancer on a set of chance mutations, we saw cancer as the rise of a new “species” in the ecosystem of the body?

In this evolutionary view of cancer, like the earth’s transition from dinosaurs to mammals, it is a changing ecosystem and not necessarily the lucky origination of a new super species that leads to a switch in the dominant population.

If the rise of cancer is due to changes in the body’s tissue ecosystem, then in addition to targeting cancer cells, we could maintain or adjust the body’s tissues to “select against” this dangerous new species.

THIS REPRESENTS A “HEALTHY TISSUE” ECOSYSTEM: A WARM CLIMATE AND LUSH GREENERY SUPPORT GIANT LIZARDS

THIS REPRESENTS AN “UNHEALTHY TISSUE” ECOSYSTEM: A COLD, BARREN LANDSCAPE THE METEOR LEFT IN ITS WAKE

9 C3: SPRING 2016

A CONVERSATION WITH SANA KARAM, MD, PhD Assistant Professor of Radiation Oncology

C ASE Y C ASS

University of Colorado School of Medicine

BY GA RT H S U N D E M

During Lebanon’s civil war, Sana Karam watched her grandmother boil water to sterilize

tumor but also the patient’s ability to see or speak

wounds. She studied critical care nursing as an undergraduate at the American University

or swallow, that cannot be considered a complete

of Beirut and as a University of Maryland grad student, caring for patients in Beirut,

success. Whenever possible, we must defeat the

Baltimore, and Seattle. She then earned a PhD in physiology and biophysics from the

disease while minimizing any negative side effects

University of Washington and was a postdoctoral fellow at Johns Hopkins before

and preserving a patient’s essential quality of life.

completing her MD and residency training in radiation oncology at Georgetown University.

In 2013, she joined the University of Colorado Cancer Center, where she treats head and

C3: You’ve only been in Colorado two years,

neck cancer patients and also manages a research lab. Here, C3 speaks with Dr. Karam

but it sounds as if you’ve found ways to keep

about her work and the path that brought her to Colorado.

yourself busy.

Karam: That’s true. Juggling lab and clinic has not

C3: How did your upbringing influence

C3: You seem to be interested in both

been easy. But the science is fascinating, and I enjoy

your path?

patient care and scientific research.

working with people and being challenged. I also

Karam: I grew up with very little, even basics such

As a researcher-physician, how would you

have three boys at home, ages 6, 10 and 13. But

as water and electricity, in a nation that was being

describe the relationship between these

my supportive husband and I are making it work.

ripped apart by civil war. At one point, our family

two areas?

And I love Colorado’s focus on nature and the

even had to flee our Lebanese village as refugees

Karam: Both are driven by a desire to improve

outdoors. It reminds me of my childhood in the

and cross the border into Syria, where we were

patient care. Many of my research ideas come

mountains of northern Lebanon overlooking the

cared for and welcomed by the kindest of people.

from patient care. When existing treatments fail,

Mediterranean Sea.

There are now more than a million Syrian refugees

you wonder why. What could have been done

living in Lebanon. It’s really heart-breaking. But

differently? Why does this cancer seem biologically

C3: What frustrates you most in your role as

tough experiences can strengthen you as a person

resistant to this treatment? I also love working with

a physician?

and make you more empathetic with people going

people, helping them think through the options.

Karam: When things don’t make sense and people

through situations where they feel powerless,

In the lab we study cancer as a collection of defec-

are being harmed as a result. I have patients with

because you understand what that feels like. I’ve

tive cells, but in caring for patients we see how

head and neck cancer, for instance, who continue

had tremendous opportunities in my life and am very

devastating it can be to people’s lives and families.

to smoke even as we are trying to save their lives.

lucky to be a in position now where I can give back.

If a certain course of treatment eliminates the

I have others who can’t make it to their treatment DEPOSI T PHOTOS

because they have no access to transportation.

Some can’t afford their medications. There are many other examples I could give you. Some of them involve policy, another area that interests me, but right now I think I have my hands full juggling the worlds of research and patient care.

C3: What do you enjoy most about your role as a physician?

Karam: When I can successfully treat a cancer, that feels terrific, of course. But even when an aggressive cancer has spread throughout a patient’s body and no treatment is available, I feel I can serve an important role by sitting down with patients and their families and helping them understand and decide among their options. The bottom line is that I genuinely enjoy caring for people and listening to

“In the lab we study cancer as a collection of defective cells, but in caring for patients we see how devastating it can be to people’s lives and families.” —Sana Karam

10 WWW.COLORADOCANCERCENTER.ORG

and addressing their concerns.

CLINICAL

CARE E RIKA MAT IC H

MD Science and Surgery ANA G L E I S N E R I S D E D I CATE D TO A TEAM AP P R OAC H, C O M B I N I N G TH E B E ST M I N D S AN D R E S EAR C H TO P R OVI D E O P TI M AL TR EATM E NTS F O R PATI E NTS

BY E R I K A MATI C H As a high school student in Brazil, Ana Gleisner,

The road to board certification took eight years

MD, PhD, dreamed of becoming a laboratory

and wound through Saint Louis University, where

scientist. But then a friend went to medical school

Gleisner completed another surgical residency

and Gleisner was intrigued by his passionate

and was chief resident. The journey continued

descriptions of learning to apply lessons in anatomy

at University of Pittsburgh Medical Center with

and physiology to help diagnose and treat disease.

a fellowship in complex surgical oncology.

Gleisner realized she would find this work highly gratifying too.

“The system in Brazil is different than in the

Finally it came time to find a new position that could nurture both her MD and PhD sides. And Gleisner wanted to collaborate with other surgeons,

ABOUT ANA GLEISNER, MD, PHD Assistant Professor, Department of Surgery Education & Training: MD, Universidade

United States,” said Gleisner. “If you pass the

medical oncologists, radiation oncologists and

entrance exam, you go to medical school straight

nurses as a team so that patients could benefit

out of high school and it takes six long years

from the experience of working with more than

RS, Brazil

to finish.”

one doctor.

Research Fellowship: Johns Hopkins

After Dr. Gleisner received her medical degree,

“When I was looking for a job, I liked the

Federal do Rio Grande do Sul, Porto Alegre,

University

she completed her residency in general surgery

multi-disciplinary approach of the University of

Residency: Saint Louis University School of

at Universidade Federal do Rio Grande do Sul,

Colorado School of Medicine,” said Gleisner. “It

Medicine, Chief Resident, Surgery

one of the most highly regarded medical schools

means each patient meets with the team directing

in Brazil. After residency, Dr. Gleisner completed

their treatment on the same day and leaves with

an abdominal organ transplant fellowship and

an understanding of what their treatment will

then joined the clinical faculty at her alma mater,

entail, based upon the group’s collective expertise.

where she performed a variety of complex general

Hopefully, it can provide some peace of mind.”

surgeries in oncology as well as adult and pediatric organ transplantations.

However, even as a successful surgeon,

In addition to the team approach, there were

Fellowship: University of Pittsburgh Medical Center, Complex General Surgical Oncology

Gleisner’s research is based in the clinic.

some familiar faces in Colorado. From her time

One of her tasks is to establish a research data-

at Johns Hopkins, Gleisner knew the work of

base following the outcomes of patients who have

science kept calling to her. Gleisner accepted a

Richard Schulick, MD, and Barish Edil, MD, both of

had liver, pancreas and other gastrointestinal

research fellowship at Johns Hopkins University

whom left Hopkins for the CU School of Medicine.

procedures. She believes the database will assist

with the plan of getting a PhD to complement

Schulick and Barish were the first surgeons in the

in informing patients and predicting with even

her medical degree.

state of Colorado to perform a minimally invasive

more precision which patients will respond to

approach to a very complicated procedure for

which treatments.

“I was working closely with faculty members in the Division of Surgical Oncology at Johns Hopkins and was fascinated by the multidisciplinary approach

pancreatic cancer patients.

Gleisner, too, employs minimally invasive

“The idea is that by following patients after cancer surgery through other therapies and

to patient care and by how well the specialty lent

techniques. While she performs breast, melanoma,

beyond, we can identify risk factors and, in a

itself to research and the adaption of innovative

and colorectal procedures, Gleisner’s emphasis is

perfect world, prevent potential issues in patients

surgical techniques,” said Gleisner.

laparoscopic liver surgery.

down the road,” said Gleisner.

Science and medicine: Suddenly it seemed like

“Liver procedures performed laparoscopically

The path to becoming a physician/scientist

Gleisner could have her cake and eat it too. During

typically result in less blood loss, less pain, and

may not have been direct, but Gleisner feels at

her research fellowship, she decided she wanted

fewer complications overall,” said Gleisner.

home at CU Cancer Center. She loves Colorado

to transition her practice to surgical oncology in the

“That translates to a shorter hospital stay and

and the opportunity to collaborate with other world

United States.

faster recovery.”

renowned physicians in the fight against cancer.

“What we can accomplish together is so much more than what we can accomplish individually,” she says.

11 C3: SPRING 2016

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All Hands

On Deck WITH EARLY-ONSET COLON CANCER ON THE RISE, CU TAKES TEAM APPROACH TO CARING FOR YOUNG PATIENTS

BY LI SA MA RS HA LL

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In the summer of 2014, Katy Davenport was leading a life many fit, Colorado thirtysomethings can relate to. She spent her days building her budding career (in real estate finance).

By night, she gathered with friends for a drink or occasional game of karaoke. She was training for a marathon and planning a trip to Mexico. And she and her husband were busily remodeling a fixer-upper they’d just bought. “That remodel was, up until then, one of the most stressful things I’d ever been through,” recalls 34-year-old Davenport, as she sits in the University of Colorado Cancer Center lobby awaiting an appointment.

On Dec. 29 of that year, Davenport awoke from a colonoscopy to life-altering news no young, healthy woman would dream of: She had Stage 3 colon cancer and likely faced a long road of surgery and chemotherapy. She was blindsided. “I’d always thought of colon cancer as old man cancer – not something that could happen to me.”

In fact, while the incidence of colorectal cancer among older patients has declined in recent years due primarily to more and better screening, cases among young patients like Davenport – while still rare – are inexplicably rising. In Colorado, studies show rates rising 2.5 percent annually among those under 50.

Nationwide, incidences are climbing by more than 5 percent per year among the 20 to 29 set. In all, about one in 10 colorectal cancer patients is 49 or younger.

“I’d always thought of colon cancer as old man cancer – not something that could happen to me.” –Katy Davenport Even more concerning: According to research published in the Journal of Clinical Oncology in 2014, younger patients tend to have more aggressive cancers that respond less favorably to existing treatments, putting them at greater risk of dying from the disease. “We are learning that this can be a very aggressive cancer in younger patients,” says the paper’s lead author Christopher Lieu, MD, director of the CU Cancer Center colorectal medical oncology program. “We need to do a better job treating it.”

To that end, Lieu has launched a research program aimed at identifying genetic differences between colorectal cancer in the young and old, in hopes of someday developing more personalized treatments. Meanwhile, he says, one key to success for people like Katy is a team approach which takes into account the myriad unique challenges younger patients face.

“Cancer is hitting them at a different point of life when they may be in school or building their career or considering starting a family, and nobody their age can relate to what they are going through,” says Lieu, adding that younger patients also tend to have more severe treatment side-effects. “We take a multidisciplinary approach with every patient. But for these young patients, it’s all hands on deck.”

D IAG N O S I S O FTE N C O M E S L AT E Davenport first noticed something wasn’t quite right in July of 2014, when her stool became looser. She wrote it off, assuming the stress of the home remodel was getting to her. By September, she noticed some blood in her stool and went to a doctor, who gave her a prescription for hemorrhoid relief and sent her home. By November, Davenport grew frightened. But she was reluctant to talk to friends, or even family about it. “No one wants to hear you talk about your poop. I just kept hoping it would go away,” she says.

On Dec. 29, she closed her eyes and drifted off, assuming her colonoscopy would reveal whatever minor problem was to blame.

When the anesthesia fog lifted, her doctor broke the news.

“She said ‘You have a 5 cm tumor in your lower colon. It doesn’t look good,’” recalls Davenport. “I was in total shock.”

Lieu says stories like this are not uncommon among younger colon cancer patients. When the disease is developing, they experience only minor symptoms and tend to downplay them.

Then, when they finally make their way to a doctor, physicians often rule out colorectal cancer because they assume they’re too young. (The American Cancer Society recommends routine colorectal screening only after age 50 in people of average risk).

One study, comparing colorectal cancer patients age 20 to 40 to those age 60 to 80, reported that younger patients often have their diagnosis delayed by more than six months. Fifty-six percent are diagnosed at Stage 3 or Stage 4.

“By the time they start to feel anything it is because the cancer has gotten really big,” says Lieu.

IT TAK E S A V I LLAG E Davenport was busy navigating insurance red tape and scheduling multiple pre-surgical appointments at another hospital when a friend suggested she get a second opinion.

“At first I was like, ‘Why? What are they going to tell me? That I don’t have cancer?’” she recalls.

She reluctantly obliged, firing off a text to CU Cancer Center radiation oncologist David Raben on a Sunday. He called her back within 30 minutes, and they spoke for an hour. On Monday,

13 C3: SPRING 2016

C ASE Y C ASS

In 2015, he and his colleagues genetically mapped RNA from tumors of 9 patients under the age of 35 and 7 patients over the age of 70, using high-throughput computer sequencing. They discovered the younger tumors contained unusually high expression of 77 genes, including ERBB2, NOTCH3, and CAV1 – which are all known to spur the cell proliferation commonly associated with cancer. Lieu presented these preliminary findings at the 2016 Gastrointestinal Cancers Symposium in January.

Now, he hopes to do further gene testing with a broader set of tumors, and use Davenport’s tumor, among others, to study what impact novel Christopher Lieu, MD, director of the CU Cancer Center colorectal medical oncology program, drugs may have on them in the lab. sharing a laugh with Katy, worked with a team of doctors and nurses to construct her treatment (FDA approved therapies already and recovery. exist to target ERBB2.)

“That tissue could have just been thrown away, but instead it she switched her care to CU. “I hadn’t even met this guy and he was treating me like a family member. I figured if everyone there will be used to help us study this disease and look at potential treatment options. It is unbelievably helpful,” he says. is like that, that’s where I want to be.”

That week, Julie Banahan, a nurse navigator with the CU A N EW STO RY colorectal cancer clinic, took the reins for Davenport, collecting Today, Davenport is cancer free, running her medical records from her previous doctors, gathering prehalf marathons again, and planning a trip to authorizations from her insurance provider, and scheduling her New Zealand. With her flowing blonde hair appointments. “I didn’t have to worry ‘Am I missing something?’ (which she thankfully never lost), clear blue All I had to do was just show up,” says Davenport. eyes, and lean athletic frame, she appears the On Jan. 20, she underwent a five hour surgery in which picture of health.

Dr. Jon Vogel removed one third of her colon. Then came 12 But she’s quick to point out that her journey is not over. rounds of chemotherapy, over the course of six months. But her “I may be done with chemotherapy, but I’m not done with care didn’t stop there. Prior to each chemotherapy session she cancer,” she says, as she waits for an appointment with health received acupuncture and nutritional counseling to help prepsychologist Laura Melton. “I can’t go back to the life I had vent side effects. She met with a genetic counselor who scoured before, and sometimes I really grieve that. I never wanted to be DNA from her blood and saliva in search of clues to what may defined by cancer, but it is part of my story now, and I’m trying have led to her cancer and might put other family members at to figure out what to take from it.” risk. (Frustratingly for Davenport, they found no clear inherited Going forward, she will have more blood tests, scans, and mutation.) When a blood clot formed in her lung, she met with appointments, and tiny aches and pains will worry her more than a gynecologist who took her off birth control pills (which can they once did. But there are, somehow, upsides to what she has boost the risk of blood clots) and found another option for been through. her. And when her side effects, including numbness, sensitivity “Cancer is scary. It brings to a young life stuff that we don’t to cold, and peeling skin, became unbearable, Lieu promptly expect to deal with until later in life: Death. Strength. Courage. switched her medications.

But I’ve realized it also opens up life in a way that is more Meanwhile, Lieu, who doubles as clinician and researcher, purpose driven,” she says. added Davenport’s tumor to a growing repository of samples Her advice to others going through it: “Love yourself and the he and other researchers around the country are collecting to people around you. Don’t waste time on things that don’t matter explore just what makes earlier-onset colorectal cancer different. to you. Relax. Have fun. Be present. And don’t be afraid to ask for help.”

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ST RY INSIDE

Adjusting to The “New Normal” After Diagnosis The moment a person hears they have cancer, the life they know can become the life they knew. Everything changes.

Targeted therapies mean that treatments for many cancers are unique. Laura Melton, PhD, ABBP, assistant professor of medicine at University of Colorado School of Medicine and board certified clinical health psychologist at University of Colorado Hospital, is working to make treatment for the psychological part of the process unique, too.

“I give the analogy of treading water.

People are just trying to keep their heads above water. An oncologist says get this treatment, get this test and that’s all they can do,” says Melton. “Hearing about what psychological or emotional help is available early in the process is a moot point for some, and rightfully so.”

Melton observes that human beings don’t deal well with uncertainty and people with cancer are confronted with life altering changes that have uncertain results: How long will I need to be off work? How will this affect my relationship?

What’s going to be different about me?

Along with physical changes brought on by chemotherapy and radiation, there are psychological changes. Melton knows that these changes are influenced by every patient’s unique background and cultural context.

“I need to know what they were like before the diagnosis – how they were before cancer is important to how they are going to deal with it psychologically,” says Melton. “I want to know whether they avoid going to the doctor, if they’re scared, in denial or have existing mental health issues.”

Melton says that once the reality of cancer sets in and treatment starts, emotional issues can start to simmer. Helping patients handle the mental component involves teaching them how to deal with their new challenges by learning to adjust unhelpful thinking and behavior.

“If you are feeling sad and you lay in bed all day and think of depressing things, you have created this spiral that keeps you depressed. So what are some different ways that we can change the behavior?” says Melton.

She says getting up and getting dressed every day makes a difference. She encourages people to get out of the house or take a walk even if they don’t feel great.

She says it creates positive energy.

Another important component of the psychological adjustment to a cancer diagnosis is normalization. People think what they are experiencing is abnormal so they isolate themselves. Melton adds, “Patients don’t necessarily understand that there is a range of what normal looks like.”

Moving forward, Melton would like to see personalized supportive care for all.

She stresses health care providers have to meet people where they are psycho­ logically and also geographically.

“We all want people to be ready to exercise or eat better but they may have their head in the sand. We can’t ignore those people,” says Melton. “And as a regional cancer center, we need to find ways to support people who live in small mountain towns or rural Wyoming or Kansas.”

Just as each patient has specific needs when it comes to treating their cancer, each patient also has specific needs regarding their emotional health.

Understanding and respecting patients’ unique psychological needs will help the truly comprehensive team at the CU Cancer Center help patients live not only longer, but better lives.

—By Erika Matich

D EPOSIT PHOTOS

In addition to daily routines and priorities, people see their past, present and future in a different light.

15 C3: SPRING 2016

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catching

THE ELEPHANT IN THE ROOM

early

COLON CANCER

BY TAY L O R B A K E M EY E R

On March 4, 2016, to mark the eighth annual Dress in Blue Day, the University of Colorado Cancer Center set up a table in the lobby of the University of Colorado Hospital stocked with blue balloons, blue candy, and blue information packets to raise awareness for colorectal cancer. Over 100 people stopped by the table to chat with the CU doctors, researchers and other experts.

One of these people was a woman in her mid-50s named Becky.

Holding back tears Becky admitted that she has never been screened for the disease because she is afraid of what the test might find. Other reasons people gave for missing their recommended screenings included forgetting or putting off scheduling an appointment and feeling ashamed about talking with their doctor about that particular part of the body.

Colorectal cancer claims 50,000 lives each year, but the reality is that many of these deaths could be prevented. Screening for the disease often catches it early, when many good options for treatment still exist. Unlike many other cancers, screening can even prevent colorectal cancer from developing.

Enter the elephant in the room: Due to stigma, fear, and good old procrastination, people are dying of a preventable disease.

In fact, one in three adults between the ages of 50 and 75 – about 23 million people in the United States alone! – are not getting the recommended screening according to the National Colorectal Cancer Roundtable (NCCRT), a national coalition dedicated to reducing the incidence and mortality of colorectal cancer in the U.S. “This is a huge public health issue because people are being diagnosed with colorectal cancer when they could have prevented it in the first place,” says Dennis Ahnen, MD, investigator at the CU Cancer Center and a steering committee member of NCCRT. Evidence shows that screening impacts both the incidence and mortality rates of colorectal cancer, meaning that not only

16 WWW.COLORADOCANCERCENTER.ORG

does screening catch early cancers in a treatable stage, but screening also discovers conditions that would lead to cancer down the road – with treatment, many of these patients will never develop cancer at all. While not everyone who should be screened completes the procedure, screening rates are up and, according to the American Cancer Society, this has been a major factor in the 30 percent decrease of colorectal cancer diagnosis and deaths in the last ten years among adults 50 and older.

“Screening for the disease works,” says Ahnen. The most well-known screening option is a colonoscopy. “This procedure is more effective than lung and breast cancer screening because it can actually prevent colorectal cancer by removing polyps.”

A colonoscopy procedure is just one of three different options that people can use to screen for the disease. In it, a flexible, Dennis Ahnen, MD lighted tube is used to look at the interior walls of the rectum and the entire colon. When physicians discover pre-cancerous polyps, they can remove the tissue before it has a chance to create the disease. The American Cancer Society recommends a colonoscopy once every ten years starting at age 50, or more often if you have a higher risk of developing the disease (ask your doctor). Other screening options include a high-sensitivity fecal occult blood test (FOBT) or fecal immunochemical test for blood (FIT), both which check for hidden blood in stool samples, or a sigmoidoscopy, in which physicians use a tube to look at the rectum walls and part of the colon. These tests are followed by a colonoscopy if a positive test occurs.

So, with these recommendations, the usefulness of screening, and the many options to accomplish it, why is there still an elephant in the room? Why are nearly 137 people a day losing

NCCRT stating that they are embracing the goal of 80 Percent by 2018. Leading the charge in Colorado is the Colorectal Cancer Task Force of the Cancer Coalition of Colorado.

To ensure that organizations can meet their goals, the NCCRT offers toolkits that provide groups with evidence based action steps to take immediately rather than losing a lot of time thinking and talking about what they can do.

“For example we are talking to insurance companies about stopping co-payments for screening and encouraging physicians to make screening a standard of care,” says Wolf.

Patient navigation will also play a huge role in meeting the 80 Percent by 2018 goal. Andrea (Andi) Dwyer, who was recently appointed to the advisory board of the NCCRT, and is a steering committee member of the NCCRT, helped create the national model of patient navigation, which is used by hospitals and health care centers all over the United States.

Patient navigation includes not only helping patients find the best treatment, but following patients along the care continuum, from diagnosis to survivorship. Dwyer and Wolf led the nation in implementing a patient navigation program for colon cancer screening in Colorado a decade ago.

“It made sense for me to get involved with the campaign because I am very familiar with making sure people know about preventive screening and getting them to the best care,” Dwyer says.

Denver itself has gotten behind the 80 Percent by 2018 effort. The capitol building and the 100 foot tall spiral steel sculpture in the Denver Technological Andrea (Andi) Dwyer Center have agreed to turn blue in March, local health fairs are encouraging screening, radio ads in both English and Spanish are being aired all over the state, and don’t miss this year’s Undy 5000 fun run, presented by the Cancer Center and the Colon Cancer Alliance on June 25!

If Ahnen, Dwyer, Wolf and the hundreds of other doctors, researchers and organizations can address the elephant in the room and reach 80 percent screening by 2018, by 2030 the effort will have prevented 277,000 cases of colorectal cancer and saved 203,000 lives. But even more than these doctors, reaching the goal depends on you. What will you do? Will you let fear, stigma and procrastination prevent you from getting screened?

Or will you take the elephant by the trunk and become part of the 80 percent that reduces your chance of becoming a colorectal cancer statistic?

DE POSIT PH OT OS

their lives to a preventable disease? Again, the answer goes back to fear, stigma and procrastination.

“There are many reasons why this may be happening,” says Ahnen. “Lack of trust, lack of education, not having insurance, fear of the procedure, or fear of what might be found can stop people from scheduling their exam.”

In order to increase the national screening rate and combat the reasons people are not getting screened, the NCCRT has initiated the 80 Percent by 2018 Campaign.

According to the NCCRT, “80% by 2018 is an initiative in which hundreds of organizations have committed to substantially reducing colorectal cancer as a major public health problem for those 50 and older. These organizations are working toward the shared goal of 80 percent of adults aged 50 and older being regularly screened for colorectal cancer by 2018.”

The initiative launched in the fall of 2014. CU Cancer Center member Holly Wolf, PhD, MSPH, was on the NCCRT steering committee at the time.

“Because of advancements in the science of treating the disease, we knew we had an opportunity to make a difference in colorectal cancer, but we had to make sure we were screening people to find it,” Wolf explains.

Wolf, along with other members of the NCCRT steering committee, helped to develop a new strategic plan to reach consumers, improve screening delivery systems, make sure that people know their rights to screening under the Affordable Healthcare Act, and celebrate people that pledged to the campaign. The result is a multi-step plan to help reach Holly Wolf, PhD, MSPH the 80 percent national screening rate by 2018. Some steps include educating and engaging clinicians, insurers, employers, and the general public, making sure that colonoscopy is available to everyone, making sure everyone is offered a stool blood test option, recruiting as many partner organizations to join the effort as possible, and implementing intensive efforts to reach low socioeconomic populations.

“We are aware that it is a very ambitious goal to raise national screening rates by 35 percent in four years, but we believe that it can be done. As screening rates rise, colorectal cancer rates are dropping and we hope this provides the incentive people need to go out and get it done,” Wolf says.

All over the United States hundreds of organizations including health care centers, hospitals, insurance companies, employers, and cancer coalitions have already signed the pledge created by the

17 C3: SPRING 2016

S U P P O R T E R

F CUS TAY LOR BAKE ME Y E R

Paying It Forward DICK AN D CATH EY FI N LON SU PPORT FE LLOWS H I P TO TRAI N N EXT GE N E RATION OF PROSTATE CANCE R R E S EARCH E R S

BY TAY L O R B A K E M EY E R During the holiday season, instead of giving gifts to

“We were both absolutely devastated. We

each other, Dick and Cathey Finlon work together

thought our lives had a straight path,” says Cathey,

to create a list of contributions they plan to make

who served on Children’s Hospital Colorado board

during the next year.

of trustees at the time. “I was familiar with the

“It’s something we have done for a long time,”

Cancer Center so I called Children’s to see if they

says Cathey. “It’s just something that feels good

could help us navigate and find someone to treat

for us.”

Dick. We were very scared and luckily, Dick was

Last year the Finlons added a new organization to their list: the University of Colorado Cancer Center.

“We found an opportunity to give back to the people that saved my life and that is very

seen by the Cancer Center within days.”

Dick and Cathey both agree that they were treated with care and compassion they had never experienced before at a medical center.

Dick and Cathey Finlon established the Finlon-Glode Endowed Fellowship Fund in Prostate Cancer Research.

“I am deeply honored by the generosity of the

“I remember we were crying and Jill (a staff

Finlons establishing the Finlon-Glode Endowed

nurse) held on to us and said ‘Don’t worry we will

Fellowship Fund in Prostate Cancer Research,”

college town of State College, Pennsylvania, where

always be here for you,’” says Cathey through

explains Glode. “The future of medicine, and all of

there are more Penn State students than towns-

tears. “It was exactly what we needed at the time.”

the breakthroughs in cancer research in particular,

meaningful to us,” says Dick.

Dick and Cathey both grew up in the rural

people. Although they knew of each other from

The prostate cancer team immediately went

ultimately begin with postdoctoral training. In the

school, they did not officially meet until they both

to work. Michael Glode, MD, CU Cancer Center

case of clinical fellowships, these are the physician-

moved to Colorado. As they say, the rest is history

member, was Dick’s attending physician. Dr. Glode

scientists who will make the discoveries that

and the couple has been married for 38 years.

wanted to tighten the original diagnosis and sent the

ultimately conquer cancer.”

“We both love to be outdoors, hiking, skiing, playing golf, fishing, you name it,” says Dick.

“Colorado is the perfect place for us, so we made it our home.”

Finlons to UCLA for a new PET scan that revealed more details about where the cancer had spread.

“When we got the scans back we were told that

“What is important to us about this gift is that we are supporting people, not only the research,” says Dick. “Without people to do the research there

the cancer had not spread throughout my body as

cannot be advances in the medical field. We both

was originally thought and could be treated as a

feel that investing in up-and-coming doctors is so

philanthropy and extensive involvement with the

local disease,” explains Dick. “I started in radiation

important for the future.”

community. Dick was the financial officer of a print-

and was cancer free by April 2013. It was astonish-

ing company and is an avid amateur astronomer.

ing to go from thinking I was going to die to being

tance of having an outstanding fellowship program.

Cathey built her career as an advertising agency

in remission within a couple months.”

At the beginning of his career Flaig was Glode’s

The couple is well known in Denver for their

owner and entrepreneur. She is very involved in local organizations, having served on numerous leadership boards, including those of Children’s

The Finlons were amazed and inspired by the care they received at the CU Cancer Center.

“There is so much collaboration between depart-

Thomas Flaig, MD, knows firsthand the impor-

fellow and is now Dick’s oncologist.

“Dr. Flaig truly embodies exactly what we are supporting,” says Cathey. “The transition from

Hospital Colorado, Denver Scholarship Foundation,

ments and a true team spirit with all of the doctors

Dr. Glode to him was smooth and professional,

Denver Metro Chamber of Commerce, Denver

we came into contact with,” says Cathey. “We were

something we both are very grateful for.”

Public Schools Foundation, History Colorado,

able to attend support lectures, talk to a nutritionist,

Junior Achievement, University of Denver Daniels

and meet with the oncology experts all in the same

College of Business, Colorado Outward Bound

building. I felt like our problem was being handled

School and American Association of Advertising

by an entire team, not just one person.”

Agencies. She is also a former President of the Denver Art Museum.

“After our experience we felt a great debt to the

A decade ago Flaig decided to pursue a career in prostate cancer under Glode.

“Dr. Glode both encouraged me and also had the ability to support my pursuit of prostate cancer research. With the Finlon Fellowship now in place,

Cancer Center and everyone who had helped us

we will have the ability to encourage current

during my treatment,” says Dick. “We collaborated

medical oncology fellows to focus on prostate

December 2012 when Dick was diagnosed with

with Dr. Glode to see how we could pay it forward

cancer research,” says Flaig.

late stage prostate cancer.

in the prostate cancer clinic. That is how we

The Finlon’s lives were turned upside down in

“The original diagnosis was pretty dire,” explains Dick.

decided on the fellowship program.”

The Finlons chose to honor Glode by naming a fellowship fund after him.

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“This gift is the first to come from my own personal impact,” says Dick. “We got a helping hand and are able to give back. It feels gratifying for me because of the motivation behind it.”

C O M M U N I T Y

N E W S

LEGACY FOR $3 MILLION: COLORADO STATE CANCER PROF EARNS FUNDING TO SAVE THE DATE

SAVE LIMBS AND LIVES

June 25: Undy 500

A Colorado State University veterinarian and University of Colorado Cancer Center investigator who is

This family-friendly 5k raises funds and awareness

dedicating her career to saving the limbs and lives of trauma victims and cancer patients becomes the

for colorectal cancer research while celebrating

beneficiary on Monday of an endowment that supports her research – and continues the university’s

survivors and honoring loved ones lost to

distinctive legacy of limb-sparing cancer discoveries.

colon cancer.

Dr. Nicole Ehrhart will be appointed to the Ross M. Wilkins, M.D. Limb Preservation University Chair in Musculoskeletal Biology and Oncology. Ehrhart is the first woman at CSU appointed to a University Chair,

July 24–25: Golfers Against Cancer

endowed with $3 million in donations. She is one of only 14 CSU faculty members holding academic

Golfers Against Cancer (GAC) is a national

chairs endowed at that level.

organization founded in 1997 by a group of

Ehrhart described her appointment to the chair as the pinnacle of her career. “I’m a veterinarian and

golfers who had lost two of their golfing buddies

I love animals, but I have a great sense of excitement about helping people, too. The greatest thing for me

to cancer. Motivated to raise money to fund

is the opportunity to do both,” she said.

JOHN EISELE/CSU PHOTOGRAPHY

cancer research, they created this annual golf tournament and auction.

August 20: Dinner in White Dinner in White is a unique, annual “pop-up party” inspired by Diner en Blanc in Paris. This popular fundraising event is like no other! The location is kept secret until one hour before the party begins, when guests (clad in all white attire) are welcomed with entertainment, music and fun.

Part of the event is dedicated to a survivor story, highlighting advances in treatment at the CU Cancer Center.

October 6: Libations for Life This event supports CU Cancer Center researchers focused on women’s cancers. This year, Julie and how the doctors and researchers at the CU Anschutz Medical Campus are changing lives every day. “Fund the Mission” – a paddle raiser emceed by 9NEWS anchor Kim Christiansen – gives attendees the opportu­nity to make gifts in support of research.

The Men’s Event (Date TBD) The Men’s Event, an institution in the philanthropic community, has increased prostate cancer awareness while supporting research to increase quality of life and survival rates. Each November, hundreds of supporters attend this event to make a significant impact on the CU Cancer Center’s work. Since 2007, this event has raised nearly $900,000 dollars in valuable private support for cancer research.

For more details about these events, visit http://events.coloradocancercenter.org

FISHING FOR A CAUSE For Jason Meninger, fishing is not only a passion, it is something that he excels in. In fact he has been fishing professionally on the Walmart FLW Bass Fishing tour since 2010. Now, after his own cancer scare followed by his sister’s breast cancer diagnosis, Jason is graciously donating 20% of his earnings on the tour to the Young Women’s Breast Cancer Translational Program at the University of Colorado Cancer Center.

Jason donated $8,000 of his 2015 earnings on the FLW Tour to Dr. Borges’ under a program he calls “Casting for a Cure.’” He was also able to secure a $2000 matching gift for his earnings at the 2015 Forrest Wood Cup Championship from the Zucker Family Foundation. Jason’s sister presented a $10,000 check to Dr. Virginia Borges, director of the Breast Cancer Research Program and Young Women’s Breast Cancer Translational Program at CU Cancer Center, on behalf of him.

“It is donations like this that allow us to start small research projects that may eventually turn into larger grants,” says Borges. “Without them it would be challenging to try new ideas in the lab that may turn into big advancements in the disease. We cannot tell you how much we appreciate Jason’s efforts.”

D EPOS IT PHOTOS

Aigner Clark will discuss her battle with cancer

19 C3: SPRING 2016

UNIVERSITY OF COLORADO DENVER

SPRI NG 2016

13001 EAST 17TH PLACE, MSF434 AURORA, CO 80045-0511

www.coloradocancercenter.org

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R ET U R N S E RV I C E R E Q U E ST E D

C3: Collaborating to Conquer Cancer Published 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: Garth Sundem | 303-724-6441 | garth.sundem@ucdenver.edu Contributing Writers: Taylor Bakemeyer, Lisa Marshall, Erika Matich Photos: Casey Cass The CU Cancer Center Consortium Members UNIVERSITIES

Colorado State University University of Colorado Boulder University of Colorado Denver INSTI TUTIONS

University of Colorado Hospital Children’s Hospital Colorado Denver Veterans Affairs Medical Center Visit us on the web: www.coloradocancercenter.org The CU Cancer Center is dedicated to equal opportunity and access in all aspects of employment and patient care.

T H E

Here Is How The “Moonshot” Will Save Lives

M E S S A G E

I

n his final State of the Union Address, President Obama

abnormalities needed to match them with targeted clinical trials

announced that Vice President Joe Biden, after losing his

of new medicines that could control their form of the disease.

son to brain cancer, would spearhead a “moonshot” to cure

In 2014 Diana Degette (D-CO) and Fred Upton (R-MI) worked

While this war led to inroads against cancer, it did not end it.

together on the 21st Century Cures Initiative to get new, effective

At the University of Colorado Cancer Center we have been at

treatments to the people who need them. This initiative, in which

the forefront of efforts that now create a new understanding of

“Cancer is not one disease.

Basic research into the biology of cancer shows us that each instance is a complex and unique mix of genetics. This work requires collaboration and support.”

the disease: Cancer is not one fight, but many related fights.

This understanding has led and is leading to new treatments and new kinds of treatments that promise to turn many formally fatal cancers into manageable conditions.

Cancer is not one disease. Basic research into the biology of cancer shows us that each instance is a complex and unique

FROM THE DIRECTOR DAN THEODORESCU, MD, PhD

We are also working with policies to support these advances.

cancer. The initiative echoes Nixon’s 1971 “War On Cancer.”

mix of genetics. One breast cancer is not the same as another, nor are two lung cancers or two bladder cancers identical.

This work requires collaboration and support. We may no

I have been honored to participate, influenced the national adoption in 2015 of the Precision Medicine Initiative, with an

longer be working with, say, all lung cancer patients, but with

initial budget of $215 million dollars meant to accelerate

a small percentage of lung cancer patients that have a specific

biomedical discoveries.

genetic alteration. Because of this, no single institution is likely

The United States has the world’s most advanced infrastruc-

to see enough patients with any subtype of cancer to draw

ture of cancer scientists and technology. This infrastructure of skill

meaningful conclusions about potential treatments. Just like the

and tools is allowing us to pick apart the biology of cancer. We

field of cancer research is working with innovative new strategies

are creating a framework of collaboration and data sharing that

to target diseases, the field as a whole is evolving new ways to

lets us understand the effects of our medicines. Our representa-

collaborate in order to test these treatments with populations

tives in government are recognizing the human and economic

large enough to demonstrate their effect.

benefits of continuing to lead the world in biomedical research.

For example, the CU Cancer Center collaborates with 15

In sum, we are poised to save lives. And it is this, watching

other major cancer research centers to share data in a partner-

patients live longer, better lives, that is the most inspiring result

ship known as the Oncology Research Information Exchange

of modern cancer research. It’s exciting to think this “moonshot”

Network (ORIEN). To date, over 130,000 cancer patients have

will generate the funding and public support needed to save

agreed to donate tumor samples that could show genetic

even more lives.

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