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Alisertib with TAK-228 excels against solid tumors, including triple-negative breast cancer


Diamond, MD, shows that cancers treated with the drug alisertib often increase communication through a pathway known as mTOR. So Diamond wondered what would happen if they used another drug, TAK-228, along with alisertib to preemptively turn off communication through mTOR. D IA MO ND

Led by Diamond and S. Lindsey Davis, MD, a phase 1 clinical trial (NCT02719691) of alisertib with TAK-228 in patients with

advanced solid tumors opened in 2016. Now results of the ongoing trial are promising. “We had multiple patients that were on the trial for a long time – a breast cancer patient who was on treatment for over a year and a prostate cancer patient whose disease continues to be under control for almost a year,” Diamond says. “I think it’s promising. We definitely had patients who saw clinical benefit from the treatment.” The trial is now expanding to an additional 20 patients, which is meant to further refine appropriate dosing and dose schedules, and to work toward identifying the characteristics of patients most likely to benefit from the combination.


Work in the lab of CU Cancer Center investigator Jennifer In a meeting of the University of Colorado Board of Regents, CU Cancer Center Director, Dan Theodorescu, MD, PhD, was named Distinguished Professor, the highest honor awarded to faculty across the CU system’s four campuses. “With a deep commitment to research and an even deeper


sense of compassion for his patients, Dr. Theodorescu is redefining healthcare,” said Don Elliman, Jr., Chancellor for the University of Colorado Anschutz Medical Campus. CU Distinguished Professors are faculty members who demonstrate exemplary performance in research or creative work, a record of excellence in classroom teaching and supervision of individual learning, and outstanding service to the profession, the university and its affiliates. In an emotional speech, Theodorescu thanked the mentors, scientific collaborators and family members who have helped and supported his career. Theodorescu closed saying, “One of my mentors told me this: follow the dream, don’t listen to the naysayers, and never give up.”

Patients with advanced cancer may be less competent to make decisions than doctors think

Get more CU Cancer Center news on our blog:

CU’s Elissa Kolva, PhD, measured the decision-making capacity of 55 advanced cancer

patients and compared their scores to those of 50 healthy adults. Overall, 44 percent of

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patients but only 8 percent of healthy adults showed impaired understanding; 49 percent of patients and 8 percent of healthy adults showed impaired appreciation; and 85.4 percent of patients versus 10 percent of healthy adults showed impaired reasoning. Interestingly, the study went on to measure doctors’ opinions of these same patients’ capacity to make decisions. Despite high levels of impairment, physicians considered 64.1 percent of these patients unimpaired, 33.9 percent moderately impaired and only one participant (1.8 percent) severely impaired. “There’s been a real shift in the relationship between doctors and patients such that we now expect patients to be involved in their care – they’re expected to be active agents and to share in the decision-making process,” says Kolva, assistant professor at the CU School of Medicine Division of Medical Oncology. “On one hand, it’s very exciting and on the other, it raises some new concerns, especially when dealing with a diagnosis that can interfere with their capacity.”



Drummer Finds New Rhythm after CU Cancer Center Clinical Trial Bob Rupp is a drummer. He works with the best musicians in the world and he’s celebrated for his contributions to the music scene in the Metro Area. There is even a day in his honor in the City and County of Denver. But in 2015, it seemed like his drumming days were numbered. “I felt a lump in my throat,” says the 60-year-old Rupp. “It felt like a big, hard marble. I had 10 tumors in my brain, so I did 15 rounds of whole brain radiation, four targeted treatments, and then chemotherapy.” Approximately six months after his first round of treatment, Rupp started feeling worse and his


cancer had spread to his chest and arm pits so his doctors referred him to Daniel Bowles, MD, at


CU Cancer Center. Bowles specializes in head and neck cancer with particular expertise in salivary

In 2013, the lab of CU Cancer Center investigator

gland cancers.

Robert C. Doebele, MD, PhD showed that “fusions”

Bowles ordered next generation sequencing that revealed Rupp’s cancer had genetic change

involving the gene TRK drive some cases of non-

known as a HER2 amplification, which is known to play a role in the development of some breast

small cell lung cancer. Now five years later, clinical

cancers. There also are effective, established therapies for cancers involving HER2.

trials are testing the drug larotrectinib (formerly LOXO-101) against advanced cancers testing positive for TRK-fusion genes. Fifty-five patients ranging in age from 4 months to 76 years, representing 17 cancer types, tested positive for TRK fusion and were treated with

In August 2016, Rupp started a clinical trial targeting HER2 cancer. Since then, he has no signs of active cancer. “I am always on the move, I get right to work. I spend a lot of time with my wife. I do things that make me happy and I say yes to everything because it might be my last chance,” Rupp says. With the help of Dr. Bowles and the CU Cancer Center, Rupp hopes to say yes to new experiences for many years to come.

larotrectinib. Overall response rate was 75 percent (44 of 55 patients). At a median follow-up of 9.4 months, 86 percent of the patients with a response

Microbiome predicts blood infections in pediatric cancer patients

(38 of 44 patients) were continuing treatment or had

A study by CU Cancer Center investigators working at Children’s Hospital Colorado shows that

undergone surgery that was intended to be curative.

changes in the microbiome, the community of microorganisms that live within the human body,

No patients discontinued treatment due to adverse

may predict or even cause some bloodstream infections associated with cancer treatment.

side-effects. “I can’t tell you how gratifying it is to see our early

Samples and records were available for 42 patients, six of which went on to develop bloodstream infection. And it turned out that these six patients had significantly reduced

lab work with genes and cells leading to a treatment

microbiome diversity compared with patients who remained free of infection. Three of the six

that is literally saving patients’ lives,” Doebele says.

patients who developed bloodstream infections had been infected with types of bacteria that

“This is the dream of all scientists who choose to

were specifically abundant in their microbiome samples. “Our results add to a growing body of literature suggesting that the microbiome matters during cancer treatment,” says Bryan Nycz, third year medical student at the CU School of Medicine and the paper’s first author. “In this case, microbiome diversity and composition may help us identify patients at greater risk for blood infections.”



go into cancer research.”

THORACIC ONCOLOGY RESEARCH INITIATIVE For a decade, Robert C. Doebele, MD, PhD has been a central figure of lung cancer research in Colorado. Now he will lead the University of Colorado Cancer Center Thoracic Oncology Research Initiative, continuing the program’s international reputation for excellence while taking advantage of new opportunities in technology and understanding to guide the program’s growth in this era of targeted treatments against cancer. “We are delighted to have a scientist of Bob’s caliber leading our program. The basic discoveries from his lab fuel our ability to design, test and offer new therapies that are extending and even


saving lives right now. With his leadership, our already excellent lung cancer research program will be in good hands for many years to come,” says Dan Theodorescu, MD, PhD, director of CU Cancer Center.

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Terry Fry spent the 2016 winter holiday in the hospital – not as a patient but as a doctor. That winter, he was trying something that had never been done before, using a new drug built from his patient’s own immune cells to treat a boy whose acute lymphoblastic leukemia (ALL) had shrugged off chemotherapy, radiation, bone marrow transplant and even a targeted treatment that was a cousin of Fry’s new drug. Fry, now a recent arrival to University of Colorado Cancer Center, had overseen much of the basic science behind the new drug while leading the Hematologic Malignancies Section in the Pediatric Oncology Branch of the National Cancer Institute, but that winter, he took a break from the lab. “I intentionally put myself in the clinical service because I wasn’t exactly sure what was going to happen. I wanted to be there in person for my patient,” he says. The boy was beyond the reach of traditional treatments. This new drug was his last real hope. In the next few pages, we’ll try to understand this new drug that Terry Fry hoped would save his young patient’s life. But to do that, we need to go back a little further than the winter of 2016. Actually, we need to go back much further.

Curing Cancer Starts with HIV Research Two billion years ago (give or take a few years), viruses learned something that would take schoolyard bullies another 1.999998 billion years to discover: It’s much easier to force someone else to do your homework than it is to do it yourself. Viruses force cells to do their homework. But instead of threatening cells with their viral little fists, viruses are much more devious – they insert their “work” alongside a cell’s own assignments so that when the cell goes through its pile of homework, it accidentally does the virus’s work, too.

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A virus’s “homework” is to make more viruses. And certain viruses are specialized to bully certain types of cells into doing it for them. For example, HIV is a “lentivirus,” which is specialized to latch onto and infect immune system T cells (which is why HIV infection undermines the immune system). Basically, the HIV lentivirus grabs a T cell and inserts its own genetic material into the T cell’s DNA, so that when the T cell replicates its DNA, it also replicates the HIV virus. But it only takes a PhD in genetics and molecular biology to see that lentiviruses like HIV could be used insert other genetic material into T cells – whatever genetic code is inserted, the T cells will manufacture. In other words, and in a twist that perhaps rights the wrongs of so many molecular biologists’ childhoods, these scientists are now bullying lentiviruses, which bully T cells into making whatever the researchers want them to make. So now the question becomes what should researchers have T cells make? It would be neat to have T cells grow tiny moustaches. But perhaps even more useful is T E R RY F RY to use lentiviruses make T cells manufacture new antibodies. If it’s been a while since you took Bio 101, you can think of an antibody like the flashlight that a T cell holds to illuminate a specific antigen. When an antibody recognizes its antigen, T cells attack. And by giving T cells new antibodies, researchers could “point” them at new antigens. If you don’t want to remember the word “antibody,” just remember they’re the things that catch antigens – call them “antigen receptors.” Actually, because these new antigen receptors are built from a little bit of this and a little bit of that, let’s call them “chimeric antigen receptors.” And because that’s a mouthful of rocks, we can shorten it to CARs. Finally, because we’re talking about CARs built into T cells, let’s just call the whole system a CAR-T. By using HIV-like lentiviruses to make CAR-Ts, scientists could theoretically program T cells to attack cells marked by pretty much any antigen. You wouldn’t want to set CAR-Ts loose against antigens found on healthy cells because they would eat these healthy cells leading to side effects such as death. But Terry Fry is the anchor of a cutting-edge team that is making Colorado a worldwide leader in the use of CAR-Ts to attack cells marked by antigens associated with cancer.



Unlike UB40, CD19 betters human life. Specifically, the gene aids the early development of B cells, one of our immune system’s flavors of white blood cell. Then, when B cells are mature and have finished their period of rapid growth, CD19 goes silent…at least, it should. When mature B cells restart CD19, the result can be the out-of-control growth of lymphoma or leukemia. But just as CD19 helps to cause these cancers, it may also help to cure them. That’s because CD19 marks these cancerous cells as different than healthy cells – it is an “antigen” that is present on the surfaces of cancerous but not healthy cells. In February of 2018, just as Broncos fans were experiencing deep schadenfreude at Tom Brady’s last second Super Bowl failure, CU Cancer Center investigator Enkhtsetseg Purev, MD, PhD, was infusing a patient with CD19-targeted CAR-T cells as part of a phase I/ II clinical trial against relapsed and refractory B-cell lymphoma. Purev earned her MD at the -Enkhee Purev Mongolian National Medical University before going on to a PhD at Temple University and a residency and fellowship at the National Heart, Lung, and Blood Institute at the National Institutes of Health, working in part in the laboratory of Terry Fry. Now also in Colorado, Purev will manage CAR-T therapies in adult patients at UCHealth University of Colorado Hospital while Terry Fry oversees CAR-Ts in pediatric patients at Children’s Hospital Colorado. An essential third member of this all-star team is Ryan Crisman, PhD, formerly of Seattle-based biotech Juno Therapeutics, who will


“CAR-T therapy has helped so many patients to achieve remission, even after other therapies have failed,” Purev says. “Now our big question is how long this remission will last.”

oversee the manufacture of CAR-T cell therapies at the nearby Gates Center for Regenerative Medicine Biomanufacturing Facility. Earlier that winter, Purev drew blood from her lymphoma patient and sent it in a bag across the street to Crisman at the Gates Biomanufacturing Facility. From there, Crisman isolated the T cells and introduced the lentivirus that inserted genetic code that made T cells manufacture CARs directed at CD19. (“Now the T cells are genetically modified to treat cancer,” Crisman says.) The next step was expanding these T cells until there were enough to be therapeutic. Then Crisman and his team used a specially designed “analytics package” to ensure the CAR-Ts were safe. And then, “the CAR-Ts were frozen to deliver back to the clinic,” he says. The ability to manufacture CAR-Ts literally within walking distance of where blood cells are drawn from patients and the living drug is eventually reinfused may seem like a little thing, but in fact is hugely important. “These patients are really sick. The ability to cut out two days of shipping to get a patient’s cells here and two days to get CAR-Ts back is really helpful. The fact that we walk cells across the street both ways lets us work closely with our doctors and researchers and decreases the downtime for the patient,” Crisman says. The fact that CU now has the capability to explore the science of CAR-Ts, manufacture them, deliver CAR-T treatments to pediatric and adult patients, and learn from the results of these treatments positions Colorado as a leader in this new paradigm of cell-based medicines. Twenty-nine days after Purev’s patient received the infusion of CD19-targeted CAR-T cells, he was back for a scan and Purev wrote in an email, “Complete response at day 29 after treatment with CAR-T cells. Aggressive lymphoma is all gone!” What seems like a miracle cure is becoming the norm. In fact, CD19-targeted CAR-T therapy leads to remission in almost 90 percent of ALL patients and about 60 percent of lymphoma patients. And remember, CAR-T therapies have only been used with the most aggressive forms of leukemia and lymphoma, those that have resisted previous therapies – those that you would think are impossible to control. “CAR-T therapy has helped so many patients to achieve remission, even after other therapies have failed,” Purev says. “Now our big question is how long this remission will last.”

CD22 The problem is that remissions created by CD19-targeted CAR-T cell therapy don’t always last. One reason for relapse may be that CD19-targeted CAR-Ts die off before the cancer does, leaving enough cancer cells to eventually restart growth. “Some patients lose CAR-T cells and this is associated with relapse,” Purev says. This is called CD19-positive relapse – cancer cells marked with CD19 still exist, only there are no more CD19-targeted CAR-T cells to attack them. But there is also “CD19-negative” relapse in which the CAR-Ts wipe out all traces of CD19marked cells, and yet the cancer returns. One theory goes like this: Imagine you are one in a crowd of people wearing red hats and suddenly find yourself running down the streets of Pamplona closely pursued by a herd of large, angry bulls. You might choose to take off that red hat. Instead, you might choose to put on a blue one. Eventually, the bulls trample and gore everyone stupid enough to insist on wearing a red hat, leaving a population of intelligent people like you that switched to blue. In other words, a smart cancer cell may ditch CD19 like a red hat, and instead put on another one that serves a similar purpose. Another theory is that the crowd of people running down the streets of Pamplona is made up of some wearing red hats and others wearing blue. Like before, the bulls trample and gore the people in red hats, leaving the population of people in blue hats, but this time individuals have not changed – the evolution of the population from “red” to “blue” is accomplished by

7 C3: SPRING 2018

selecting for blue. In cancer, this would be like some cells wearing CD19 and others wearing another “hat” from the start, and when CD19-targeted CAR-T cell therapy eradicates the CD19 cells, it leaves these other cells wearing other hats to drive CD19-negative relapse. A third theory is that everyone starts out wearing both red and blue hats, and some people are smart enough to take off the red one. But no matter how a population of cancer cells loses CD19, we know the color of the other hat. The hat is colored CD22. Do you remember the patient that Terry Fry treated over the 2016 winter holiday? The new drug that Fry was using for the first time was a CD22-targeted CAR-T cell therapy. The patient he treated was the first of 21 patients ranging from seven to 30 years old treated with CD22-targeted CAR-T cell drug known as JCAR018. Twelve of these 21 patients achieved complete remission, including 11 of 15 who were treated with the trial’s highest dose. Here’s a very important point: Almost all of these patients had relapsed after CD19-targeted CAR-T cell therapy, meaning that doctors may be able to use first one drug and then when it fails, switch to the other. Even better, they may even be able to use both at the same time.

CD19 and CD22 As we’ve seen, CD19 and CD22 are parallel roads that cancer can take to the same destination. Barricade CD19 and cancer cells can take CD22; barricade CD22 and cancer cells may take CD19. But what happens when you barricade both roads at once? “Now that we have CAR 19s and CAR 22s, we’re starting to see trials that treat them both at the same time,” Fry says (for example #NCT03233854). And he sees Colorado as the place where this will happen. “I’ve been in this long enough to know that the programs that are successful ensure that developing treatments is always a two-way street – you do your lab work, take it to the clinic, and then take your clinical observations back to the lab,” Fry says. “What we’re seeing with CAR-T cells emphasizes that it’s always bench-to-bedside and back again. Colorado has a long history of strong immunology research, both at CU and at National Jewish and that’s what it’s going to take to improve these therapies. The next generation of this field is going to take what we’ve learned back to the laboratory to understand it.”

Back to the Laboratory Combining CD19 with CD22 CAR-Ts is just the start. Fry also plans to open a trial of CD33 CAR-Ts against pediatric ALL. Then, of course, with three CAR-Ts on the table, there will be opportunity to sequence and combine these treatments, and to find the best strategies against specific kinds of cancer, both in the blood and perhaps even against solid tumors. And Fry points out that “CD’s” are only one possible target for CAR-Ts. For example, CU Cancer Center investigator Nick Foreman, MD, is exploring CAR-Ts aimed at the well-known breast cancer gene HER2. “The success with CAR 19 creates the opportunity to think about doing the same thing with other antigens and other cancers,” Fry says. Futuristic strategies may even include gene editing on the tumor side of the equation – using lentiviruses or even the geneediting technology CRISPR (see next page), researchers may be able to force cancers to express certain antigens. For example, instead of being forced to discover targets like CD19 and CD22 that happen to already exist on cancer cells, doctors could insert a new genetic target into cancer cells that makes them naturally visible to the immune system. “I think that one of the perceptions has been that, okay, now with CAR-Ts, we pretty much have at least the B cell malignancies locked up,” Fry says. “But having 50 percent of our patients in remission at one year is not enough. It’s already a paradigmchanging treatment, but as our experience matures it tells me that we really have a long way to go.”




CRISPR CAR-T You are made up of many kinds of cells, including cells of the immune system that are specialized to fight viruses. But viruses don’t only infect multicellular organisms like you. They also infect single-celled microbes. These microbes don’t have armies of specialized virus-fighting cells at their disposal. But they aren’t completely without an immune system. One strategy of the microbe immune system is to store a library of virus mug shots packaged with little bombs that go off if the virus appears. The way the microbe does this is by grabbing bits of viral DNA (the “mug shots”) and shoving them into a backwater of its own DNA, each separated from the next by repeating patterns called “clustered regularly interspaced short palindromic repeats” or CRISPR regions. So, for example, the microbe could end up with a genetic sequence like TACOCAT and then a section of viral DNA called a “spacer” and then another TACOCAT. Next to this TACOCAT-viralDNA-TACOCAT system is something called a CRISPR-associated gene or “Cas gene.” The Cas gene is the bomb – when it’s activated, it cuts cleanly through DNA. Here’s how it works: The microbe carbon copies the entire CRISPR/Cas system (TACOCAT-viralDNA-TACOCAT-Cas) as RNA, which floats around the microbe ready to latch onto matching DNA. That matching DNA, of course, belongs to a virus. And when the CRISPR latches onto the matching, viral DNA, Cas chops it in half. Goodbye virus. Researchers use CRISPR/Cas to edit DNA. With two CRISPR/Cas systems, scientists can snip DNA in two places, which is usually used to precisely cut out a gene. They can also ask the system to carry along a new gene to stitch in place of the one it removes. If this sounds a bit like lentiviral gene editing described in the accompanying article, that’s because it’s very similar: lentiviruses can be used to put a new gene somewhere in a cell’s DNA; CRISPR/Cas can be used to replace a gene in cellular DNA or to put a new gene exactly where you want it in a cell’s DNA. CRISPR/Cas is also relatively cheap and easy. CRISPR has been vilified as a possible way to create designer babies. But even more immediately, look for CRISPR as a way to treat diseases. Clinical trials are planned to use CRISPR to cut and replace faulty genes that cause diseases like the inherited blood disorders sickle cell anemia and beta thalassemia. And CRISPR is also being studied as a less expensive, more precise way to engineer CAR-T cells to fight cancer.

9 C3: SPRING 2018

A CONVERSATION WITH DOUGLAS H. THAMM, V.M.D., DACVIM Barbara Cox Anthony Professor of Oncology



Director of Clinical Research, Flint Animal Cancer Center

Doug Thamm is a physician-scientist, learning about cancer through his experiences

a lot of what we do routinely requires sedation,

treating and studying patients. Only, his patients happen to have four legs. Here we

we have the opportunity to biopsy over and over

speak with Thamm about the unique opportunities of veterinary medicine and how his

again, getting little pieces of tumor tissue each

own cancer diagnosis 25 years ago influenced his career.

time that can tell us things like how the cancer in changing in response to therapy or whether a

C3: We understand you took a year off from vet school to treat NonHodgkins lymphoma. Can you tell us how your own cancer experience guided your career?

C3: And since then has veterinary oncology caught up with human oncology? Thamm: Actually, it some ways it’s ahead of human oncology! One thing about having fewer

Thamm: The really interesting thing about

vets treating cancer is there just aren’t enough of

my cancer is that when I was in vet school,

us to specialize. There aren’t veterinary breast or

veterinary oncology wasn’t what it is today. It

sarcoma or hem-onc specialists. We sort of have

wasn’t something that had crossed my mind as a

to be Jacks of all trades, treating and studying a

specialty. I’d done a lot of research as an undergrad

wide variety of cancers. Sometimes that lets us see

and knew I wanted a career that had a component

the forest for the trees – see the big picture, when

of research – then after my personal experience of

maybe some human oncologists only see things

cancer, I kind of said, “Hey I wonder what’s going

within their subspecialty.

on with canine oncology?” It was kind of like the little spark that made me check it out.

C3: Such as?

drug is doing what it’s supposed to be doing in the tumor tissue. And there’s much more flexibility in combination therapies – we can put a new drug in with chemotherapy, radiation therapy or surgery; in contexts where it has the chance to be much more effective. That couldn’t be done so quickly and easily in humans.

C3: We’ve been talking about the difference between veterinary and human oncology, but do you also see places where the fields are converging? Thamm: I think one of the things, that has very recently come to the fore is the era of

Thamm: Well, I’d argue that we may have been

immunotherapy – and dogs have immune systems

a little ahead in the approach of defining a cancer

that are exactly like human immune systems.

by its molecular driver rather than its microscopic

Tumors show up in dogs and have learned to avoid

appearance – because we see many cancer types,

the immune system just like humans. In contrast,

we’re positioned to see patterns between types,

mouse tumors usually don’t evolve in the same

for example, instead of calling a tumor “breast” or

way to avoid the immune system. Researchers are

“lung” cancer, we might see it as ALK-positive or

trying to do all these crazy things with mice when

EGFR-positive cancer, defining the cancer by the

there’s a huge population of dogs walking around,

genetic changes that created it.

a third of whom are going to get cancer and may benefit from these immunotherapies.


C3: Does that mean there are actually advantages to studying cancer in dogs compared to studying the disease in humans?


Thamm: Our goal as veterinarians is, first and

Thamm: Sure, there are a couple advantages.

foremost, to improve the health and welfare

For example, human clinical trials generally can

of animals, but we have the potential to go

test new drugs only after everything else has failed.

one better. We have the opportunity to answer

Because there’s no accepted standard of care in

questions that could translate into better therapies

veterinary medicine, we can study new treatments

for humans as well.

much earlier in the course of care. And because


C3: So we help dogs and learn something, too?



MD What it Really Means to be a Doctor EVEN IN THE HI-TECH WORLD OF RADIATION ONCOLOGY, CHAD RUSTHOVEN PUTS PATIENTS FIRST B Y E R I K A M AT I C H Ask a kid what they want to be when they grow

Rusthoven is part of CU’s renowned thoracic

up and the answers are often predictable – doctor,

oncology team improving outcomes for people

lawyer, cop, firefighter. As a child, Chad Rusthoven,

with lung cancer around the world.

MD always said he wanted to be a doctor – it

“When I was a resident,” Rusthoven recalls,

seemed like a good career choice, frequently

“Brian Kavanagh (MD, MPH, chair of radiation

reinforced by both teachers and parents. Over the

oncology), Ross Camidge (MD, PhD, director

years, he’s learned that being a physician in the

of thoracic oncology), and Bob Doebele (MD,

field of radiation oncology is a far more complex

PhD, director of the Thoracic Oncology Research

and rewarding journey than he ever imagined.

Initiative) were just beginning to look at the

After earning his undergraduate degree in

combination of radiation and targeted therapies

psychology from the University of Florida honors

in lung cancer. Five years later, their work has

college, Rusthoven committed to pursuing

defined some of the key treatment paradigms in

medicine and spent another 10 years in training,

the national guidelines for lung cancer patients with

including medical school at University of South

targetable mutations.”

Florida, internship at Georgetown, and ultimately

As a radiation oncologist, Rusthoven’s job is to

CHAD G. RUSTHOVEN, MD Assistant Professor, CU School of Medicine

Cancer Network (NCCN) brain tumor and small-cell

his residency in radiation oncology at University of

help his patients live longer, improve symptoms, and

lung cancer guidelines, which set the standard-of-

Colorado Hospital.

to minimize the side effects of therapy. Sometimes

care for the oncology care in U.S.

“There were a number of fields that interested

the treatment options are limited, though, and

For example, in a recent study published in the

me in medical school, including internal medicine,

Rusthoven believes that may be when some of his

Journal of Clinical Oncology, a group of CU-lead

infectious disease, and emergency medicine.

patients need their physicians the most.

radiation oncologists and surgeons, with Rusthoven as senior author, analyzed post-treatment

Ultimately, I decided on oncology, which ended

“As oncologists, there is always something

up being a wonderful choice for me,” Rusthoven

we can do. For some, it is treating with the hope

outcomes for over 80,000 patients with stage I lung

says. “It’s a multidisciplinary field, that’s constantly

of cure or improving quality of life. But in some

cancer. Importantly, the authors found differences

evolving and advancing. But above all, oncology

cases, people just need to speak to someone

in post-treatment outcomes between surgery and

allows you to support people going through a major

understanding who cares about what they are

radiation that appeared to increase with age, which

challenge in their lives, which is such a privilege and

going through,” he says.

could influence decision-making among older

a uniquely human experience.” After completing his radiation oncology

Rusthoven’s bedside manner was recently recognized with an induction to the Gold Humanism

patients who are eligible for either treatment. “The culture of research at CU is to go wherever

residency in 2015, Rusthoven was offered

Honor Society, a distinction voted on by current

the data leads you, and we’ve been fortunate

a position to stay on as a faculty member at

UCH residents and fellows in recognition of faculty

enough to follow those leads to some exciting

the University of Colorado Hospital, with a

members who embody humanism in medicine.

research questions over the years. Here, I also

specialization in the treatment of lung and

In addition to his interest in patient-centered

brain tumors. “Working in the lung and CNS oncology

have the advantage of working with some of the

oncology, Rusthoven is also an active researcher

brightest and most open-minded oncologists

and author. He has had notable success early

around,” he says. With old-school bedside manner and an

programs at UCH has really been a dream job for

in his career, with original research and opinion

me,” he says. “It is an incredible environment to

contributions to leading medical journals including

openness to ongoing scientific advancement,

work in, with a culture of compassionate, patient-

the Journal of Clinical Oncology and the New

Chad Rusthoven hopes to be one of CU’s radiation

centered care and colleagues who are some of the

England Journal of Medicine. Rusthoven also serves

oncology leaders for the next generation in the

world’s leading experts in oncology.”

as a panel member for the National Comprehensive

rapidly advancing field of cancer care.

11 C3: SPRING 2018

Invisible These Breast Cancer Patients are Still



In 1974, First Lady Betty Ford went public with her breast cancer diagnosis and subsequent mastectomy, launching breast cancer into the national consciousness. Watergate was still fresh in everyone’s minds, and Mrs. Ford said that part of the reason she spoke so openly about breast cancer at a time when the subject was taboo is that she wanted no cover-ups in the Ford Administration. Ford’s decision to share her experience resulted in what researchers called the “Betty Ford Blip.” Her story raised awareness of the disease, leading millions of women to go for screening. As a result, diagnoses of breast cancer in the United States rose sharply, and with awareness and early detection, thousands of women were able to treat breast cancer at an earlier, more manageable stage. Nearly 20 years later, in 1992, the pink ribbon became the national symbol for Breast Cancer Awareness Month. Now, twenty-six years later, without fail, the month of October is awash in pink ribbons and calls for awareness and early detection. But even as Angelina Jolie added a new burst of steam to the campaign of awareness that Betty Ford started, a group of breast cancer patients was being left behind. Once breast cancer metastasizes into other areas of the body, it becomes much more dangerous. And while the National Cancer Institute spends more than $500 million dollars per year on breast cancer research, only two to five percent of this funding goes to

study how the disease spreads. First there was Betty Ford. Then there were pink ribbons. Then there was Angelina Jolie. Now a new generation of breast cancer patients is pushing to increase awareness for a group of breast cancer patients that has been largely overlooked this whole time, namely those with metastatic disease.

FROM STAGE II TO STAGE IV Christine Howard was diagnosed with Stage II breast cancer in 2012 when she was 41 years old. Breast cancers at this stage are considered curable. Christine underwent surgery, radiation and chemotherapy which included Herceptin (trastuzumab) for a year. Howard says she knew the cancer had spread to a lymph node, and she thought about the possibility of recurrence despite completing the intense treatment program, but she put it out of her mind as much as possible and moved on with her life. Then in January of 2016, Howard was having some back pain and recurrent

me to get my affairs in order,” says Howard. “I didn’t feel comfortable with the care I was receiving, so I switched to UCHealth University of Colorado Hospital (UCH) and found Dr. Kabos. I felt so much better immediately.” Peter Kabos, MD, deputy director of the University of Colorado Cancer Center’s Breast Cancer Research Program, found that Howard’s cancer had spread to her bones. He immediately changed the plan for her care, giving Christine a targeted treatment against a protein called human epidermal growth factor or HER2, and another against estrogen receptors (ER), which were driving her cancer. In addition, Bennie Lindeque, MD, PhD, a professor of Orthopedics at CU School of Medicine, performed surgery on Howard’s legs which had been weakened by the cancer. Then came another blow. They found the cancer in Howard’s brain as well. “I was starting to have a hard time on occasion,” says Howard. “When I was driving, I would feel fuzzy but that could

“WE NEED MORE RESEARCH,” SAYS HOWARD “WHAT WORKS FOR ME MAY NOT WORK FOR SOMEONE ELSE...” pneumonia, and during the course of treatment, she learned the cancer had come back. “When I learned the cancer had returned, my physician at the time told

have been chemo-brain. My boyfriend took me in for brain MRI and new scans showed spots on my brain.” Howard had three sessions of stereotactic radiation surgery, which

13 C3: SPRING 2018



is precisely targeted form of radiation commonly used to treat brain metastases from breast cancer. Shortly thereafter, she enrolled in a clinical trial to keep her cancer from spreading any further. After a detailed discussion about standard of care therapy and the available clinical trials, Christine decided to enroll in an innovative study using a combination of three drugs that she could take orally at home.

“TRIPLE POSITIVE” BREAST CANCER There are three well-established predictive markers of breast cancer. They are estrogen receptors (ER), progesterone receptors (PR), and the growth factor receptor HER2, these receptors may be blocked with targeted drugs to stop cancer growth. Breast cancers lacking these three markers are referred to as “triple-negative” but clinicians and scientists are quickly learning more about cancers that have all three receptors, which are often called “triple-positive.” There are treatments against each target individually, but when multiple drivers are present, as in “triplepositive” breast cancer, blocking one


often results in cancer nimbly switching to driving its growth with the other two. When you first meet Christine Howard, you would never know she has advanced cancer. Christine’s hair has grown back following chemotherapy, and because of the surgery to strengthen her legs, she gets around well. Not only does she have metastatic breast cancer, but her cancer is the “triple-positive” form of the disease. Serendipitously, in 2017 when Howard learned that her cancer had returned, a clinical trial to treat triple-positive breast cancer had just opened at CU Cancer Center. The study combines tucatinib, which inhibits HER2, with letrozole targeting ER and PR hormone receptors, and the drug palbociclib, which targets CDK proteins that help cancer cells rush through the process of replication. The three had not been tried together until Elena Shagisultanova, MD, PhD, a breast cancer specialist at UCH, hypothesized there could be a way to target all three drivers at the same time with better results than targeting combinations of any two. The clinical trial is open nationwide through the Academic Breast Cancer Consortium, giving access to this exciting novel combination across the United States. “When metastatic cancer spreads to the brain, it can be especially challenging,” says Kabos. “Many medications aren’t effective in the brain, but exciting early clinical trial data for tucatinib shows that it may be one of the drugs that can penetrate the blood-brain barrier to combat brain metastases. It was the ideal choice for Christine at the time.” The tucatinib, palbociclib and letrozole clinical trial has allowed Christine more time with her loved ones and friends. It has also given her time to pursue her new passion: Howard is passionate about raising awareness about metastatic breast cancer. She wants

to tell people that the sea of pink we see each October is not always helping scientists find new, more effective treatments for women with more advanced breast cancers. “We need more research,” says Howard “What works for me may not work for someone else. And I am hoping that if the combination I’m on stops working, maybe a year from now research could lead to something else available.” First through Facebook communities and now through the organization Living Beyond Breast Cancer, Howard has also become a patient advocate for other women living with metastatic disease. When Betty Ford shared her breast cancer story, she brought the disease out of the shadows. Angelina Jolie gave awareness another boost when she had surgery to reduce her risk of getting cancer. Christine Howard is hopeful that she, in some small way, can remind us that women with advanced breast cancer require and deserve the same kind of attention as first ladies and movie stars. *The tucatinib, palbocilib and letrozole trial is coordinated by the Academic Breast Cancer Consortium and currently open for enrollment at the University of Colorado Cancer Center; University of Texas Health and Science Center in San Antonio, TX; Stony Brook University, NY; University of Arizona, Tucson, AZ; and University of New Mexico, Albuquerque, NM and will also be accruing patients at Northwestern University, Chicago, IL. The trial is funded by the Pfizer ASPIRE Award in Breast Cancer Research. Cascadian Therapeutics and Pfizer are providing the study drugs tucatinib and palbociclib.

For more information about trial eligibility and participation, contact or


Funding Research for Advanced Cancers Metastatic Breast Cancer In 2016, the National Cancer Institute spent $522.6 million for breast cancer research. But only about $13 million, or 2-3 percent, went to research in metastatic breast cancer.

On the philanthropic side, only one U.S. non-profit, METAvivor, dedicates 100 percent of its research funding to metastatic breast cancer. “Getting research funds of any kind is a challenge,” says Heide Ford, PhD, CU Cancer Center’s associate director for basic science. “But advanced cancers present unique challenges. Often patients are not well at diagnosis, sometimes they can’t tolerate aggressive treatment. We want to discover medications that improve length of life and quality of life. It’s a long, expensive process.” Ford’s work focuses on the parallels between normal development and tumor progression. She also examines how cancer cells utilize developmental programs to spread and survive in areas of the body beyond the primary tumor. “By better understanding how breast cancer spreads through the body, and particularly how it adapts to and grows in secondary sites, we may be able to develop drugs that block those pathways,” says Ford. “If we can understand the pathways that allow breast cancers to thrive at sites beyond the original tumor site, we might be able to apply what we learn to other kinds of cancer.”

In 2018:

266,120 40,920

women will get breast cancer

women will die of breast cancer

2% - 3% Only

of NCI breast cancer research funding goes to metastatic breast cancer

1 in 8

will develop breast cancer in their lifetime

15 C3: SPRING 2018



When it comes to healthcare, what really matters to patients? In 2015 two physicians, Leana Wen, MD, MSc, Commissioner of Health for the City of Baltimore, and Suhavi Tucker, MD, from Mount Sinai Hospital, took to the streets of Washington, DC to find out. After interviewing people at coffee shops, senior citizen homes, metro stops, and community centers, what the researchers discovered surprised them. It turned out that rather than a doctor’s intelligence, training or even skills, at the top of the list of things participants wanted were a doctor who listens to them, a doctor who is caring and compassionate, and a doctor who explains well and is transparent and open. According to the study, “the doctor/ patient relationship remains at the heart of people’s perceptions of healthcare.” CU Cancer Center investigator, Amanda Dempsey, MD, PhD, MPH, puts this idea at the center of her research in cancer prevention. And


she shows that as much as cancer prevention depends on actions like smoking cessation and vaccination, equally important is how we talk about these things. It turns out that in preventing cancer, communication is key.

THE PREDICAMENT OF THE HPV VACCINE According to the Centers for Disease Control (CDC), in the United States the human papilloma virus causes 30,700 cancers in men and women each year. Worldwide, the number is closer to half a million. However, in the last decade since the CDC recommended the HPV vaccination, HPV-associated cancers have dropped 64 percent. Despite the proven effectiveness of the HPV vaccines only 60.4 percent of children aged 13 to 17 have started the vaccination series in the United States. If vaccination rates were higher the incidence of HPV would be even lower. “The HPV vaccine has been around for over a decade yet there are low

vaccination rates in the United States, especially compared to other countries,” explains Dempsey, associate professor of pediatrics at the CU School of Medicine. She’s not kidding: Thanks to an effort to distribute HPV vaccine for free at schools, Australia is on track to be the first country to completely eliminate cervical cancer. Dempsey believes there are three major reasons for the United States’ low rate of HPV vaccination. “First, past research shows that providers treat the HPV vaccine differently than other vaccination,” Dempsey explains. Specifically, studies have found that rather than treating the HPV vaccine like any other vaccination against disease, physicians feel the need to point out to parents that HPV is considered a sexually transmitted virus, possibly clouding parents’ perceptions of the vaccine by conjuring the taboo of teenage sexual activity. “Second, media tends to treat the vaccine as controversial,” she says. A

quick internet search proves her point: Many articles at alternative news sites claim harm from HPV vaccines, and even though FDA and CDC articles cite studies thoroughly debunking the safety myth, the fact that safety concerns are even mentioned may sour some patients on the need for vaccination. “Finally,” Dempsey says, “people perceive it as a new vaccine despite the fact it has been around for years and millions of people have been vaccinated.” The perception that the vaccine is new can make it seem experimental or unproven, leading some parents to a wait-and-see attitude about vaccination. In other words, according to Dempsey, the overarching reason that people in the United States fail to get the HPV vaccination is lack of effective communication. “I thought, if only we could help to improve communication between providers and their patients, we could increase vaccination rates,” she says. And so she designed a study to do just that.

A COMMUNICATION INTERVENTION To figure out if helping doctors talk to their patients would have an effect on vaccination rates Dempsey and her team created a program made up of an HPV fact sheet library, a tailored parent education website, HPV-related disease images, an HPV decision aid, and two and half hours of communication training for healthcare providers. In total 16 primary care practices in Denver participated in the study, with 188 medical professionals who saw 43,132 adolescent patients. Half the practices would use Dempsey’s kit and the other half would continue with business as usual. After the study concluded in 2015,

there were obvious differences between “intervention” and “control” practices. The intervention practices saw an 11.3 percent increase in adolescents initiating the vaccine series while the control practices saw a 1.8 percent increase. Additionally, at intervention practices, teens who started the vaccination series were more likely to complete it. Dempsey and her team are excited to see that something as simple as optimizing communication can have a substantial impact on vaccination rates. However, they also know that there is a long way to go to get vaccination rates to where they should be. “Increasing vaccination rates is hard and takes lots of interventions,” says Dempsey. “This is not a magic bullet that will completely get rid of the problem, but it is a good start.”

NEXT STEPS Now that Dempsey has shown that the communication intervention works, she is trying to get more primary care practices to use it. “We know from surveys taken at the end of the study that the communication techniques and fact sheets were most commonly used by the providers,” she says. “Hopefully we can use this information to make a simplified version of the intervention and take it to practices all across the state.” Intervention practices had such positive results from the study that over 90 percent of health care professionals at these clinics said they would continue to use the components in the future. “We are not reinventing the wheel by any means,” says Dempsey. “We are taking what doctors already do (communicating with their patients) and making it better and more effective. A small amount of time and training can make a big difference.”

HPV 101 Human Papillomaviruses (HPV) are not one, but approximately 200 different viruses. According to the National Cancer Institute, more than 40 types of these viruses can be spread from person to person through sexual contact, leading to HPV infection. Most of the time these infections are not cause for concern, however persistent infections from certain HPV viruses can lead to cell changes and ultimately cancer. In 2006 the Food and Drug Administration approved a vaccine to prevent these infections in girls. Shortly after in 2009 the vaccine was also approved for boys. The vaccine is most effective at preventing infection if it is given before the patient is sexually active. Because of this it is recommended that patients start their vaccination series at ages 11 or 12, but it can be given as young as 9 years old. The HPV vaccine works by stimulating the body to produce antibodies that help your immune system bind to and eliminate HPV virus. The vaccine is made from virus-like particles (VLP’s) that resemble the natural virus enough to encourage the body to create antibodies but lack viral DNA, and thus are not infectious.

17 C3: SPRING 2018



Remembering Bette A SISTER’S GIFT SPEEDS DISCOVERY IN PANCREATIC CANCER B Y E R I K A M AT I C H “Dr. Leong is a very kind, compassionate, loving

and their families, the experience is life changing.

man, who made us all feel that he took a special

For families left behind the experience can be

interest in Bette,” says Carr. “He took all the time

motivation to do what they can for the patients and

necessary to explain exactly what was happening

families that inevitably follow.

in her body, what she could expect from the

The numbers are grim. Pancreatic cancer will

treatment, and was always encouraging, but not in

kill 80 percent of people diagnosed within a year.

such a way as to minimize the very real possibility

That means that 43,090 of the approximately

that this disease might kill her.”

54,000 people who develop pancreatic cancer will

Leong acknowledges that treating patients

die within 365 days. Of the people diagnosed with

with pancreatic cancer is difficult. There are only

pancreatic cancer five years ago, only eight percent

two widely used therapies, neither of which works

are still alive today.

particularly well. There also is no test for early

“My sister and I were very close,” says Anne

detection, meaning that at the time of diagnosis

Carr, of McCall, Idaho. “We were best friends,

more than 50 percent of pancreatic cancers will

we shared everything. When I lost her, it left a

have already spread to other parts of the body

big hole. That’s what inspired me to give my

making it much more difficult to treat. Though

whole estate to research.”

pancreatic cancer is the fourth leading cause of

Carr made a $1 million estate commitment in

cancer-related deaths in the United States, federal

honor of her sister Elizabeth Carr Arnold, “Bette”

funding for pancreatic cancer research has been

as she was affectionately known. This happened

only about a fifth that of the other top-five cancers

weeks after Bette passed away from pancreatic

(lung, colon, breast and prostate).

cancer, just 18 months after diagnosis. In addition to memorializing Bette with the Bette

“There is no question it is gratifying when any patient’s family compliments the quality of the

Arnold and Anne Carr Pancreatic Cancer Research

care they received,” says Leong, an investigator

Fund, Carr also wanted to acknowledge the

at CU Cancer Center. “Mrs. Carr has taken the

compassionate care of Bette’s medical oncologist,

compliment to a new level with her generous gift.”

Steven Leong, MD.


For people diagnosed with pancreatic cancer

Bette was active and apparently healthy when it


became obvious something was not right. She was diagnosed with pancreatic cancer in June 2016. That is when Bette and her husband, Ed Arnold, sought out Dr. Leong for a second opinion. “There are risk factors for pancreatic cancer

have not found the right approach yet for

those risk factors,” says Leong. “We have so much

pancreatic cancer.”

better ways to manage the effects of this disease.” Carr could not agree more and hopes her gift

team discover these better approaches so that other patients will have a better chance of beating the disease than Bette did, and other families

is optimistic but cautions there is a lot to learn.

won’t have to watch their loved ones ravaged

“It’s an exciting time in cancer science,”


Carr is hopeful her gift will help Leong and his

will speed the search for better treatments. Leong

says Leong. “We have had some success using


that increase the survival of patients. We just

but many people who develop it don’t have any of to learn and we need to find better treatments and



by the disease. “Dr. Leong has dedicated himself to curing this

immunotherapy to rev up the immune system

disease and I want to do what I can to move it

against tumors. We have also seen other therapies

along,“ says Carr. “I hate this disease and I want

targeting cancer cells while sparing healthy cells

to get rid of it.”



Ballard Spahr Remembers Beloved Partner, Roger P. Thomasch When Denver trial lawyer Roger P. Thomasch C /O BALLARD SPAH R

was diagnosed with cancer in 2016, members of his law firm, Ballard Spahr, rallied around their beloved colleague. They ordered wristbands embossed with “No One FIGHTS Alone!” and made a cardboard cutout of their missing officemate, which they carried to various office gatherings when Mr. Thomasch was out of the office receiving treatments. When he shaved his head before chemotherapy, the office staged a head-

CU’s Scott Holden Honored with Fellow Award Former University of Colorado Assistant Professor Scott Naylor Holden, MD, died suddenly on March 5th, 2017 at age 50 and now Genentech, his employer of 14 years, has established a fellow award fund in his honor. Scott joined CU as an oncology fellow and became chief fellow before joining the faculty in 2001. As a member of the Developmental Therapeutics Program, Scott spent three years conducting many Phase I studies before leaving CU in 2004 to take a position at Genentech where he worked in the Oncology Early Clinical Development Group. During his tenure at Genentech he provided clinical oversight for early stage oncology programs and managed a very talented group of medical directors and clinical scientists. In addition to his passion for helping patients,

shaving fundraiser to support CU Cancer Center, where Mr. Thomasch was treated until his death in 2017. The entire firm joined in, with most of Ballard’s other offices holding fundraising activities. “He was our leader, our partner, our mentor, our colleague and our friend,” said Steve Suflas, who followed Mr. Thomasch as Denver Managing Partner. Mr. Thomasch was a partner at Ballard Spahr for three decades and tried more than 100 cases to verdict during his 50-year career. He was a fellow of the prestigious American College of Trial Lawyers and the International Academy of Trial Lawyers. He was ranked by The Best Lawyers in America for 30 years and, for more than a decade, was named by Super Lawyers as a “Top 10 Colorado Lawyer.” Chambers USA: America’s Leading Lawyers for Business awarded him its highest ranking 14 years in a row. More importantly, Mr. Thomasch was admired as much for his kindness and loyalty as for his successes in the courtroom. “His energy and spirit, and innate decency, pushed us to do and be better,” said Ballard Spahr Chair, Mark Stewart. With the gifts that poured in to honor Mr. Thomasch, Ballard Spahr is carrying forward his memory and advancing the search for a cure.

Scott was also an avid drummer and played in two bands together with several Genentech and ex-Genentech bandmates, culminating in a performance at the 2017 ASCO conference. Scott was a unique and special person who touched many people over the course of his oncology career. His wit and his enthusiasm for early drug development remain warm memories for all his colleagues at Genentech and at University of Colorado. Additional support for this award can be directed to:

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19 C3: SPRING 2018



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C3: Collaborating to Conquer Cancer Published twice a year by University of Colorado Anschutz Medical Campus 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 | Contributing Writers: Taylor Abarca, Erika Matich Photos: Trevr Merchant The CU Cancer Center Consortium Members UNIVERSITIES

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Why CU Cancer Center is expanding access to cancer clinical trials, across Colorado In 1971, when President Richard Nixon signed the National

Network (ORIEN) since 2013, CU Cancer Center shares

Cancer Act, doctors and researchers thought cancer was

molecular genetic data with 17 institutions across the U.S. This

one disease that would have one cure. Now we know that

means that instead of waiting to enroll 500 patients with

cancer is many related diseases, with hundreds of different

a specific genetic mutation on a clinical trial, these hospitals

causes and many hundreds of possible treatments. This new

work together to reach the required number. At the same

understanding is incredibly exciting – it means that we have

time, we are working to expand access to clinical trials for our

the opportunity to match just the right patient with just the

patients in Colorado. The fact is that cancer treatment can be

right drug. But it also presents an incredible challenge.

involved, and it may be impractical for patients to visit Denver

The challenge is in the numbers.

for weekly chemotherapy infusions or spend many days away

Say it takes 500 patients with a specific genetic mutation

from family and friends while admitted to UCHealth University

to test a new drug. If all of the 10,000 new adult oncology


patients treated every year at UCHealth University of Colorado Hospital were eligible and

of Colorado Hospital. By offering clinical trials at UCHealth locations up and

enrolled in a clinical trial of

“What this means is that it can

this drug, we could test

take years or decades to enroll

20 such drugs every year! But, nationally, only

enough patients draw conclusions

about three percent of

about a new treatment.”

cancer patients will join a

down the Front Range, in the rural eastern half of the state, throughout the mountains and along the Western Slope, CU Cancer Center hopes to move cutting edge care closer to

clinical trial, and rather than all being eligible for the same

patients who need it, while speeding the approval process of

clinical trial, these patients are spread across hundreds of

important, new drugs.

cancer subtypes. What this means is that it can take years or

As more drugs treat smaller populations with specific

decades to enroll enough patients draw conclusions about

genetic mutations, testing these drugs gets harder and harder.

a new treatment. And for less common kinds of cancer,

But this new reality is forcing the field of cancer research

gathering 500 patients at a single hospital is simply impossible.

to work in new ways – only by sharing our findings and

That’s the problem. University of Colorado Cancer Center is working hard to be part of the solution. As part of the Oncology Research Information Exchange


expanding access to life-saving clinical trials can we move the field forward. This increased collaboration and connectivity benefits us all.


C3: Collaborating to Conquer Cancer Spring 2018 Edition  

The biannual magazine of the University of Colorado Cancer Center

C3: Collaborating to Conquer Cancer Spring 2018 Edition  

The biannual magazine of the University of Colorado Cancer Center