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.
Stomach cancer is the fifth deadliest cancer in the world. Inflammation damages the stomach and causes harmful changes. First, the pre-cancerous cells start to show up. These cells cause the person’s body to make intestinal genes instead of stomach genes and can then lead to stomach cancer. However, we still have many questions about how and why pre-cancerous cells appear in the stomach in the first place. One important question is where the pre-cancerous cells come from. Scientists believe that some types of stomach cells can directly become pre-cancerous cells, but we do not fully understand which stomach cells can do this. Our research group looked at mice and humans with inflammation and damage in the stomach. We found that a stomach cell called a “pit cell” turned on intestinal genes. This meant that pit cells were pre-cancerous cells. This finding was surprising because scientists had already discovered that other cell types, not pit cells, become pre-cancerous. In our research project, we will learn more about why pre-cancerous pit cells appear. In the future we hope to develop drugs to stop these cells. We want to eventually develop ways to prevent pre-cancer from turning into cancer.
Acute myeloid leukemia (AML) is a deadly blood cancer that’s difficult to treat. Sometimes AML starts with a mistake in our cells. Think of DNA like a library of instruction books for your body. Imagine if pages from two different books accidentally got glued together—that’s what happens in AML when two different genes get stuck together to create a cancer-causing fusion protein. These fusion proteins take over the cell’s control system and make cancer cells grow without stopping.Our research team found that we can fight these cancer-causing fusion proteins by blocking other proteins that help them work. When we block these helper proteins, the cancer cells stop growing and start turning into normal white blood cells. We’ve shown that drugs blocking a helper protein called Menin can make cancer cells change back toward normal. Doctors are now testing these drugs in patients with AML. However, we’ll probably need to use several drugs together to completely cure this cancer.Our team also found two more important proteins called KAT6A and KAT7. These proteins help write the instructions that keep cancer cells growing. We’re studying how KAT6A and KAT7 work together with fusion proteins to cause leukemia. Understanding how these proteins cooperate to cause AML will help doctors create better treatments that cure more patients while causing fewer side effects.
Bladder cancer is the 5th most common cancer in the United States and causes about 17,000 deaths each year. When it spreads to other parts of the body, patients usually live less than two years. In the past few years, a new type of treatment called antibody drug conjugates (ADCs) has changed how bladder cancer is treated. One of these drugs, enfortumab vedotin (EV), targets a protein on bladder cancer cells called NECTIN4. When EV is used alone or with immunotherapy, this new therapy can shrink tumors in nearly 70% of patients at first. Sadly, most patients with bladder cancer become resistant after about a year, which means that the cancer stops responding to the treatment.We first thought this resistance might happen because tumors lose expression of the target NECTIN4. But when we looked at tissue samples from patients whose cancer stopped responding, we found most resistant tumors still had it. This project will explore other reasons why resistance happens and how to delay or reverse it. This includes looking at how the drug is processed inside cells, how it gets broken down, and how immune cells around the tumor may play a role. We will study both cancer cells and patient samples to see what changes occur as resistance develops. We will also test new drug designs, try other ways of targeting NECTIN4, and build new lab models from patients whose cancers are resistant. This work could lead to better treatments not only for bladder cancer but also for other cancers treated with ADCs.
Funded by the Stuart Scott Memorial Cancer Research Fund
About 15% of human cancers are caused by viruses. By stopping these viruses, we can reduce cancer cases. Kaposi sarcoma and pleural effusion lymphoma (PEL) are cancers caused by a virus called KSHV. We don’t have enough treatments to stop KSHV from spreading.This project will study how a protein called Angiogenin (ANG) helps stop KSHV from spreading. As a secreted factor that promotes blood vessel formation, ANG can help tumors grow, but we discovered an important anti-viral activity of ANG in Kaposi sarcoma. We found that when KSHV becomes active in primary effusion lymphoma, it creates fragments of tRNA (a type of RNA) that block viral replication. ANG helps make these fragments, and without ANG, KSHV spreads more.The goals of this project are:To see how ANG stops KSHV from spreading.To understand how ANG and tRNA fragments affect protein production.This research could greatly help cancer patients, especially those with Kaposi sarcoma and pleural effusion lymphoma. By learning how ANG stops the KSHV virus, new medicines could be made to stop the virus and cancer from spreading, which may be applicable to treating other tumor-causing viruses. With better treatments, patients could live longer. Overall, this research could lead to new ways to treat virus-related cancers, giving patients hope for better outcomes and a better life.
Immunotherapy is a transformative cancer treatment. It helps the body’s immune system find and kill cancer cells. This treatment has saved many lives, but some patients still do not respond. To help more people, we need to learn why immunotherapy works in some cases but not in others. One answer may be in the gut. The human gut has trillions of bacteria. Some of these bacteria can make immunotherapy stronger. They may even help fight cancers in other parts of the body, like the lungs, skin, or breast. Our team recently found a new type of gut bacterium that helps immunotherapy work better. We are now studying how this bacterium helps the immune system fight cancer outside the gut. We look at the substances these bacteria make and how they support immune cells, even inside tumors. Our goal is to turn these findings into new treatments. This could allow more patients to benefit from immunotherapy and bring new hope to people living with cancer.
Endometrial cancer is a type of cancer that starts in the inside part of the uterus (womb). Gaining too much weight can increase the risk of getting this cancer. Current treatments can be very hard with many side effects and sometimes do not work. We need safer and better ways to prevent this cancer and save lives. Before cancer starts, some women develop a condition called atypical endometrial hyperplasia (AEH). If AEH is not treated, it can turn into endometrial cancer. The main treatment now is surgery. Surgery is not always safe for overweight patients or for women having other health problems. Another option is a hormone medicine called progesterone, but it does not always work. We are studying a medicine called semaglutide, which is already used to reduce body weight. Semaglutide is safe medicine. Early studies showed that Semaglutide helps progesterone work better, but it is not clear how it works together. In our animal studies, using semaglutide and progesterone together helped animals gain less weight, live longer, and slow cancer growth. In our research, we will test both drugs together in overweight animals that are more like human’s disease. We will also study how semaglutide may reduce the risk of cancer. If this research works, semaglutide combined with progesterone could lower the risk of cancer in women. This could save lives and give women safer, better options for their health.
Childhood AML is a devastating blood cancer with high rates of treatment failure and relapse. Some types of AML are especially difficult to cure because they have high levels of a protein called MECOM. These AMLs reawaken signals that are normally only active in healthy blood stem cells. We know that high levels of MECOM are bad in AML, but targeted drugs have not been developed. In this proposal, we will use cutting edge technologies to test for weak spots in the MECOM protein itself. This will allow us to develop targeted drugs that can attack those weak spots. In this way, we aim to develop new medications to treat and cure childhood AML.
Lymphoma is one of the most common blood cancers. Treatments have helped many people, but for some, the cancer comes back after treatment. When that happens, it can be harder to treat. New research shows that finding shared targets in different types of lymphoma could lead to better treatments.
Cancer does not grow alone. It is surrounded by other cells called “stromal cells.” These stromal cells can sometimes help the cancer grow or resist treatment. But we still do not know exactly how they work or how many different types there are. In this project, we will use special tools to study these cells one by one. One tool is called single-cell sequencing, and another is called the CosMx Spatial Molecular Imager. These tools help us look closely at tumor cells and stromal cells to see how they work together.
We will also use lab models made from real patient samples. These models will help us watch how cancer and stromal cells behave together, both in lab dishes and in mice. We can then test new treatments that block the bad interactions between these cells. Lastly, we will use gene-editing technology to learn how cancer cells escape the immune system and resist treatment.
By better understanding how stromal cells support lymphoma, we hope to find new ways to treat the disease and help more people survive.
Our bodies are home to trillions of tiny living things called bacteria. A growing amount of research shows that these bacteria can play a role in how cancer starts and grows. Most scientists have focused on this connection in the gut, which is packed with bacteria. It might also be true for the lungs, but this is much harder to study because the lungs have far fewer bacteria. Right now, we can only identify which bacteria are there. To learn how these lung bacteria might affect cancer, we need to understand what they are actually doing. Unfortunately, our current tools are not sensitive enough to show us. We are creating two new ways to look at lung bacteria in cancer tissue from patients. These tools will let us see not only which bacteria are there, but more importantly, which of their genes are turned on. A gene that is “turned on” can tell us what a bacterium is doing. This will help us form new ideas about how they could be involved in lung cancer. This work will provide the first detailed picture of how bacteria might be involved in lung cancer. Understanding their role could lead to new tests to find lung cancer earlier or to identify people who are at a higher risk. It could also help us discover new ways to prevent lung cancer. We might even be able to design personalized treatments that change a person’s unique mix of bacteria to help fight cancer.
T cell therapy uses a person’s own immune cells to fight cancer. It has cured some blood cancers, like leukemia and lymphoma. But it does not work well for solid tumors in organs such as the lung, pancreas, or colon. My research asks why—and how to fix it.One problem is how the cells are grown before they go back into the body. Today, most labs use a “one size fits all” recipe. That recipe helps T cells multiply, but it does not train them for the tough job inside a solid tumor. Another problem is that people are different. Age, sex, and health history can change how T cells grow and work. A third gap is knowledge: we do not fully know what these cells do once they enter a tumor.To solve these challenges, I am building new tools to fine-tune how T cells are prepared and to track how they work in tumors. I will test many preparation methods at the same time and combine advanced imaging and AI to find the best recipes that make T cells that get into tumors, last longer, and fight cancer cells more effectively. The goal is simple: smarter, stronger T cell treatments for solid tumors. If successful, this work will guide doctors to match the right recipe to each patient and cancer. That could mean better responses, fewer side effects, and longer lives.
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