Grant Archive - Page 4 of 143

Thomas Hägglöf, PhD

The immune system protects us from infections, but it also plays an important role in fighting cancer. While many cancer treatments now focus on using the immune system to attack tumors, these treatments don’t work for everyone. To improve these therapies, we need to better understand how different immune cells behave inside tumors. Our research program focuses on a specific type of immune cell called the B cell. B cells are best known for making antibodies, but recently it was discovered that they are also found inside many types of tumors. Some B cells seem to help the body fight cancer, while others may actually help cancer grow. Right now, we don’t fully understand which B cells do what, or how. Our project will track how B cells enter tumors and how the tumor environment changes their behavior. We will use advanced tools in mice to follow B cells over time and test how certain stress signals, like low oxygen or changes in nutrients, affect how B cells grow and function. This work aims to discover better ways to boost the helpful B cells and block the harmful ones. By learning how to control these B cells, we hope to make immune-based cancer treatments work better for more people. Our ultimate goal is to use the immune system more effectively to help patients survive and thrive after a cancer diagnosis.

Haopeng Xiao, PhD

In honor of Ariel Ungerleider Kelley & Shoshana Ungerleider and in memory of Steven Ungerleider, V Foundation 2026 Sonoma Epicurean

Metabolism is how cells use nutrients to make energy and build the molecules they need to live. Cancer cells, unlike healthy cells, can change these processes. This rewiring helps them grow faster, resist stress, and avoid death. Learning how this happens may lead to new treatments.Our lab uses data-driven tools to study cancer metabolism. One of our main methods is mass spectrometry. This tool measures thousands of proteins and metabolites, and these molecules are the building blocks of metabolism. By measuring them in cancer, we can create a clear picture of how cancer cells use their metabolism to their advantage. These large datasets also allow us to use machine learning to find hidden patterns and weak points that cancer depends on.With this approach, we found a protein that controls the levels of cysteine, an amino acid that cancer cells need to grow and survive. The protein works by sensing and adjusting cysteine levels in cells. We are now testing if it can be a new drug target to kill cancer cells. In the future, we will use similar methods to find more hidden rules that let tumors survive. Our goal is to turn these findings into better cancer treatments that directly target cancer’s unique metabolic needs.

Hannah Garner, PhD

Breast cancer is the second most deadly cancer for women in the U.S. and Canada. This is mainly because some kinds of breast cancer are aggressive and spread to other organs, which makes them very difficult to treat. However, new research has shown that some cells that are part of the immune system are very important in cancer spread, opening the door for new treatments. My previous work found that breast cancer changes the way that these immune cells develop and how they work. These changes help cancer spread. This project will study how this happens. We will use advanced technologies and laboratory models that recreate many aspects of breast cancer. This will allow us to understand how tumors change the immune system. We will study important cells of the immune system at different stages of their development to understand how they are changed by breast cancer. We will study how breast cancer changes the bone marrow, where these cells form. We will also study samples of cancer and immune cells collected from breast cancer patients at hospitals. This will let us link our lab findings with real-world cases to make sure that our research will help patients. Finally, our project will test new ways to stop the immune system from helping cancer spread. This may help prevent or treat the aggressive types of breast cancer and help more patients to survive this disease.

Valerie O’Brien, PhD

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.

Emily Heikamp, MD, PhD

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.

Jonathan Chou, MD, PhD

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.

Jessica Tucker, PhD

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.

Joon Seok Park, PhD

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.

Vishal Chandra, PhD

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.

Richard Voit, MD, PhD

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.