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.
The immune system has special cells called T cells that can find and kill cancer. Scientists can now take a patient’s own T cells and change them in the lab so they recognize that patient’s specific cancer, then give the cells back as a treatment. This approach has already saved many lives. However, for some brain and blood cancers, the cancer finds ways to wear down these T cells or hide from them, so most patients eventually get sick again.Scientists have found many small genetic changes that can make T cells stronger and help them survive longer in the body. The problem is that testing each change one at a time in patients would take decades and enormous resources, time that people facing these cancers do not have.Our project solves this problem by building a single treatment made up of many different T cells. Each cell carries one of these genetic improvements. This lets us test many changes at the same time instead of one at a time, which will speed up our search for what actually works. We also use a new, safer editing method along with a tracking tool. This tool lets us see which changes help T cells survive longer and fight cancer better, first in laboratory models and then in patients.Our project focuses on one type of brain cancer, glioblastoma, and one type of blood cancer, multiple myeloma, since both currently have limited treatment options. However, our hope is that this approach will not stay limited to these two cancers, and can be adapted to help patients with many other types of cancer as well.
Funded by the Stuart Scott Memorial Cancer Research Fund
Cancer is not a single disease, but many. Of those, pancreatic cancer is one of the deadliest. Current treatments help only a small number of patients, and doctors still cannot predict who will respond well and who will not. New treatment strategies are urgently needed. Our research studies immune cells that live inside tumors. Some of these immune cells help hide and protect the tumor rather than attacking it. However, we recently made an unexpected discovery: some of these cells can change sides and begin attacking the tumor and helping us. We want to understand why this happens. Why do some cells switch sides while others do not? What signals tell them to change? Answering these questions could reveal new ways to improve cancer treatment. To do this, we will study immune cells in pancreatic tumors and compare what we learn with samples from patients. We will look for clues that show which tumors contain immune cells that can be changed into cancer-fighting cells. This work will improve our understanding of how the body’s defenses respond to cancer. It may also help doctors identify patients who are more likely to benefit from treatment and guide the development of new therapies for pancreatic cancer and other hard-to-treat cancers.
Glioblastoma is a deadly brain cancer that is very hard to treat. One reason is that a tumor can contain many different types of cancer cells. A treatment may kill some cells, while others adapt and survive. These surviving cells can help the cancer keep growing or return after treatment. Our project will study how glioblastoma cells escape drugs that block a key signal for cancer growth. These drugs can block their main target, but some cancer cells still find ways to survive. They may turn on backup signals or use the same signals in new ways. We want to learn which cells escape, when they do so, and where these survival signals come from inside the cell. We will use artificial intelligence to create protein-based sensors that work like tiny “signal detectors.” These sensors will let us watch growth signals inside living cancer cells during treatment. We will study one cell at a time, rather than only looking at the tumor as a whole. This can help us find small groups of cells that respond differently and may otherwise be missed. We will also test our sensors in tumor models made from patient cancer cells. Our goal is to find the signals that allow glioblastoma cells to survive treatment. We can then look for ways to block these escape routes. This research could lead to better drug combinations that stop cancer cells from adapting to treatment. In the future, these findings may help treatments work longer and improve options for people living with glioblastoma.
We are studying a new type of radiation therapy that acts like a GPS-guided missile because it is injected into the patient, goes straight to tumor cells that have the target, and delivers radiation to kill the cells. One drug called 177Lu-PSMA-617 is used to treat prostate cancer that has spread to other parts of the body. Unfortunately, this treatment only works in 45% of patients. Our goal is to understand why some patient’s tumors do not respond to this treatment so we can figure out ways to improve this. To do this, we first must learn more about how this drug works and how it kills cells. We will look at how prostate cancer cells grow and divide during treatment and find ways to increase cell death. We will do this in cells in a dish and in real tumors from patients. We will also make models that look like prostate cancers and grow cells in different patterns to look at how different mixtures of cells in a tumor affects treatment response.
Every year, more than 20,000 women in the United States are diagnosed with ovarian cancer. Most respond to treatment at first, but nearly all will relapse, at which point there are very few treatment options. Hence, new treatments for relapsed ovarian cancer are urgently needed. Part of what makes this cancer so deadly is that tumors become resistant to drugs. Tumors also spread to fatty tissue in the abdomen, where fat cells feed the cancer cells and protect them from treatment.Our research focuses on a protein called NMNAT2. This protein helps cancer cells make NAD+, a molecule they need to grow, survive, and resist treatments. We found that ovarian cancers with high NMNAT2 are more aggressive and harder to treat. NMNAT2 also helps cancer cells use fat cells to spread. Crucially, NMNAT2 is highly expressed in ovarian cancer but rarely found in normal tissues. This makes it a safe and precise drug target.In the proposed studies, we will test how NMNAT2 drives drug resistance and tumor spreading. We will also test whether blocking NMNAT2 makes tumors easier to treat by changing their immune environment. By understanding how NMNAT2 is controlled, we aim to develop new treatments for treatment-resistant ovarian cancer and improve outcomes for patients with this deadly disease.
CAR-T therapy is a cancer treatment that uses a patient’s own immune cells, called T cells, to find and kill cancer. It has transformed treatment for some blood cancers, but it has not worked nearly as well for solid tumors such as pancreatic cancer. One major reason is that solid tumors create a hostile environment that can weaken T cells and stop them from fighting.Our goal is to make CAR-T cells smarter, stronger, and safer. Pancreatic tumors release signals that normally help them hide from the immune system. We want to turn one of those signals into an alarm. We will engineer T cells so that when they sense this cancer-associated signal, they switch on their strongest cancer-fighting abilities. In other words, the tumor itself would tell the T cells, “Cancer is here—start fighting.” This approach could help T cells survive longer, attack pancreatic tumors more effectively, and remain less active in healthy tissues. That could make treatment both more powerful and safer for patients.If successful, this research could open a new path toward effective CAR-T therapies for pancreatic cancer and, in the future, other solid tumors that are currently very difficult to treat.
Our immune cells help us fight injections, for example, the flu. Our immune cells also help our bodies fight cancer cells. Famous studies by Drs. Allison and Honjo, where they did experiments by injecting cancer cells into mice to study how the immune system fights cancer discovered “ways” cancer cells use to hide from immune cells. Those discoveries were then used to make drugs that “wake-up” the immune system; those drugs are known as immunotherapies. But these drugs don’t work for all patients. This means there are other “ways” cancer cells hide from our immune system. Our goal is to discover these other ways, but not by using cancer cells. Instead, we are doing experiments using unique and special cells that are not cancer yet, but on their way to becoming cancer. We call them “pre-malignant” cells (pre-malignant = pre-cancer). By using these unusual and novel cells, we want to discover new ways that cancer cells use to escape from the immune system and to make drugs that reverse this, so we can develop the next generation of immunotherapies.
Each year, thousands of young adults are diagnosed with IDH-mutant glioma, the most common brain cancer in people aged 35 to 44. Even with treatment, these tumors eventually return and take lives far too soon. A new drug approved in 2024 brought real hope. But it helps only about half of patients, and many treated tumors still fail to respond. The hardest part is that the same mutation, treated with the same drug, can mean recovery for one person and decline for another. Our research aims to explain that difference and make resistant tumors treatable. These tumors are shaped by tiny chemical marks on DNA that switch genes off. We believe the drug works by erasing these marks, freeing the genes a tumor needs to grow into healthy-like cells. In tumors that resist, those marks appear locked in place. To learn why, we will compare tumors that respond against tumors that do not. We will study patient samples taken before and during treatment. And we will test whether a second drug can unlock resistant tumors in the lab.If we succeed, we will understand why the same drug helps some patients but not others. That knowledge could let us design new drug combinations for the patients who have the fewest options today, switching tumors that resist treatment back into a state that responds. Because the same biology appears in other cancers, our findings could improve care for many patients well beyond those with brain tumors.
White blood cells protect us from infection by fighting bacteria and viruses. When we get sick, these cells create inflammation to help us kill germs. Inflammation can make us feel achy, tired, and feverish, but it is a sign that our immune systems are working. Once the infection is gone, the inflammatory response stops and we feel better.Leukemias are cancers of white blood cells. Our group studies a rare leukemia called chronic myelomonocytic leukemia (CMML). People with CMML have inflammation even when they do not have an infection. As a result, many patients feel like they have the flu all the time. Common symptoms of CMML include fatigue, fevers, night sweats, and weight loss. We believe that decreasing inflammation in the body may help CMML patients feel better and live longer.We have found that a type of white blood cell called a neutrophil may be an important source of abnormal inflammation in CMML. Neutrophils release sticky webs made of DNA and proteins. These webs are called neutrophil extracellular traps, or NETs. In healthy people, neutrophils produce NETs to trap germs when they are sick. CMML patients produce large amounts of NETs even when they are not sick with an infection. Our group has discovered a protein called neonatal NET inhibitory peptide, or nNIF, that blocks NET formation. In this project, we will test whether nNIF can lower NET levels in a mouse model of CMML. We believe that reducing NETs will also reduce inflammation. If successful, this work could lead to new treatments that improve the lives of people with CMML.
Funded by the Dick Vitale Pediatric Cancer Research Fund
Bone cancer is one of the most painful cancers in children and teenagers. Many patients live with severe pain that makes it hard to walk, play, or sleep. Doctors often rely on opioid pain medicines, but these drugs can cause serious side effects. We still do not know why bone tumors cause so much pain or how pain is linked to tumor growth. Our research studies special nerve cells that sense pressure. As a bone tumor grows, it pushes against the hard walls of the bone. We think this pressure turns on these nerves. In our earlier studies of adult bone cancer, we found that these nerves play a major role in cancer pain. Now we will test whether the same process happens in childhood bone cancer. We will also study whether these nerves send signals that help tumors grow. If they do, blocking these signals could reduce pain and slow cancer at the same time. Our goal is to find safer, non-opioid treatments for children with bone cancer. This work could change how we think about cancer by showing that physical forces and the nervous system work together to shape disease. We hope these discoveries will lead to better treatments and improve the lives of children with bone cancer.
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