Tomi Akinyemiju, PhD

Funded by the 2021 Victory Ride to Cure Cancer

Black patients are more likely to die from breast, prostate, lung, and colorectal cancers than White patients. There are many reasons for these differences, including barriers to accessing treatment. In recent years, scientists have created new and better treatments that match a cancer’s unique biology, changing the way that we treat the disease. The first step to getting these therapies is genomic testing, which looks closely at the cancer to understand what might be causing it. Black patients are less likely to get genomic testing and these new therapies than White patients. If we don’t improve access to genomic testing, Black patients will continue to experience barriers to life-saving treatments, causing even bigger differences in survival between Black and White patients. In this study, we will look at the factors that cause differences in genomic testing between Black and White patients. We will also interview Black patients and cancer doctors about their experiences and preferences related to genomic testing. We will use our results to create strategies to improve access to genomic testing for Black patients. In the future, we hope to use our strategies at Duke Cancer Institute and in community hospitals in the Duke Cancer Network to reach cancer patients who are mostly Black, rural, and low-income, a group with large barriers to genomic testing.

Sascha Tuchman, MD, MHS

Funded by the 2020 Victory Ride to Cure Cancer

African Americans develop a form of blood cancer called multiple myeloma more often than Caucasians. On average, African Americans live less long with it. That may be in part because African Americans take part in clinical trials less often. Clinical trials are studies designed to develop new treatment drugs. Those trials can sometimes help people to live longer with this illness. We are trying to improve how many take part in clinical trials at UNC. We are creating an easier, more comfortable doctors’ office to get care at and take part in trials at UNC. We are making it easier for African American researchers at UNC to work on this important issue. We will make a video that shows what clinical research is. It will show why it can be helpful to take part in research. The video will be shown to African Americans and other patients treated at UNC. The UNC team will compare how many African Americans join multiple myeloma trials before and during this grant. If more African Americans enroll in multiple myeloma trials after the grant begins, it would show that these efforts have helped solve this problem. That may help African Americans with multiple myeloma to live longer. IT will also help make important progress in this research.  

Linda Sutton, MD

Funded by the 2020 Victory Ride to Cure Cancer

Cancer is caused by changes that happen in the genes of cancer cells. Special tests can find genes that start or promote cancer growth. New drugs can target cancer causing genes and kill cancer cells. The Duke project team wants to increase awareness and use of both the special tests and the new drugs. The project will bring a group of experts together to talk about patient cases and help find the best medicine for patients. If medicines are not available, the project team can find clinical trial options for patients. The team will also provide training to doctors and nurses on new tests for cancer genes and medicines. We will create information to help patients learn about the special gene tests and how the results can help the doctors choose the right medicine to treat their cancer. When the project is finished, the team hopes to provide the information and tools created to other local doctor’s offices and patients.


Ronny Bell, PhD

Funded by the 2020 Victory Ride to Cure Cancer

African Americans have the highest percentage of new cancer cases in the United States and the worst outcomes. Other diverse populations have difficulty getting to a cancer treatment center or need help figuring out the system one they arrive. Some people die from cancers that can be prevented or treated, simply because they are not aware of all of the treatment options. Cancer care can be very difficult because many times a patient has more than one doctor who is part of their care team. This can be scary and may make some people choose not to get cancer treatment, even if they can be cured. WFBCCC wants to make sure that everyone has access to the best cancer care possible. This may include patients participating in research that may improve outcomes for them but also may help provide information that can help tailor treatments for the next generation of cancer patients. It is important to make sure all populations are represented in studies that look at new treatments or supports for cancer patients. To meet that goal, we created a population health navigator program- people who are from the community who can help people learn about cancer, how to prevent it, what screening is required and what treatments are available. If someone is diagnosed with cancer, the navigator will assist that person by helping to remove barriers to care and will talk with patients about clinical research as part of their care. 


Ian Davis, MD, PhD

Co-funded by the Dick Vitale Gala, and WWE in honor of Connor’s Cure

Years of cancer research have shown that combining therapies virtually always works better than when therapies are used alone. Recently, medications have been discovered that change the way genes are turned on and off. At the same time, treatments have been developed that use the body’s own cells to find and attack cancer cells. Each of these treatments have been shown to work alone on specific cancers. Each has known limits. However, the combination has not been studied. Our project explores whether combining these treatments will improve our treatments for childhood cancer. We are especially interested in if combining these therapies will increase the success of cellular therapies. Our proposal initially studies one specific medication that is already approved for use in children. We will also evaluate a large group of possible medications. We expect that our results will quickly result in a clinical trial for children. In addition, it may lead to a new treatment approaches for many cancers.

Adam Palmer, PhD

Funded by the Constellation Gold Network Distributors

Non-Hodgkin Lymphomas are common cancers which can be cured in some patients by combinations of multiple chemotherapy drugs. Currently, these treatments consist of giving many drugs at the same time, waiting some weeks to recover from side effects, and repeating the cycle several times. We have discovered that in the most common combination therapy for Non-Hodgkin Lymphomas, while the use of many chemotherapies kills more cancer cells, the drugs do not enhance one another’s activity. Instead, certain drug pairs interfere with one another’s effects. This suggests that treatment might be more effective at killing cancer cells, and cure more patients, if this interference were avoided. This could be accomplished by giving certain chemotherapies at different times from each other. We will study a few lymphomas and measure how chemotherapies interact to determine which should or should not be given at the same time. A computer model will simulate how tumors respond to combinations of drugs given at various times. This simulation will use measured drug interactions to predict which treatment designs will be most effective at killing cancer cells. We will test these treatments on human lymphoma cells, and compare them to the current ‘all-drugs-at-once’ strategy. If this research finds a more effective approach to treatment, it can next be tested in animals, and eventually in human clinical trials. Ultimately we hope to identify a simple change in the use of already approved medicines that has the potential to cure more cases of lymphoma. 

Marjory Charlot, M.D.

Funded by the Victory Ride to Cure Cancer

All cancer patients should have the opportunity to get very good care through research studies. Research studies are important to make cancer treatments and survival from cancer better but very few people of color are treated on cancer research studies called clinical trials. One way to solve this problem is to use specially trained staff to help cancer patients better understand clinical trials.  These staff are called patient navigators. In this project, we will use patient navigators to teach and support patients asked to be in a cancer research study.  These navigators will work as a team to make sure that all African Americans who receive care at the Cancer Center are considered for a clinical trial.  In order for the patient navigator to know which patients may be fit to participate in research, we will use information from the medical record to create a list of patients that could be asked about their interest to get treatment with a clinical trial. The patient navigator will use this list to contact patients and will teach patients about clinical trials and connect patients to finance counselors, social workers and other helpful community services as needed. To understand if the project is a success, we will compare the total number of patients, by race, treated on a cancer research study before and after the project.

David Soto-Pantoja, Ph.D.

Funded by the Stuart Scott Memorial Cancer Research Fund

Our immune system operates on a balance of cells that can destroy infected or cancerous tissue and cells that prevent attacking healthy tissue. This balance is affected during cancer where cells that attack the tumor become inactivated. This allows further growth, cancer spread (metastasis) and eventual death of the patient. To address this problem researchers have developed drugs known as immune checkpoint inhibitors. These drugs activate T cells, a type of immune cell, to attack the tumor. Cancer patients treated with these drugs have seen major increases in survival. However, due to these drugs tipping the balance to a more active immune system, it can cause harmful side effects. These side effects cause interruptions in treatment plans which can result in disease progression. Currently, we do not have tests in the clinic that are able to predict these side effects. Therefore, there is an urgent need to understand how these side effects develop. Cancer cells consume abnormal levels of nutrients and release factors that can be sensed by blood circulating cells. We believe that these changes can be sensed by mitochondria. The mitochondria are organelles in cells that regulates energy metabolism. With new technological advancements, we can measure how this organelle changes in function in patients’ blood cells. We propose to test how patient blood cells energy changes. We predict that patients that develop side effects will have a lower cellular energy levels. Our study will provide a marker to predict side effects before they develop. We will also study genes that regulate cell energy metabolism to identify drug targets aimed at reducing the onset of side effects. Therefore, our studies will provide a personalized approach to cancer treatment to improve outcomes while preserving their quality of life.

Hector Franco, Ph.D.

Funded by the Stuart Scott Memorial Cancer Research Fund

Ovarian cancer is one of the deadliest cancers among women worldwide. In 2019, nearly 22,240 new cases of ovarian cancer will be diagnosed in the US, and approximately 14,070 women will succumb to this disease. Most women respond well to the standard treatment, however, the majority of these patients (with estimates up to 75%) experience a recurrence of the disease due to acquired resistance of the tumor cells to chemotherapy.

This proposal is aimed at understanding what makes ovarian cancer cells resistant to therapy with the goal of discovering new avenues for therapeutic intervention. We will use state-of-the-art genome sequencing techniques to measure the changes that occur in primary ovarian tumor samples compared to recurrent tumor samples collected from the UNC Cancer Hospital. Our goal is to define how genes are being regulated in ovarian tumors in order to identify the molecular switches that are responsible for turning on genes that give rise to resistance. We hypothesize that these molecular switches (known as enhancers) are hijacked by the tumor cells for the activation of genes that give rise to resistance. We aim to identify their locations throughout the genome and determine which ones are responsible for drug resistance. Completion of this project will increase our knowledge about an understudied new facet of ovarian cancer, advance the way cancer research is conducted, provide a new set of biomarkers with diagnostic and prognostic potential, and highlight new targets for controlling cancer cell growth.

Yarui Diao, Ph.D.

Funded by the Dick Vitale Pediatric Cancer Research Fund

Rhabdomyosarcoma is the most common childhood cancer. Its most hard-to-treat subtype, fusion-positive alveolar Rhabdomyosarcoma (FP-ARMS), is mainly caused by chromosome translocations that form a “fused oncogene” called PAX3-FOXO1 or PAX7-FOXO1. Although the genetic mutations leading to FP-ARMS has been known for decades, the effective therapy to treat FP-ARMS patients is still lacking: less than 50% of the patients are cured, and patients survival rate is less than 10%. In FP-ARMS translocation, a piece of DNA is “fused” to another piece of DNA. Such fused DNA sequence not only consists of the protein-coding genes but also of the non-coding DNA sequences. These non-coding sequences used to be called as “junk DNA”, but more and more studies have shown that they play essential roles in human diseases, including cancer. However, in FP-ARMS, we know very little about whether or how the “fused” non-coding DNA sequences contribute to cancer. In this study, we will take advantage the newly developed technology to address this question that has never been asked: how the “fused” non-coding DNA sequences contribute to tumor development. Our work will help to understand the mechanism that control FP-ARMS development, and in the future, to provide new drug targets for better therapies. More importantly, since chromosome translocation is frequently observed in many childhood cancer types, our pioneer work will also establish the new methods that can be applied to study other pediatric cancers.

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