Designed to identify, retain and further the careers of talented young investigators. Provides funds directly to scientists developing their own independent laboratory research projects. These grants enable talented young scientists to establish their laboratories and gain a competitive edge necessary to earn additional funding from other sources. The V Scholars determine how to best use the funds in their research projects. The grants are $200,000, two-year commitments.
Funded by the Dick Vitale Pediatric Cancer Research Fund
Diffuse midline glioma is a deadly brain tumor that affects children. Radiation is the main treatment, since surgery and chemotherapy do not work well. New drugs are being tested, but they are not proven yet. To find better options, we built a new method that combines gene disruption with detailed study of brain tumors. This lets us test the role of many genes in new ways. We found genes that may help tumors respond better to treatment. Now, we will study how these genes work. Our goal is to discover new treatment combinations that can help children with glioma live longer and healthier lives.
Funded by the Dick Vitale Pediatric Cancer Research Fund
My group investigates specific features of pediatric bone tumors that allow them to survive. One cancer we are interested in is Ewing sarcoma. Ewing sarcoma is a common bone tumor in children. It is challenging to treat, particularly when the cancer has spread. We have become interested in a protein that is important for Ewing sarcoma cells. We want to understand what this protein does in cells. This will help us to kill Ewing sarcoma cells. We are also working with chemists to make new drugs to disrupt its activity. We will test these in Ewing sarcoma cells. Our hope is that these studies will eventually lead to new treatments for Ewing sarcoma.
Funded by the 2026 Dick Vitale Gala in memory of Lucas Ticola
Brain cancer is an unwelcome guest that sneaks into a kid’s brain. Doctors can usually see and take out the cancer, but it gets really difficult when the cancer enters normal brain areas. This sneaky move by cancer is called invasion. The problem is that these cancer cells are so small and tricky that even our best medical scanners can’t find them. It is like the cancer is playing a game of hide-and-seek in the kid’s brain and escaping from the doctor’s tools.We know some of the places the cancer hides, but we don’t understand why it chooses certain paths or how it moves so easily. So, what we did was take a super close-up look at how brain cancer behaves using a special research tool. This is a way to see exactly what is going on inside individual cancer cells. Our first look tells us that brain cancers are like masters of disguise — they can look like normal brain cells, especially when they are hiding among them, and it seems they might even be “talking” to the normal cells around them.We will dive deep into how these cancer cells chat with healthy brain cells and what special tools or genes they use to travel so well. We believe figuring this out could put the brakes on cancer’s sneaky move. It could lead to new treatments that stop their play and talk, making treatment much more effective and helping many kids.
Funded with support from Hockey Fights Cancer in honor of Ben Stelter
Glioblastoma (GBM) is the deadliest adult brain cancer. Even with standard of care treatment, survival rates are low. A major challenge is that the brain’s protective barrier blocks most drugs. The tumor also weakens the immune system, making it harder for treatments to work. CAR-T cell therapy is a promising treatment that trains T cells, a special immune cell, to recognize and attack cancer cells. It works well in other cancers, but not GBM. Normally, T cells follow signals from proteins called chemokines and cytokines to locate and fight disease. However, GBM blocks these signals, stopping T cells from working properly. Our study will develop a new immune gene therapy using a harmless virus called AAV to help the immune system fight GBM. This therapy reprograms nearby brain cells (called astrocytes) to send signals that attract and activate immune cells, including CAR-T cells. Our gene therapy will deliver two key proteins: CXCL9 (which attracts T cells) and IL-2 (which helps them grow and stay active). This targeted approach ensures a steady immune response right at the tumor. We will combine this immune gene therapy with CAR-T cells to improve their ability to find, survive, and attack the tumor. Our research will study how AAV works in the brain, activates CAR-T cells, and which AAVs can be used in human clinical trials.
Funded by the V Foundation Chicago Epicurean in honor of The Debbie Jones Family
Cancer immunotherapy with checkpoint receptor inhibitors (ICIs) causes autoimmune side effects. These side effects occur in most patients treated with ICIs. These side effects are debilitating and difficult to treat. My goal is to find treatments for ICI side effects. I developed new mouse models where ICIs induce the same autoimmune side effects as in humans. I will use these models to understand why ICIs are toxic. I will also understand how to treat the side effects of ICIs.
Pancreatic cancer is one of the most difficult cancers to treat, with only about 1 in 10 patients living five years after diagnosis. New and more effective treatments are urgently needed. One promising option is CAR-T cell therapy, which uses a patient’s own immune cells to fight cancer. While this treatment works well in blood cancers, it has not been successful in solid tumors like pancreatic cancer. One major challenge is the environment around the tumor, which lacks nutrients and weakens the immune system. This makes it hard for immune cells to survive and do their job. Our research aims to solve this problem by using a single target to improve both the immune cells and the tumor environment. We have found that changing how immune cells use energy can help them stay stronger and last longer in the body. At the same time, targeting how cancer cells grow makes the tumor more vulnerable to attack. By combining these two strategies, we hope to improve how well CAR-T cells work against pancreatic cancer. With support from the V Foundation, we will test this approach in models of pancreatic cancer. If successful, this work could lead to better treatment options for people with pancreatic cancer and potentially other hard-to-treat cancers as well.
Colorectal cancer (CRC) is frequently diagnosed when it has already spread to other parts of the body. When caught early, 65% of patients survive for five years, but if the cancer has spread, only 12% survive that long. This makes it critical to understand what causes CRC to spread and find better ways to treat it. Cancer spreads when certain genes become more or less active. Scientists have mostly studied how genes are turned on and off, but recent research shows that another process, called post-transcriptional regulation, is also important. This refers to all the steps that happen between when a gene is copied into RNA to when it is turned into a protein. These steps, such as modifying, transporting, or breaking down RNA, add another layer of control over how much of a protein a cell makes. RNA-binding proteins (RBPs) help manage this process. But when RBPs don’t work properly, cancer cells may grow and spread more easily. We will use a genetic screening method to find all RBPs that play a role in cancer spread. By studying these proteins, we hope to better understand how CRC spreads and discover new ways to stop it.
Myeloid cancers are a group of blood diseases that happen when blood-forming cells in the bone marrow become abnormal. These changes often come from genetic mutations. One important mutation occurs in a gene called ASXL1, which is linked to the development of blood cancers and associated with poor prognosis. However, it remains unclear how ASXL1 mutations could drive blood cancers in humans. We recently found that, in younger mice, ASXL1-mutant blood stem cells do not grow out of control. But in older mice, these mutated cells do grow and expand. These suggest that aged bone marrow environment (BMM) may help these abnormal cells grow and cause leukemia. We also found that in older mice, the bone marrow has more inflammation and a higher number of stromal cells (cells that support blood cell growth), which can be mitigated by anti-aging therapy. In this project, we will study how aged BMM helps these mutant cells grow and test if targeting the aged environment alters the development of blood cancers. By understanding this process, we hope to find new ways to treat or even prevent blood cancers in humans.
Funded with support from Hockey Fights Cancer powered by the V Foundation presented by AstraZeneca
Cancer cells are always growing, and they need nutrients to keep up this fast growth. An exciting idea is that we might be able to starve cancer cells without harming healthy cells by getting rid of nutrients that cancer cells need. A drug being developed right now called ADI-PEG20 destroys a nutrient called arginine, which is an amino acid that is used to make protein and is particularly important for cancer cells. My lab studies what happens when cancer cells don’t have enough arginine. We want to understand how ADI-PEG20 works, how to improve it, and which cancers to treat with it. We have found that restricting arginine disrupts ribosomes, the machines that build new protein, causing them to get stuck and abandon their jobs early. We want to study three things to figure out how this impacts ADI-PEG20 treatment. First, why is protein production in cancer cells so sensitive to arginine levels? Next, what machinery in the cell is responsible for causing “starved” ribosomes to press the eject button in the middle of doing their jobs? Finally, what effect does this have on a cancer cell? This work will help us understand how a nutrient like arginine can directly control very important processes in the cell like protein production. It will also reveal how we can take advantage of cancer’s dependence on arginine to shrink tumors.
Multiple myeloma and AL amyloidosis are incurable cancers of blood cells. These blood cells are called plasma cells. There is only one therapy that is available for AL amyloidosis patients. In severe stages, AL amyloidosis patients survive less than one year. Amyloidosis plasma cells cause damage to the body by spilling in the blood a sticky protein. These sticky proteins attach to each other and build up in the heart. Buildup of proteins in the heart causes progressive poor function. AL amyloidosis is a major cause of malfunctioning of the heart and death. To cure AL amyloidosis, we need drugs that 1- stop plasma cells from spilling sticky proteins; 2- kill the cancer plasma cells; and 3-remove the buildup of sticky proteins from the heart. These drugs do not exist, because we do not know how sticky proteins get spilled and why the build-up is not removed.Recently, our lab found out how sticky proteins get out of amyloidosis plasma cells. We also showed that if we stop this process, cancer cells die. Finally, we discovered that cleaner cells that should remove sticky proteins from the heart are reduced and do not function in amyloidosis patients. Based on these data, we will make two novel drugs. One will stop spillage of sticky proteins and kill cancer cells. The other will remove sticky protein from the heart without the need of cleaner cells. Our work is doable and will create therapeutic options for AL amyloidosis patients that could cure their disease.
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