VELOSANO 2 ANNUAL REPORT

VE LOSANO 2
ANNUAL REP O RT
Table of Contents
Living Hope6
VeloSano 2 | By the Numbers
8
VeloSano 2 | Top 10 Lists
9
VeloSano 1 | Research Update
11
Where The Money Goes
12
Case CCC Pilot Awards
30
VeloSano Partners35
Big Wheelers presented by KeyBank
36
VeloSano 2 Steering Committee
37
The Future of Cancer Care at Cleveland Clinic
38
The Power of Every One39
VELOSANO 2 | ANNUAL REPORT
Brian Bolwell, M.D. and
Stewart Kohl, VeloSano
Founder at the start line
during VeloSano 2
Thank you for being part of our VeloSano family. Our primary goal, as you are aware, is to fund
cancer research, and continue to make scientific discoveries that lead to better outcomes, and,
ultimately, cures. For the second year, I had the honor of overseeing the selection process for the
VeloSano Pilot Awards and the designation of the VeloSano Impact Awards. The Pilot Awards are
scientific proposals made by Cleveland Clinic researchers from many different specialties. They
have become very competitive, and this year we had over 60 applications. This required two
separate levels of review. The first was to determine the top 30 that would be ranked, and the
second was the actual ranking.
Eighteen scientific leaders judged these applications. After significant deliberation, 15 awards
were distributed, at an amount of $100,000 per award (this is greater than the $75,000 per
award we were able to allocate last year). These awards included studying genomic mutations in
a variety of cancers, including colon cancer; studying cancer stem cells and brain tumors; novel
precision therapies for leukemia; and many other outstanding projects. The dollars raised from
VeloSano are of vital importance to stimulate this extremely promising research.
The VeloSano Impact Awards are granted to large-scale projects that are among our Cancer
Institute’s highest priorities. Examples include using xenografts to create avatars of human
cancers; studying and preventing the development of blood clots in patients with selected tumors;
and establishing a novel protocol for freezing ovarian tissue to preserve fertility.
Cleveland Clinic is the home of many world-renowned scientists and researchers. VeloSano is
allowing us to make meaningful discoveries right now, that will translate into improved patient
care. This is a big deal. We are extraordinarily grateful for these opportunities, and we plan on
continuing to work very hard to advance this field with the dollars raised, thanks to all of you.
We will look forward to seeing you at VeloSano 3 in July. Bike to cure!
Sincerely yours,
Brian J. Bolwell M.D., F.A.C.P.
Chairman, Taussig Cancer Institute
Medical Chairman, VeloSano
5
As VeloSano continues to grow, we are focused on not only
Riders, Virtual Riders and Volunteers from
bringing in significant funds to advance cancer research but also
these special groups will be recognized
to continually enhance and evolve.
as Living Hope in various ways, including
With that, we are taking our former term that was specific
to cancer survivors only (Living Proof), and evolving it to
incorporate both current patients and survivors.
That new term: Living Hope.
on their personal fundraising pages
on velosano.org and throughout event
weekend, to name a few.
While we strive for the day when there
will be no more cancer, for now, join us in
honoring our Living Hope community.
VELOSANO 2 | ANNUAL REPORT
J. Mark Brown , Ph.D.
From Cancer Patient to Cancer Researcher
In April 2013, I joined Cleveland Clinic as a basic science staff
member in the Lerner Research Institute and in August 2013 I was
unexpectedly diagnosed with stage III colon cancer. After two major
surgeries, 6 months of intensive chemotherapy, and state of the art
medical care given at Cleveland Clinic - I am now cancer free! Being
a cancer survivor myself and experiencing the world class care that I
have received from my colleagues at Cleveland Clinic, has ignited a new
passion for cancer research in my laboratory. My laboratory’s research
has historically been focused on nutrient metabolism, and now we
are leveraging our expertise in this area to find new cures for cancer.
Proceeds from last year’s ride provided funding for my laboratory to
study how we can treat liver cancer (hepatocellular carcinoma), and we
now have exciting findings of new potential drug to treat liver cancer.
7
VeloSano 2 | By the Numbers
$3,000,000
1,300
Riders from ...
65%
increase in Riders
from VS 1 to VS 2
913
Volunteers
228
Riders at least doubled their minimum
commitment to become Big Wheelers
147
Living Hope Participants
(cancer survivor / cancer patient community)
raised for
cancer
research
and
3
states, DC,
and Ontario countries
214
Virtual Riders
18,000+
Gifts received from all 50
states, DC and 25 countries
VELOSANO 2 | ANNUAL REPORT
VeloSano 2 | Top 10 Lists
Top 10 Fundraising Teams
1.
Cleveland Clinic
$301,954
2.
The Riverside Company
$210,527
3.
Big Galoots Bicycle Club
$203,652
4.
Cleveland StARTup Collective
$202,291
5.
Taussig Cyclotrons
$147,217
6.
Cleveland Indians
$135,156
7.
Team Key$69,010
8.
Jones Day
$67,018
9.
Cardinal Health
$66,180
10. Make It Rain
$64,238
Top 10 Fundraising Riders
1.
Marc Harrison
$262,600
2.
Joanne Cohen
$172,372
3.
Stewart Kohl
$144,655
4.
Paul Dolan
$51,973
5.
Bob Rich
$47,423
6.
Michelle Amato
$28,531
7.
John Fung
$20,000
8.
Hiroyuki Fujita
$17,812
9.
Matt Litzler$17,635
10.
Larry Pollock$16,970
Top 10 Fundraising Virtual Riders
1.
Jorge Garcia
$10,760
2.
Zumi Pig$6,015
3.
Peter Dougherty
$3,450
4.
Jaroslaw Maciejewski
$3,402
5.
Brian Bolwell
$2,925
6.
Shlomo Koyfman
$2,775
7.
Jenna Oliverio
$2,151
8.
Brian Laliberte
$1,529
9.
Yogen Saunthararajah
$1,365
10.
Eric Tischler$1,270
9
Why I Ride
VELOSANO 2 | ANNUAL REPORT
Justin Durla
Lathia, Ph.D. (left)
VELOSANO 2 RIDER
VeloSano 1 | Research Update
Reversing Immune Cell Suppression and Enhancing
Cytotoxic T Cell Response in Glioblastoma by Targeting
Myeloidderived Suppressor Cells
Principal Investigator: Justin Durla Lathia, Ph.D.
Co-Investigator: Michael Vogelbaum, M.D., Ph.D.
The immune system ensures normal tissue function by responding to injury and
When the suppressive immune cells were targeted,
infection to minimize damage. While the immune system is tightly regulated,
tumors did not grow as well and contain many
in malignant tumors, such as those in the brain, its function is suppressed by
immune cell populations that have the capacity
the tumor cells and the recruitment of unique immune cell populations with
to target and kill tumor cells. This is an attractive
suppressive function. The goal of our VeloSano pilot grant was to determine
strategy as it allows the body’s immune system
how recruited suppressive immune cells function in brain tumors and explore
to function to eliminate the tumor. This approach
strategies to target them. We were able to identify a pathway that therapy-
is complementary to immune-based therapies
resistant tumor cells use to amplify the function of these suppressive immune
being currently evaluated as our approach targets
cells and this work will be published shortly in a top-tier journal, Stem Cells.
suppressive immune cells while many current
We also explored several ways to target these suppressive immune cells
therapies are attempting to increase immune
and found that a conventional chemotherapy, 5-fluoruracil, could eliminate
system function. Based on these observations, we
these cells in pre-clinical models. We found that we could effectively target
are initiating a pilot clinical trial in which we will
suppressive immune cells at a dose 20-fold less than what is routinely given.
track suppressive immune cells in patients after
they receive 5-fluoruracil. Once we can demonstrate
the ability to target suppressive immune cells, we
are hoping to initiate a larger scale trial to look
at how this strategy may be combined with other
therapies.
11
$3,000,000
You gave 100%, so will we.
Pilot Awards
The VeloSano Pilot Awards provide seed funding for cancer research
activities being performed across the Cleveland Clinic enterprise.
Utilizing a competitive application and peer-review selection process,
the goal of the VeloSano Pilot Awards is to support projects with a high
likelihood of leading to successful, future extramural grant funding. The
focus of these one year grants is to build upon and transition recent
advancements in cancer genetics and epigenetics and basic and
translational tumor immunology.
Impact Awards
The VeloSano Impact Awards are distributed by the VeloSano Medical
Chairman to satisfy the critical needs of the Cleveland Clinic cancer
program. Whether a piece of equipment, advanced technology,
recruitment or laboratory expenses, the VeloSano Impact Awards are to
address strategic priorities that will advance the investigational abilities
in the area of cancer research. These awards are meant to ensure
that our caregivers and patients have access to the best talent and
technology available.
VELOSANO 2 | ANNUAL REPORT
(L–R)
Federico Aucejo, M.D.
J. Mark Brown, Ph.D.
Daniela Allende, M.D.
PILOT AWARD
Targeting Lipid Metabolism to
Prevent Hepatocellular Carcinoma Progression
Principal Investigator: J. Mark Brown, Ph.D.
Co-Investigators: Federico Aucejo, M.D. and Daniela Allende, M.D.
Obesity represents a rapidly expanding health care burden in developed countries, and is recognized as a
major risk factor for the development of many types of cancer. In particular, hepatocellular carcinoma (HCC)driven mortality is strikingly associated with obesity. HCC is known to be predominantly driven by hepatitis
B (HBV) or hepatitis C (HCV) viral infection. However, highly effective vaccines targeting HBV and curative
anti-HCV drugs are now readily available, which will likely result in a sharp decline in viral-driven HCC over
the next decade. In contrast, the incidence of obesity-driven HCC is poised to rise at an alarming rate as the
obesity epidemic continues to grow. Importantly, the molecular mechanisms linking obesity to HCC are not
known. Furthermore, animal models that recapitulate human-relevant obesity related disease progression are
lacking. To address these gaps our team has established both viral- and obesity-driven mouse models of HCC
that allow us to model human-relevant disease progression. We have also begun establishing patient-derived
xenografts of obesity-driven HCC to study molecular mechanisms driving malignancy. Most importantly,
we have identified a novel lipase drug target for prevention of obesity-driven HCC, and have established
collaborative efforts with major pharmaceutical companies to rapidly move lead compounds from bench to
bedside. Significance: These studies will lay the foundation for next generation targeted therapeutics for HCC,
and have broad implications for many other obesity-linked cancers.
13
Xiaorong Gu, Ph.D.
PILOT AWARD
Novel, Precision Therapy for Relapsed NPM1-Mutated AML
Principal Investigator: Xiaorong Gu, Ph.D.
Co-Investigator: Yogen Saunthararajah, M.D.
NPM1 is the most commonly mutated gene in de novo Acute Myeloid Leukemia (AML). Despite being
considered a more favorable risk in AML, only ~50% of patients exhibit long-term survival due to relapse
that is resistant to treatments. One reason is that current treatments intend cytotoxicity, via p53, the master
transcription factor (TF) of apoptosis. Unfortunately, p53-system is frequently attenuated by genetic alterations
in AML, subverts this common apoptotic intent, causing resistance in vitro and clinically. Meanwhile, normal
hematopoietic stem cells (HSC) with intact p53 are destroyed, causing substantial toxicities including death.
Therefore, new treatments that use pathways other than p53/apoptosis for cell cycle exits are needed.
Cell cycle exits by differentiation do not require p53. Myeloid differentiation is driven by only a few master
TFs, suggesting disruption of master TF function underlies differentiation-arrest. We discovered that NPM1 is
a co-factor for the master TF PU.1, and in mNPM1 AML, PU.1 and NPM1 dislocated from the nucleus into
the cytoplasm. Inhibition of nuclear-cytoplasmic exporting (KPT330, CRM1-inhibition) restored both mNPM1
and PU.1 into the nucleus, triggering terminal monocytic differentiation. We also discovered that mNPM1AML appears to respond to nanomolar concentrations of retinoic acid (ATRA) with terminal granulocytic
differentiation. Realistically, neither single agent CRM1-inhibition nor single agent ATRA will be curative. It
is possible, however, that resistance to one may increase susceptibility to the other. We will investigate the
molecular mechanisms underlying differentiation-arrest and its pharmacological reversal, in order to develop
rational p53-independent, non-cytotoxic, and combination differentiation treatments to salvage chemorefractory mNPM1-AML.
VELOSANO 2 | ANNUAL REPORT
Babal Kant Jha, Ph.D.
PILOT AWARD
Developing a Potent Pharmacologic Inhibitor of Sonic Hedgehog
Transcription Factor Glioma-Associated Protein (GLI) for the
Treatment of Drug Resistant Myeloid Leukemia
Principal Investigator: Babal Kant Jha, Ph.D.
Co-Investigator: James Phillips, Ph.D.
Proliferation of hematopoietic stem and progenitors cells are tightly regulated and are quiescent under
steady state condition however, they can be induced to proliferate by activation of various oncogenic signals.
Recent studies suggest that signaling pathways involved in embryonic development including Hedgehog (Hh)
signaling are aberrantly activated in leukemia. GLI genes, commonly known as Gli code, encode transcription
factors that regulate pro-survival genes at the distal end of the canonical Hh pathway. For the last several
years the focus has been on targeting the Hh-GLI axis using inhibitors of SMO, an upstream modulator
of Hh-GLI signaling axis, which has met with limited success. This is because oncogene-driven signaling
pathways, in particular RAS/RAF/AKT, circumvent the Hh-GLI axis to converge on and drive GLI to a higher
activating state. Thus, GLI serves as a node for the convergence of various oncogenic signals. Inhibition of
GLI-dependent transcription affords a unique mechanism of action. Using structure guided drug designing
approach we are developing a highly specific inhibitor of GLI that will terminate GLI induced transcription
detrimental for cancer cell survival. GLI proteins are constitutively activated in many types of human cancers
that include myeloid leukemia, epithelial cancers of the GI tract, brain tumors, melanoma, pediatric solid
tumors, liver, lung, breast, pancreatic and prostate cancers. KRAS is mutated in 30% of all human cancers,
and in ~40% of myeloid leukemia. Our current study directed towards the development of a new class of GLI
inhibitors may have important impact for the treatment of various cancers.
15
Jaroslaw Maciejewski,
M.D., Ph.D.
PILOT AWARD
VELOSANO 2
VIRTUAL RIDER
Use of Metformin to Prevent and Treat Aging-Related Myeloid Neoplasia
Principal Investigator: Jaroslaw Maciejewski, M.D., Ph.D.
Co-Investigators: Daniel Lindner, M.D., Ph.D. and Tomas Radivoyevitch, Ph.D.
Mutations are discrete defects in genes which if acquired in specific tissues can result in cancer. Many
different mutations have been recently discovered which can either initiate or lead to progression of leukemia.
Myelodysplastic syndrome is an example of a slowly progressing leukemia affecting increasing numbers of
patients in the US. In MDS and many other leukemia’s one the most commonly altered (mutated genes) is
called TET2. Mutations affecting the function of this gene promote leukemia and thus the defect in the gene
may constitute a relevant target for specific drug development. To date, no targeted, selective drugs effective
in TET2 mutations have been developed. Our hypothesis, supported by preliminary results, suggest that one
could generate drugs that would increase the remaining activity of the partially damaged TET2 and therefore
restore the appropriate function of this gene in leukemic cells. Our data also suggests that one of the already
existing agents used in other disease may be effective in increasing TET2 function and overcoming the effect
of mutations. If indeed mouse and other experiments to be performed in this project show that this is the
case, we could quickly use an old drug in a new targeted application. Consequently, our proposed study
has the potential to generate a new, effective and selective therapy for leukemia and MDS characterized by
defects in the TET2 gene.
VELOSANO 2 | ANNUAL REPORT
Edward V. Maytin, M.D., Ph.D.
PILOT AWARD
Minimally Toxic Approach for Breast Cancer Metastases:
Capecitabine-Enhanced Photodynamic Therapy
Principal Investigator: Edward V. Maytin, M.D., Ph.D.
Co-Investigator: Sanjay Anand, Ph.D.
Breast cancer (BrCA) that has metastasized to the skin of the chest wall is a particularly difficult problem
because these tumors are notoriously resistant to chemotherapy. Currently, the only effective option for
local control of BrCA skin metastases is ionizing radiation therapy (RT); this shrinks the tumors after
repeated treatments, but also causes severe side effects (blistering, chronic ulcers, and radiation dermatitis).
Photodynamic therapy (PDT) is a new form of cancer treatment that in contrast to RT, causes no scarring,
fibrosis, nor genetic mutations. PDT employs two components: (1) a drug, called a photosensitizer (PS),
which builds up specifically within tumor cells; (2) intense visible light, which activates the PS to kill the
cancer cells. PDT is currently used for treatment of superficial skin cancers such as basal cell carcinoma, and
should theoretically also work for cutaneous BrCA metastases. To increase the effectiveness of PDT for BrCA,
we propose to combine PDT with a chemotherapeutic agent (capecitabine; CBN) already used routinely
for breast cancer. Based upon our discovery that the active component of CBN has a remarkable ability to
increase PS accumulation within BrCA cells, we will ask whether giving CBN in combination with PS leads
to higher PS accumulation in tumors, as compared to the accumulation after giving PS alone. Experiments
will be performed in mice with cutaneous breast cancer. The results of this study, if positive, should allow us
to propose a clinical trial of combination CBN-plus-PDT as a non-scarring alternative to RT for patients with
cutaneous BrCA.
17
Alberto Montero, M.D.
PILOT AWARD
VELOSANO 2
VIRTUAL RIDER
Targeting the Achilles’ Shield of Triple-Negative Breast Cancer
by Androgen Blockade
Principal Investigator: Alberto Montero, M.D.
Co-Investigators: Jame Abraham, M.D. and Mohamed Abazeed, M.D., Ph.D.
Breast cancer can be divided into four major subtypes: luminal A, luminal B, HER2 type, and triple negative
breast cancers (TNBC). TNBC is the only breast cancer subtype that cannot be targeted with hormone
therapy and/or trastuzumab (Herceptin). In part, this is why TNBC are more aggressive and have a poorer
prognosis. Our research is focused on studying how specific gene changes in TNBC may be useful in
developing new therapies. Namely, we have identified the receptor for the male hormone, androgen, as a key
molecule for making some TNBC resistant to traditional chemo- and radio-therapy. Although several studies
have shown that some women that contain the androgen receptor in their tumor may respond to drugs that
block androgen signaling, our work suggests that a majority of women with TNBC that express androgen
receptor can benefit from androgen blockade when combined with DNA damaging drugs or X-rays. Our
proposal seeks to translate these findings to inform early phase clinical studies that will implement this new
treatment paradigm in breast cancer.
VELOSANO 2 | ANNUAL REPORT
Kwok Peng Ng, Ph.D.
PILOT AWARD
Non-Cytotoxic Probes to Renew AML Differentiation
and Spare Normal Stem Cells
Principal Investigator: Kwok Peng Ng, Ph.D.
Co-Investigators: Yogen Saunthararajah, M.D. and Drew Adams, Ph.D.
The human body is made up of specialized cells, e.g. liver cells, heart cells, etc. During gestation, these
cells develop from a single fertilized egg cell to the billions of cells that form the complex multicellular body
through a process known as cellular differentiation. Cellular differentiation persist in adulthood when adult
stem cells produce daughter cells (progenitors) that rapidly divide and mature to the myriad of specialized
cells required for tissue maintenance and repair. During each division, progenitors progressively specialize
until they reach their terminal differentiated state where they stop dividing, e.g. becoming a heart cell or
nerve cell. Cancer is a disease of unregulated progenitor growth emerging from gene mutations that blocks
terminal differentiation. Conventional chemotherapy kills dividing cells indiscriminately by causing stress that
activates a cell suicide program. Unfortunately, suicide program genes are the most commonly mutated genes
in cancer cells, which in essence, removes the suicide program from these cells. Consequently, conventional
treatments do not eradicate the cancer, but instead destroy normal dividing cells that have an intact suicide
program, leading to the severe side-effects typical of chemotherapy. Our research will develop drugs for a
new and distinctive approach to treating cancer that is based on restoring cancer cell differentiation rather
than activating the cell suicide program. We have very promising molecules that we have identified through
a search for compounds that renews cancer cell differentiation. We will improve these compounds with the
goal of one day testing this non-toxic, non-suicide-based approach to treatment in the clinic.
19
Craig Peacock, Ph.D.
PILOT AWARD
Mechanisms of Acquired Chemoresistence in Small Cell Lung Cancer
Principal Investigator: Craig Peacock, Ph.D.
Co-Investigator: Mohamed Abazeed, M.D., Ph.D.
With a world-wide, estimated 1.6 million new cases a year, cancer of the lung has easily been the most
lethal over the past several decades. While only 10-15% of these cases are diagnosed as small cell lung
cancer (SCLC), it is nonetheless a major contributor to cancer deaths in its own right, due to the outsized
lethality of this disease. At first, most SCLC patients have disease that is very sensitive to chemotherapy, but
the almost inevitable emergence of a drug-resistant form of the cancer within 12 months of diagnosis, results
in less than 5% of these surviving for five years. This dismal statistic has not changed for over thirty years.
To deliver desperately needed, lasting treatment responses to these patients, we must find new approaches
that can be used to either prevent or delay the development of relapsed disease, or improve its clinical
management. By establishing cutting-edge, laboratory models, we have both addressed the shortage of fresh
tissue that has hampered earlier progress in SCLC research, and enabled us to administer successive rounds
of chemotherapy to tumors that are initially sensitive. We can then follow development of resistance in these
tumors, in real-time. This includes analysis of the genetic changes that accompany this process, with the
expectation of identifying a vulnerability via which we can significantly improve outcomes for these patients.
VELOSANO 2
VIRTUAL RIDER
VELOSANO 2 | ANNUAL REPORT
Jianfei Qian, Ph.D.
PILOT AWARD
Developing a DKK1-DC Vaccine for Immunotherapy of Multiple Myeloma
Principal Investigator: Jianfei Qian, Ph.D.
Multiple myeloma (MM) is a plasma cell cancer characterized by tumor cell accumulation in the bone
marrow; it remains incurable in most patients. Vaccination may help the immune system control disease
early and prevent MM progression. An effecive vaccine must include protein fragments that can recognize
MM cells and kill them. Currently we lack such a vaccine for MM because no one has found suitable
MM-associated protein fragments. Our previous results show that a protein, Dickkopf-1 (DKK1), is highly
expressed by MM cells from all patients studied and is absent in normal tissues except placenta and prostate.
We also found certain immune cells called dendritic cells specifically recognized DKK1 and effectively
killed MM cells in test tube experiments and mouse models of MM. We hypothesize that DDK1’s broad
expression in myeloma cells but highly restricted expression in normal tissues, together with its ability to
inihbit the activity of bone-forming cells, make DKK1 an ideal and universal target for MM immunotherapy.
To develop DKK1-dendritic cell vaccines for all MM patients, we identified a long DKK1 protein fragment
that can potentially bind with immune system molecules crucial for immune recognition and killing of foreign
molecules and abnormal cells. In this project we will complete preclinical studies necessary for a first-inhuman pilot study that we have designed. Completing this project will enable us to optimally translate
our well-established myeloma vaccination concept into the clinic through collaboration between experts in
vaccines, MM immunology, and clinical care that is unique to our comprehensive cancer center.
23
Violette Recinos, M.D.
PILOT AWARD
Inhibition of Histone Methyltransferase with Novel Epipolythiodioxopiperazines
(ETP) Alkaloids in Pediatric High Grade Glioma
Principal Investigator: Violette Recinos, M.D.
Pediatric high grade glioma (HGG), which ranks among the most deadly childhood cancers has recently
been shown to be linked to certain genetic mutations. Two of these mutations within the histone H3.3 gene
H3F3A (K27M and G34R/V) have been shown to be influenced by epigenetic factors whereby the cell’s
environment can cause changes to the DNA and result in altered function.
Our goal is to show that specific mechanisms related to these genes may be involved in tumor growth and
contribute to therapeutic resistance and tumor recurrence. Targeting these pathways may provide a new
therapeutic approach. We will expand preliminary results from our lab showing Chaetocin, a histone lysine
methyltransferase (HMT) inhibitor, effectively killed 5 of 7 pediatric HGG including two with H3 K27M
mutation to include four newly synthesized epipolythiodioxopiperazine (ETP) alkaloid derivatives. These ETP
agents are structurally and functionally distinct and have been shown to be effective for cervical, lung, renal
and breast cancer at low concentrations. We will evaluate ETP effectiveness on tumor growth and survival
through in vitro and in vivo studies using tumor cells as well as non-tumor control cells.
Results from this investigation will (1) advance our understanding of epigenetic regulation in solid brain
tumors, (2) possibly show that epigenetic targeting may be more beneficial than or synergize with current
therapies, (3) specifically identify agnets that may target the H3 K27M tumor subtypes and ultimately
improve survival in pediatric brain tumor patients as well as other pediatric and adult cancers.
VELOSANO 2 | ANNUAL REPORT
Brian Rini, M.D.
PILOT AWARD
Exploration of CD8+ T Cell Infiltration and Other Immune Microenvironment
Parameters in Primary Renal Cell Carcinoma Tumors as Biomarkers of Response
to Checkpoint Inhibitor Therapy
Principal Investigator: Brian Rini, M.D.
Co-Investigators: James Finke, Ph.D. and Christopher Przybycin, M.D.
Harnessing the immune system to treat cancer has been a long sought-after goal in cancer medicine.
Recently, a class of agents known as checkpoint inhibitors has been tested in patients with advanced cancers
and has demonstrated anti-tumor effects. These agents effectively remove the brakes of a person’s immune
system, allowing a patient’s natural anti-tumor immunity to kill cancer cells. We are now testing the safety
and effectiveness of these agents in patients with a type of kidney tumor called renal cell carcinoma. Patients
will be given one or two doses of either a single drug or a combination of drugs prior to surgical removal
of the kidney tumor. The safety of this approach will be tested, along with whether or not these medicines
cause the tumor to shrink. Importantly, many studies on the tumor tissue and blood will be done to look at
specific immune cell populations to see if they can predict which patients might benefit the most from this
approach. The hope is that this clinical trial will lend insight to allow for the rationale further development of
these agents in kidney cancer patients.
VELOSANO 2 RIDER
25
Steven Rosenfeld,
M.D., Ph.D.
PILOT AWARD
Enhancing the Efficacy of Kif11 Inhibitors for the Treatment of Glioblastoma
Principal Investigator: Steven Rosenfeld, M.D., Ph.D.
Glioblastoma (GBM) is the most common and malignant of primary brain tumors. In spite of well over
half a century of dedicated clinical research, the outcome for patients afflicted with GBM still remains grim.
Three features particularly contribute to the highly malignant nature of this disease. First, GBMs, like many
cancers, proliferate uncontrollably. Second, while these tumors rarely metastasize outside of the brain, they
invade diffusely through the brain, producing a profound degree of neurological disability. Finally, GBMs,
like several other cancers, contain within them a small population of cells—referred to as “tumor initiating
cells” (TICs)—that are highly resistant to conventional treatment and which cause the inevitable recurrence
of tumor after radiation and chemotherapy. What is desperately needed is a “target” that is required for
both GBM proliferation and invasion, and for survival of both TICs and nonTICs alike. The underlying
theme of this proposal is that the mitotic kinesin Kif11 is an ideal target for GBM. We have recently shown
that clinically available Kif11 inhibitors kill both TICs and nonTICs and also block GBM invasion. However,
translating these encouraging laboratory results into a treatment that benefits patients in the clinic will
require that we address two questions: 1) how can we prevent the development of resistance to Kif11
inhibitors and 2) how can we optimize the delivery of these inhibitors to brain tumors. Our central hypothesis
is that targeting resistance to Kif11 inhibitors and enhancing their delivery/retention in the CNS can make
them very effective GBM therapeutics with minimal local toxicity and reduced systemic toxicity.
VELOSANO 2 | ANNUAL REPORT
George Stark, Ph.D.
PILOT AWARD
New Strategies for the Preferential Killing of Cancer Stem Cells
Principal Investigator: George Stark, Ph.D.
Co-Investigator: Sarmishtha De
Most tumors consist of two types of cells. The major type is sensitive to many drugs, and the killing of these
cells is responsible for the initial favorable responses that are often observed. Unfortunately, tumors also
contain a minor type, called cancer stem cells, and the regrowth of an initially sensitive tumor is likely to be
due to the ability of these stem cells to resist most therapies. We are seeking novel points of vulnerability
of cancer stem cells, so that therapies can kill both tumor cell types initially, thus avoiding recurrence. We
have found that a new drug, CBL137, kills both stem and non-stem cancer cells, but remarkably kills the
stem cells preferentially. The drug works by preventing the expression of proteins that are essential for cancer
stem cell survival. Current Phase I clinical trials show that CBL137 has minimal toxicity at effective doses.
In initial experiments with a mouse model of glioblastoma, we show that administration of CBL137 in the
drinking water provides a substantial improvement in survival from human tumors that have been implanted
into the brains of the mice. We are also working with a second class of drugs, called STAT3 inhibitors,
which are also reported to kill cancers stem cells preferentially. We will now test the beneficial effects of
CBL137 and STAT3 inhibitors alone, in combination with each other, and in combination with standard-ofcare therapies, using stem cells from cancers of the breast, prostate, and lung. Positive results can quickly be
translated to clinical trials.
27
Angela Ting, Ph.D.
PILOT AWARD
Understanding the Full Spectrum of Epigenetic Vulnerability in Cancer Through
the Delineation of DNA Methylation Function in Gene 3’ End
Principal Investigator: Angela Ting, Ph.D.
Abnormal DNA methylation (an epigenetic mark) is a hallmark of human cancers, and drugs that target the
DNA methylation machineries are used for treating certain cancers. However, effective targeting of DNA
methylation changes as a cancer therapy demands a full understanding of the biological impact of these
cancer-associated defects so that we can exploit all aspects of epigenetic vulnerability in cancer as well as
anticipate unintended side effects of any epigenetic therapy. DNA methylation in the beginnings of genes
(promoters) can shut off gene expression without affecting the DNA sequence, much like a light switch
turning off a lamp without cutting the wires. Through whole genome mapping efforts, we now appreciate
that cancer-associated DNA methylation frequently occur in the ends of genes (3’ ends). In colon cancer, we
discovered a novel association between DNA methylation at gene 3’ ends and RNA processing, which can
result in the production of different amounts of the protein or altered proteins with unique functions. Our
observation raises the exciting possibility that DNA methylation can affect gene expression not only as an on/
off switch in gene promoters but also analogously to a dimmer switch modulating light levels when it occurs
in gene 3’ ends. We aim to delineate how gene 3’ DNA methylation regulate RNA processing and anticipate
such knowledge to broadly and significantly aid in understanding of how cancer behaviors are shaped by
non-promoter DNA methylation. Ultimately, these insights will accelerate our ability to develop therapies
targeting epigenetic changes in cancer.
VELOSANO 2 | ANNUAL REPORT
Bin Zhang, Ph.D.
PILOT AWARD
Novel Roles of LMAN1 Mutations in Colorectal Cancer Development
Principal Investigator: Bin Zhang, Ph.D.
Every year over 50,000 people die of colorectal cancer, making it the third most common cause of cancer
death in the United States. Genomic studies have shown that colorectal cancer is a highly heterogeneous
disorder. Subgroups of cancer, defined by different combinations of gene mutations, may not respond well
to the standard course of treatment and require more personalized therapies. Finding and understanding
new pathways associated with oncogenes and tumor suppressor genes are critical for developing the most
effective personalized treatment approaches. We have shown that a gene (LMAN1) previously not known
to be associated with cancer is frequently mutated in colorectal cancer. Patients lacking LMAN1 expression
had significantly worse prognosis than those with normal LMAN1 expression. LMAN1 is involved in
controlling protein secretion. Our in vivo and in vitro studies support a hypothesis that LMAN1 functions as
a novel tumor suppressor by regulating the secretion of interferon beta. This proposal is aimed at identifying
molecular mechanisms for the loss of LMAN1 expression in colorectal cancer and understanding how LMAN1
mutation promotes formation and development of colorectal cancer. Although interferon is effective against
certain types of leukemia and melanoma, it has not been indicated for colorectal cancer treatment. Our
results suggest that a subgroup of patients with LMAN1-deficient cancer can also benefit from an adjuvant
interferon beta therapy.
29
Case Comprehensive Cancer
Center Pilot Awards
Cleveland Clinic is part of the Case
Comprehensive Cancer Center (CCC), which
is designed to promote research collaboration
across the three member institutions:
Cleveland Clinic, Case Western Reserve
University, and University Hospitals. Team
science is increasingly important for successful
cancer research, and the Case CCC is an
excellent example of such teamwork, working
across these three organizations.
Case CCC had numerous teams participate in
VeloSano 2, and as part of our collaboration
they received $250,000 of the VeloSano 2
total raised. They used these funds to grant
five Case CCC VeloSano Pilot Awards that are
detailed on the following two pages.
VELOSANO 2 | ANNUAL REPORT
PILOT AWARD
Targeting the cAMP-CREB1 Axis to Treat Platinum
Resistant High-Grad Serous Ovarian Cancers
Principal Investigator: Analisa DiFeo, Ph.D.
Co-Investigator: Vinay Varadan
This project is a collaboration between PI Analisa DiFeo, a basic/translational
cancer researcher focusing on ovarian cancer, and Co-PI Vinay Varadan, a
computational cancer genomics researcher. They aim to identify novel pathways
for the targeted treatment of chemo-resistant ovarian cancer. The proposal
involved the application of a computational method, termed InFlo, to identify
dysregulated groups of genes from mRNA expression data. They present solid
preliminary data showing that cAMP activity mediates platinum resistance in
ovarian cancer, and they propose that a specific CREB1 inhibitor H-89 can be
used in combination with platinum treatment to overcome resistance to the
latter. Two aims are proposed: Aim 1: Assess efficacy of H-89 on overcoming
platinum resistance in vivo. Aim 2: Identify pharmacodynamics and therapeutic
susceptibility biomarkers of H-89 and platinum therapy in PDX models.
PILOT AWARD
Development of Intravenously Injectable ß-Glucan
Treatment for Regulating Granulocytic Myeloid-Derived
Suppressive Cells
Principal Investigator: Julian Kim, M.D.
Co-Investigator: Mei Zhang
The proposal is based on preliminary data developed by Dr. Zhang demonstrating
that ß-glucan structures (particularly BG34) can alter the suppressive immunity
function of granulocytic MDSC (Gr-DMSC) towards and inflammatory (M1)
phenotype, and the observation made by Drs. Kim and Zhang in their ongoing
polyclonal T-cell immunotherapy trial in melanoma of the emergence of an
increase MDSC population following adoptive T-cell transfer.
This is a proposal based upon exploring the impact of a soluble betaglucan, BG34, or Gr-MDSC’s that are through to be important in cancer. The
investigators believe that the administration of this agent has potential as an
immunomodulatory strategy for cancer therapy. The proposal seeks to study the
effects of BG34 on GR-MDSC’s in vitro using mouse and human cells and using
a mouse melanoma model system.
31
PILOT AWARD
Identification of Surface Proteins Required
for Internalization of Therapeutic Exosomes
Principal Investigator: Huiping Liu, M.D., Ph.D.
Co-Investigators: Cliff Harding, Jan Olof LÖtvall and Cheryl Thompson
This proposal looks to identify differences in exosome surface proteins and interrogate how this
impacts the dynamics of cellular uptake. As multiple cell types generate exosomes, generating this
information is critical for future mechanistic studies and therapeutic development.
PILOT AWARD
Development of New Type of Therapeutics Selectively Targeting Bax or Bak
Principal Investigator: Shigemi Matsuyama, DVM, Ph.D.
Co-Investigator: Drew Adams
This is a proposal based upon identifying novel small molecules that regulate BAX/BAK-mediated
cell killing. The investigators have developed a cell based tet-inducible model system that has been
validated and tested using some compound libraries. This work has led to the identification of several
hits that will be explored further along with new hits from their proposed screening.
PILOT AWARD
Develop HTS Assay for Screening GPT2 Inhibitors
to Target P13KCA-Mutated Colorectal Cancers
Principal Investigator: Zhenghe (John) Wang, Ph.D.
Co-Investigator: Drew Adams
The preliminary evidence underlying this proposal is strong, suggesting that GPT2-specific inhibitors
will be more potent and less toxic than Aminooxyacetate (AOA), an inhibitor of GPT2 which is nonspecific as it inhibits and transaminases, and thus would have a more favorable therapeutic index
than AOA. PIK3CA, which encodes the p110a catalytic subunit of P13K, is the most frequently
mutated oncogene in human cancer.
VELOSANO 2 | ANNUAL REPORT
1
IMPACT AWARD
Precision Targeting of Therapeutic Resistance in Cancer
Principal Investigators: Mohamed Abazeed, M.D. (1), Ph.D. and Shlomo A. Koyfman, M.D. (2)
Abazeed VELOSANO 2 RIDER | Koyfman VELOSANO 2 VIRTUAL RIDER
2
Patients that do not respond to traditional cancer therapies have the poorest clinical outcomes and suffer
due to resistance of their tumor to palliation. Our research program focuses on identifying the genetic
changes that give rise to resistance in cancer and to use this information to develop personalized treatment
strategies. We have generated a large body of data describing the genetic landscape of resistance in cancer
and we are focused on targeting specific genetic changes with greater precision. To advance the translation
of these findings, we have coupled the Cleveland Clinic’s robust clinical infrastructure with state-of-the-art
methodology developed in our laboratory to develop primary xenografts from several cancer lineages. These
avatars of human cancers are ideal platforms for enhancing the genetic understanding of cancer because they
recapitulate the genetic complexity of human tumors. Our team is poised to lead the incorporation of these
models into clinical practice.
IMPACT AWARD
Preserving the Fertility of Women with Cancer: Ovarian Tissue Freezing
Principal Investigators: Tommaso Falcone, M.D. (3), Rebecca Flyckt, M.D. (4)
As treatments for cancer become increasingly effective, more women are surviving their cancers and
focusing on childbearing. Unfortunately, the treatments involved in effective cancer care can also be severely
damaging to the ovaries. Many women suffer menstrual dysfunction, infertility, or premature menopause after
their cancer treatments.
3
Until recently, women undergoing chemotherapy had limited options for fertility preservation. The gold
standards, egg and embryo freezing, cannot be used for girls who have not undergone puberty, and they are
also not options for adult women who must pursue immediate treatment of their cancers.
In the past several decades, ovarian tissue freezing has emerged as a promising new approach to fertility
preservation in adult women and girls. Instead of a handful of eggs or embryos, frozen ovarian tissue may
contain thousands of viable oocytes. To date, at least 60 live births have been recorded worldwide using
this technique, and the numbers are increasing every year. The American Society of Reproductive Medicine
still considers ovarian tissue cryopreservation to be experimental in humans and this procedure can only
be performed under an IRB approved protocol with detailed informed consent. Cleveland Clinic now offers
ovarian tissue freezing for both pediatric and adult populations under such a protocol. The protocol involves
a brief minimally invasive surgical procedure to harvest the tissue and then the tissue can frozen and
reimplanted years later once treatments are complete and fertility is desired.
Ovarian tissue freezing provides an opportunity for fertility preservation to patients who might not otherwise
have any options. We are excited to be offering this innovative treatment at Cleveland Clinic for those who
need it.
4
33
IMPACT AWARD
Colon Cancer Metastasis
Principal Investigators: Emina Huang, M.D. (1) and Xiaoxia Li, Ph.D. (2)
The purpose is to define the underlying clinical and molecular behavior of this most lethal presentation of colon cancer,
to identify new strategies to prevent progression from localized disease to metastatic disease, and to save lives from
this disease.
Increasingly, patients present with metastatic colon cancer that require combined management by surgeons and
medical oncologists, both of whom are advised by pathologists. This project brings together insights from these three
disciplines as well as the molecular expertise from the Lerner Research Institute to tackle both the understanding
and treatment of metastatic colon cancer. Survival is dismal. Even in best case scenarios more than 50% of patients
with metastatic disease die from cancer. A better understanding of this disease leading to novel treatment approaches
is clearly needed. First, we will examine the microenvironment of both primary and metastatic cancer lesions with
examination of stromal elements including lymphocytes and fibroblasts. Another element of this microenvironment,
required for all tumors to grow and to metastasize, is the vascular supply. Secondly, we will examine these lesions
with regard to epigenetic regulation, well known to exert regulation in both primary and metastatic lesions.
IMPACT AWARD
1
2
Cancer Thrombosis
Principal Investigators: Alok Khorana, M.D. (3) and Keith McCrae, M.D. (4)
Khorana & McCrae VELOSANO 2 RIDERS
This project will consist of new clinical research programs that explore novel approaches to the management and
prevention of cancer-associated thrombosis. These programs focus on clinical trials that employ agents such as
statins, anti-platelet agents and direct oral anticoagulants. These trials, as well as a newly-opened cancer thrombosis
clinic (CAT) are a rich source of clinical samples for analyses that will be performed. New biorepositories containing
samples from patients with glioblastoma, pancreatic cancer and leukemia have been developed over the last year, and
a forth biorepository focusing on patients presenting to the CAT clinic for evaluation of venous or arterial thrombosis
will be initiated. The goals of our studies will be to (1) better define basic mechanisms that underlie the development
of venous and arterial thrombi in patients with cancer, in particular those receiving chemotherapy, (2) test the efficacy
of novel anticoagulants and anti-platelet agents in cancer by developing quantifiable measures of platelet, hemostatic
and vascular activation in patients that will be assessed before and during therapeutic interventions, (3) develop
animal models of cancer-associated thrombosis to allow development of mechanism-based interventions, and (4)
create and expand biorepositories of fractionated plasma, leukocytes, platelets and microvesicles that will be an
invaluable resource for future initiatives.
3
IMPACT AWARD
Chronic Myelomonocytic Leukemia (CMML)
Principal Investigator: Jaroslaw Maciejewski, M.D., Ph.D (5)
Maciejewski VELOSANO 2 VIRTUAL RIDER
Chronic Myelomonocytic Leukemia (CMML) is a protracted and progressive leukemia occurring mostly in the elderly.
With the increased life expectancy of the US population, the number of individuals affected by this condition is
expanding, lending increasing urgency to the proposed investigations. CMML represents a continuum of clinical stages,
including low-risk disease, advanced CMML and CMML-derived secondary acute leukemias (sAML). In addition, many
early, indolent cases remain unrecognized, labeled as reactive monocytosis of unclear significance. Our investigators
will also involve these entities.
The overarching aim of our proposal is the creation of a center for treatment of CMML, that, due to clinical and
research excellence, will achieve national and international recognition. The short-term goals of the center will include
improved management of CMML. Long-term goals will include development and application of curative therapies for
CMML. The scientific focus is on the introduction of effective targeted therapies to be developed through a team effort
of laboratory scientists, medicinal chemists and clinicians. Members of our team have already established a track
record of scientific productivity and fruitful collaborations that have contributed to progress in CMML.
4
5
VELOSANO 2 | ANNUAL REPORT
Partners Make VeloSano Possible
F O U N D IN G
The financial and/or in-kind support of our partners allows
VeloSano to successfully and safely operate the event, as
well as allocate every dollar raised by participants directly
to cancer research at Cleveland Clinic. Thank you to each
and every one of our amazing partners – we couldn’t do this
without you!
S UPP ORT I NG
CO N TR IB U TIN G
S POK E
P E DA L
A XL E
MEDIA
S P E CIA L TH A N K S
B IK E S H O P
star
HARLEY-DAVIDSON
TM
35
Big Wheelers presented by KeyBank
Our Big Wheelers are Riders who at least double their minimum fundraising
commitment, thereby accelerating the pace at which we can impact advances
in cancer research. There were 228 Big Wheelers in VeloSano 2, and each one
earned a cozy VeloSano Big Wheeler fleece to wear proudly around town. Help us
send a Big Thank You to our Big Wheelers – they’re a big deal!
Pete Accorti
Ross Agnor
Vlad Agranovich
Benito Alvarez
Michelle Amato
John Anderson
Keith Arian
Sandra Avis
Greg Avis
Kathy Bass
Mike Bauer
Coleen
Becker-Dowdall
Craig Belec
Laurie Benic
Mike Bosner
Nancy Bradshaw
Mark Brandt
Ali Brawner
Sarah
Brawner-Dyke
Steve Briggs
Chad Broski
Marc Byrnes
Julie Callsen
Denise Carkhuff
Jeff Carpenter
Hetty Carraway
Bob Case
AJ Chardiet
Armando Chardiet
Victoria Chardiet
Thomas Chung
Tom Cicarella
Andy Clarke
Michael Coburn
Joanne Cohen
Terence Connor
Chandler Converse
Paul Cusato
Curtis Danburg
Tyler Danburg
Jonathan Dandes
Jerry Davidson
Jillian Davis
Lynn Dieter
Paul Dolan
Kevin Dooley
Dave Doren
John Dougherty
Don Dreier
Alan Duffy
Stephanie Duffy
Jack Efta
Courtney Eiler
Bassam Estfan
Doug Fanta
David Faturos
Tim Fenner
Judy Ann Forbes
Amanda Fox
Hiroyuki Fujita
John Fung
Beth Fung
Monica
Gali-Chardiet
Fred Geis
Fran George
Stan Gerson
Samir Ghousheh
Dave Grinnell
Ira Grossman
Beth Grubb
Lindsay Guzowski
John Haas
Darin Haines
Steve Hallam
Cassi Handler
Lauren Hanna
Marc Harrison
Kathy Hart
Larry Hatch
Dan Haynes
Graham Hearns
Matt Hein
Brian Held
Mike Hermsen
Angela Higham
Larry Hirsh
Richard Hollington
Michael Jacobs
Vickie Johnson
Steve Jones
Andy Jones
Deborah Junior
Steve Karklin
Matt Keppler
Jeff King
Larry Klein
Stewart Kohl
Donna Kohl
Zach Komorski
Cindy Koury
George Kreiner
Lisa Krejci
Amy Kubacki
Jeff Kula
Anthony LaPlaca
Margaret LaPlaca
Samantha LaPlaca
Justin Lathia
Amanda Lathia
Eric Laurence
Dennis Lehman
Alicia Lenhart
Brinton Lincoln
Matt Litzler
Anna Lowenstein
Christine Lynch
Kevin Lynn
Nancy Lyon-Stadler
Paul Madonia
Alane Malerick
Kate Malone
Craig Manchen
Lisa Manning
Matt Manosky
Scott Marlow
Deborah Marotta
Robert May
Keith McCrae
Robert Mccreary
Linda McHugh
Jamie McKeon
Daniel McNeil
Tom Milewski
Laura Mimura
Robbie Mocilnikar
Jessica Mocilnikar
Greg Montagano
Dan Moore
Edward Moore
Jeff Moore
Mike Mullen
Bill Mulligan
Latham Murfey
Brad Nagle
Jen Neundorfer
Michael Ohm
Dario Ortiz
Len Pagon
Alan Papa
Armida Parala
John Patrick
Rob Pawlak
Brad Peck
Steve Penton
Tracy Pesho
Matt Peters
Nicole Peters
Michael Petras
Michael A. Petras
Katherine Petrey
Brad Pohlman
Julia Pollock
Larry Pollock
Jason Radel
Sunay Rastogi
Craig Reagor
Sharon Reichart
Feza Remzi
Bob Rich
Paul Rich
Brian Rini
Bill Riter
Tom Roe
Mark Rood
Mark Ross
Tom Roulston
John Saada
Cindy Sackett
Jessica Sacks
Joe Santoli
Joe Scaminace
Bill Schiemann
William Schiemann
Ryan Schreiber
Morgan Schreiber
Brittany Schreiber
Matt Segal
David Seiger
Renee Singley
John Sinnenberg
James Soukup
Tim Spiro
Nick Stambula
Randall Starling
Andy Stephenson
Tim Stover
Rich Stovsky
John Suh
Bart Swain
Sheila
Swartzlander
Jeff Syslo
Ilaria Tamagno
Kelly Tompkins
Mike Toth
Mary Toth
Colleen Tredway
Shane Turner
Robbie Twells
Rodney Twells
Barry Underwood
Jason Valent
Jack Varney
Rose Viny
Dominic Visconsi
Bob Waitkus
Sally Wajahn
Rob Watson
Robin Weaver
Ron Weinberg
Terri Weinberg
Morris Wheeler
Shirley White
Jeff Wilson
Kelly Wolff
Blair Wood
Donald Wroble
Kirk Zehnder
VELOSANO 2 | ANNUAL REPORT
VeloSano 2 Steering Committee
CO - CHAIRS (Below, L-R)
Stewart A. Kohl
Paul J. Dolan
The Riverside Company
Cleveland Indians
MEDICAL CHAIR
Brian J. Bolwell, M.D.
HONORARY CO - CHAIRS
John Anderson
Norma Lerner
WKYC Channel 3
The Lerner Foundation
TEAM VELOSANO (Below, L-R)
Mohammed Farunia, Associate
Kandis Schreiber, Director
Nicole Peters, Senior Director
Beth Brand, Assistant Director
Pete Accorti
Talan Products
Phil Alexander Brandmuscle
Mike Bauer Master Lock Company LLC
Mark Brandt
McGladrey
Bill Braun
Eaton
Marc Byrnes
Oswald Companies
Kara Carter
Orion Advisory, LLC
Armando Chardiet Cleveland Clinic
Loren Chylla
The Adcom Group, Inc.
Andy Clarke
Blount International
Joanne Cohen
Cleveland Clinic
Chandler Converse
CBRE | Brokerage Services
Delos Cosgrove, M.D.
Cleveland Clinic
Sam Covelli
Covelli Enterprises
Caroline El Sanadi
Case Western Reserve Univ.
Trina Evans KeyBank / KeyCorp
Samir Ghousheh Cardinal Health
David Gilbert
Greater Cleveland Sports Commission
Marcus Glover
Horseshoe Casino Cleveland
David Goodman
Squire Patton Boggs
Jerry Grisko
CBIZ, Inc.
Jack Haas
Sensical Companies / UN1TUS
Brian Hall
Innogistics LLC
Marc Harrison, M.D.
Cleveland Clinic
Jody Herzog Fleet Feet Sports
Tom Hileman Hileman Group
Andy Jones MCPc
Steve Jones, M.D.
Cleveland Clinic
Craig Manchen Retired Former Owner
(Highland Group Industries)
Paul Matsen Cleveland Clinic
Linda McHugh Cleveland Clinic
Heather Moore Heather Moore Jewelry
Bill Mulligan Primus Capital
Jennifer Neundorfer flashstarts
Len Pagon Next Sparc, LLC
Mike Petras Cardinal at Home / Cardinal Canada
Larry Pollock Lucky Stars Partners LLC
Lauren Rich Fine Howard & O’Brien Inc.
Tim Richards Cleveland New 102-FM
Joe Roman Greater Cleveland Partnership
John Saada Jones Day
Mark Siegel Forest City Enterprises
Renee L. Singley The Lerner Foundation
John Sinnenberg Cyprium Capital
LT Slater Takoda Group LLC
Jacob VanSickle
Bike Cleveland
Morris Wheeler Drummond Road Capital Inc.
37
The Future of Cancer
Care at Cleveland Clinic
Patient Support Is Paramount in New Cancer Facility
The psychological impact of a cancer diagnosis is profound. “When someone
hears that they have cancer, it is a life-changing two or three seconds,” says
Cleveland Clinic Taussig Cancer Institute Chairman Brian J. Bolwell, M.D., FACP.
“They are filled immediately with anxiety and fear. A cancer diagnosis may not
always be a medical emergency, but it is always a psychological emergency.”
Light and Space for Patients
The open-plan first level — suffused with natural
light from floor-to-ceiling windows — also will
contain an outpatient pharmacy; a retail store
stocked with items to meet cancer patients’ needs,
such as skin care lotion for dry hands; and a
cafeteria with food offerings to accommodate
special dietary needs and medical conditions.
Cleveland Clinic’s new cancer care building, opening in 2017, is designed
for easy access to the array of patient support services intended to reduce
cancer’s psychological stress. Those services will occupy most of the first floor
of the $276 million, 377,000-square-foot outpatient tower currently under
construction.
•
Conserving Resources, Aiding Well-Being
•
•
“We strongly believe in the benefits of such programs, which range from reiki to
relaxation therapy to mentoring,” Dr. Bolwell says. “They are not always easy to
quantify scientifically. But what we do know is that patients with cancer and a
psychiatric diagnosis consume six times more healthcare resources than those
without a psychiatric diagnosis. If you manage anxiety and other stress-related
issues, you can significantly reduce resource utilization. It is also the right thing
to do for the well-being of patients and their families.” Dr. Bolwell and other
Cleveland Clinic officials toured numerous cancer facilities around the country to
compile best-practice ideas for the new building’s design. Patient comfort and
convenience were paramount on their lists. “In almost every cancer facility, the
thing that I really did not like were the lines in which patients had to wait to get
their blood drawn,” Dr. Bolwell says. “A quote from a cancer patient that sticks
with me is, ‘If I have six months to live, waiting four hours to get chemotherapy
is a big deal to me.’ We have dedicated a lot of space in the new building to
try to make sure that does not happen.” That includes a sizable blood-testing
laboratory on the first floor.
The first floor will be home to:
•
•
•
•
A resource center where patients and families
can access printed and online cancer information.
Art and music therapy spaces.
A boutique where patients with chemotherapy
associated hair loss can receive free wigs, caps
and scarves.
A wellness center for reiki, reflexology, guided
imagery, facials and other aesthetic services.
A private prosthetics fitting area.
The 4th Angel Mentoring Program, an initiative
begun by figure skating champion and Cleveland
Clinic cancer patient Scott Hamilton to provide
patients with free, confidential, one-on-one
advice and support from a trained volunteer and
cancer survivor.
A spiritual area where patients and families can
go for prayer or meditation.
“There is a reason for having all these services on
the first floor of our new cancer center,” Dr. Bolwell
says. “We want to show patients as they first walk
in that this is a warm and inviting atmosphere, and
that we understand what they are going through.
We understand that they are scared, and we have a
lot of caregivers and programs right in front of them
to help.”
The Power of Every One Centennial Campaign
finished 2015 with $175.8 million in total
commitments for the year, bringing the overall
total to more than $860 million. Launched
in 2014, the historic $2 billion philanthropic
campaign will continue until Cleveland Clinic’s
100th anniversary in 2021. Every gift that
supports the campaign is helping to make the
highest-quality healthcare accessible to the
greatest number of people through projects
and programs that put patients first, including
the new Cleveland Clinic Cancer Center to
open in 2017.
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