Ronny Bell, PhD

Funded by the 2021 Victory Ride to Cure Cancer

Dr. Ronny Bell is a Professor in the Department of Social Sciences and Health Policy at the Wake Forest School of Medicine and Director of the Office of Cancer Health Equity at Atrium Health Wake Forest Baptist Comprehensive Cancer Center. Dr. Bell’s research focuses on disparities that impact health outcomes and health care access for racial/ethnic minority and underserved populations.

Karen Winkfield, M.D., Ph.D.

Funded by the 2019 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.

Michael Kastan, M.D., Ph.D.

The Duke Cancer Institute and the College of Veterinary Medicine at N.C. State University formed a Comparative Oncology Consortium (COC), taking advantage of their expertise and national leadership in their respective disciplines and their geographic proximity. The goals are to collaborate in pre-clinical and clinical cancer research activities in order to advance our understanding of both cancer causation (a high incidence of specific cancers in specific dog breeds provides opportunities to identify new cancer susceptibility genes and environmental factors in cancer causation) and of behaviors and genetics of specific tumor types, as well as to coordinate clinical trials in humans and canines so that novel therapies can be tested in both settings, with information gained in one setting informing the other. In addition to response outcomes of these cancer therapies, the ability to use biomarkers and pharmacology in the canine models can be a novel addition to the characterization of these new cancer therapies and these insights could result in significant enhancements of clinical trial designs (including dosing, scheduling, and combination therapies) when these treatments are tested in human clinical trials. Cost savings and improved clinical trials design would help encourage pharmaceutical companies to use the canine models as part of the assessment process and would benefit the canine patients by giving them access to these novel therapies.

Yuliya Pylayeva-Gupta, Ph.D.

V Scholar Plus Award – extended funding for exceptional V Scholars

Pancreatic cancer is a very aggressive disease. It is the 3rd leading cause of cancer deaths in the USA. Only 8% of patients who can undergo surgery will survive past five years. Late diagnosis and lack of good treatment options are some of the reasons for this outcome. Recent progress in cancer immune therapy showed effect in cancers such as relapsed leukemia and metastatic melanoma. Unfortunately, immune therapy was not effective in patients with pancreatic cancer. One explanation for this result is that pancreatic cancer blocks immune responses against cancer. Thus, understanding how cancer promotes immune suppression is vital to our ability to treat this deadly disease. Our initial work has revealed that B cells promote growth of pancreatic cancer and resistance to immunotherapy. However, it is not clear how B cells promote cancer growth, and how targeting these cells can benefit patients. We propose to understand how B cells function in pancreatic cancer. The goal of this research project is to find new targets that can block immune suppression in pancreatic cancer. Using both mouse models of pancreatic cancer and patient samples, we hope to identify B cell based targets in pancreatic cancer. We ultimately hope to translate our findings into effective therapies that may also work with existing immune therapy treatments.

Michael Kastan, M.D., Ph.D.

The Duke Cancer Institute and the College of Veterinary Medicine at N.C. State University formed a Comparative Oncology Consortium (COC), taking advantage of their expertise and national leadership in their respective disciplines and their geographic proximity. The goals are to collaborate in pre-clinical and clinical cancer research activities in order to advance our understanding of both cancer causation (a high incidence of specific cancers in specific dog breeds provides opportunities to identify new cancer susceptibility genes and environmental factors in cancer causation) and of behaviors and genetics of specific tumor types, as well as to coordinate clinical trials in humans and canines so that novel therapies can be tested in both settings, with information gained in one setting informing the other. In addition to response outcomes of these cancer therapies, the ability to use biomarkers and pharmacology in the canine models can be a novel addition to the characterization of these new cancer therapies and these insights could result in significant enhancements of clinical trial designs (including dosing, scheduling, and combination therapies) when these treatments are tested in human clinical trials. Cost savings and improved clinical trials design would help encourage pharmaceutical companies to use the canine models as part of the assessment process and would benefit the canine patients by giving them access to these novel therapies.

John Cavanagh, Ph.D.

Recently, researchers in the program have discovered a synthetically accessible class of molecules that appear to increase the effects of novel anticancer drugs by several orders of magnitude.  The overarching goal is to reduce the working concentrations of ALL anti-cancer drugs in order to mitigate serious side effects.  Here, we propose to develop and screen our new molecules with both novel and existing chemotherapeutics against a variety of cancer cell lines in order to define the optimum combination treatment. 
 
Also we are working on tumor formation. 
 
The life and death of cells must be balanced if tissue homeostasis is to be maintained-there should neither be too much growth nor too little death.  Normal cells accommodate this balance by invoking intrinsic programmed cell death, referred to as apoptosis.  Apoptosis is triggered via three signaling pathways.  If apoptosis does not occur correctly and cells do not die, then malignant tumors form.  It is no surprise therefore that countless cancer therapeutics are being developed to control apoptosis. 
 
It is known that all three apoptosis signaling pathways route through a protein known as caspase-3.  If caspase-3 fails to function, then cell death does not happen correctly and cancer occurs.  It is known that a calcium-binding protein known as calbindin-D28K binds to caspase-3 and stops it functioning.  If we can stop calbindin-D28K from interfering with caspase-3, apoptosis would occur normally and the risk of cancer developing would be significantly reduced.  Consequently calbindin-D28K is a particularly powerful target for anticancer drug development. 

Corinne Linardic, M.D., Ph.D.

Funded by the Apple Gold Group

Rhabdomyosarcoma (RMS) is the most common soft tissue cancer of childhood.  Because RMS has features of skeletal muscle, we and others have been trying to understand how muscle development pathways inside the tumor cells have gone awry.  This project will study the role of a protein called SFRP3, which although it takes part in normal muscle formation, is co-opted to support RMS tumor formation.  We aim to understand in more detail how SFRP3 works in RMS, and how to block it.  Our goal is to someday use SFRP3 blockade as a therapeutic intervention.

John Cavanagh, Ph.D.

Funded by a challenge grant with

North Carolina State University

The Jimmy-NCSU V Cancer Therapeutic Program allows young researchers the opportunity to work on multiple facets of cancer research in a set of diverse labs, each investigating different approaches for developing cancer therapeutics.

Enhancing cancer drugs
We have discovered molecules that increase the effects of anticancer drugs by several orders of magnitude.  Our goal is to reduce the working concentrations of all anti-cancer drugs in order to mitigate serious side effects.  We will develop and screen our new molecules with both novel and existing chemotherapeutics against a variety of cancer cell lines in order to define the optimum combination treatment.  Initial screens show effects against breast, renal and colon cancer cell lines.

Cell death and tumor formation
The life and death of cells must be balanced.  Normal cells accommodate this balance by invoking programmed cell death pathways, referred to as apoptosis.  In cancer cells, these pathways are defective and normal cell death does not occur, leading to tumor formation.  In addition, faulty apoptosis causes tumor cells to be resistant to chemo/radiation therapies.  If we could make apoptosis occur properly, we slow down tumor formation and overcome this resistance.

The protein caspase-3 controls apoptosis.  If caspase-3 fails to function, cell death does not happen correctly.  We also know that the protein calbindin-D28K binds to caspase-3 and stops it functioning.  If we can stop calbindin-D28K from interfering with caspase-3, apoptosis would occur normally and the risk of cancer developing would be reduced.  Consequently calbindin-D28K is a powerful target for anticancer drug development.

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