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.
Our immune system contains cells that keep it in balance, but some of these cells actually stop the body from attacking tumors. We found that a promising cancer drug can change these cells, turning them from tumor protectors into tumor fighters. Our project studies how this change happens, and how we can use it to help patients. We use specially designed mouse models of pancreatic cancer to perform these studies. These models let us tag the immune cells of interest with a fluorescent tag so that we can track the cells even after we give the drug and the cells change their job. This allows us to study how our drug works with other cells to cause the immune cell switch into tumor-killing cells, and to help us determine how the changed cells actually fight the cancer cells. We are comparing the genes of the changes cells to unchanged cells to determine a unique signature of these cells – which we will then look for in patient tumors.This research is important because it could explain why some patients respond well to cancer therapies that use the immune system, while other patients do not. If we can find out which patients are most likely to benefit from this style of drug, doctors could better match patients to the right drugs. We can also design better future drugs for other patients, bringing us closer to cancer care built around each patient’s unique needs.
Over a lifetime, our skin is exposed to sun, pollution, and other injuries. To survive this damage, skin adapts in surprising ways. It can carry early cancer-causing changes in cells that still look normal, until the right trigger turns them into cancer.This raises a broader question: if skin can hide the seeds of skin cancer, could it also hide a cancer that starts somewhere else? Leukemia is a bone marrow cancer that circulates in blood. Doctors check the bone marrow to see if treatments work, but leukemia can return even when the marrow looks clear. We wondered whether leukemia cells could escape treatment by hiding in skin and later cause relapse.In leukemia patients we studied, we found traces of leukemia in skin that appeared healthy. Patients with more leukemia signal in the skin had worse outcomes. We found that in mice, leukemia cells formed small hidden pockets in the skin and could transmit leukemia through small skin grafts. This gives us a new tool to study how leukemia gets into the skin and how to clear it.This project aims to determine whether leukemia truly hides in normal-looking skin, how it gets there, and whether we can remove it. If successful, the skin could become an easier place to test for hidden leukemia and a gentler target for treatment to help prevent relapse.
Funded by the Stuart Scott Memorial Cancer Research Fund
New cancer drugs that help the immune system have improved survival for many people with melanoma. But they often do not work well for acral melanoma, a type of skin cancer that grows on the palms, soles, and under the nails. Acral melanoma is the most common type of melanoma in Black, Asian, and Hispanic patients. Patients with this cancer also tend to do worse after immune treatment than patients with other forms of melanoma.Our team studied tumors from patients with acral melanoma to learn why this happens. We found that a protein called BRD4 may be important. BRD4 comes in two forms. One form helps turn on signals that allow the immune system to see and attack cancer. The other form may help cancer cells survive.In acral melanoma, a change in the BRD4 gene may reduce the helpful form and increase the harmful form. When this happens, immune cells may have a harder time finding and killing the cancer, even during treatment.Drugs that block BRD4 already exist, but they block both forms at once. This may be one reason they have not worked well. Our project will study what each form does, where it is found in the tumor, and how it affects nearby immune cells. We will then test whether blocking the harmful form while keeping the helpful form can make immunotherapy work better.
Funded by the Dick Vitale Pediatric Cancer Research Fund with support from Hockey Fights Cancer and Jeffrey Vinik
More children are surviving brain cancer than ever before. However, when a brain tumor comes back, it is still very hard to cure. Medulloblastoma returns in more than 30% of patients, even after intensivetreatment. This raises two important questions: Is some cancer left behind after treatment? Can we find it sooner? We hope to answer these questions with a new test that uses only a small amount of spinal fluid. The test is called a “liquid biopsy.” It looks for tumor DNA in the fluid around the brain and spinal cord. In patients with medulloblastoma, we can find signs of cancer using only a teaspoon of spinal fluid. In some cases, the test may find cancer before it can be seen on a scan. Our goal is to offer this test to more patients through a Children’s Oncology Group clinical trial. We will study whether the test helps doctors choose the best treatment for each young child. This project brings together two leading labs at the University of Washington and Children’s Hospital Los Angeles. Our results could change how doctorswatch and treat brain tumors. We hope this work will help more children with medulloblastoma survive. The test may also help patients with other types of brain cancer, expanding its impact even further.
Funded by the Dick Vitale Pediatric Cancer Research Fund
Some children are born with changes in their genes that increase their risk of cancer. Doctors do not always know which children are at the highest risk or how often they should be checked. One common condition linked to childhood cancer is neurofibromatosis type 1 (NF1). Children with NF1 can develop tumours in the brain, nerves, and other parts of the body. They may also have other serious health problems. However, not all changes in the NF1 gene cause disease. This makes it hard for doctors to know which children need closer monitoring and which do not.Dr. Yiming Wang’s research will help answer this question. His team will build a detailed map of NF1 gene changes and their effects. Using new laboratory tools, the team will study thousands of NF1 gene variants. They will test how each variant affects the normal work of cells. This will help identify which gene changes are harmful and which are harmless.The findings could help doctors make more accurate diagnoses and reduce uncertainty for families. They could also reduce the number of unnecessary tests. Most importantly, they could help identify children who are at higher risk and need closer follow-up. This may allow dangerous tumours to be found earlier, when treatment can be more effective.In the future, this work could help doctors choose the best care for each child. It could improve the lives of children with NF1 and support better cancer care for many families.
Funded by the Dick Vitale Pediatric Cancer Research Fund
Aggressive childhood cancers, including neuroblastoma and certain types of leukemia, are driven by a protein called MYC. MYC acts like the gas pedal in a car, telling cancer cells to grow and divide. When MYC gets stuck in the “on” position, tumors grow quickly and become harder to treat. Even though MYC is one of the main causes of these cancers, scientists have struggled for many years to develop drugs that can block it.Our research takes a different approach. Instead of trying to stop MYC directly, we study the cell’s natural braking system. A protein called PP2A normally helps keep MYC under control by telling the cell when MYC should be turned off and removed. In many high-risk childhood cancers, this natural brake no longer works, allowing MYC to stay active and drive cancer growth.Our goal is to learn exactly how PP2A controls MYC and why this process breaks down in cancer. We will combine advanced imaging tools with studies using pediatric cancer cell lines to see how these two proteins work together and how their connection changes in tumors.This research could lead to a new way to treat childhood cancer. Instead of blocking MYC itself, we hope to restore the cell’s natural ability to control it. The knowledge gained from this project will provide the foundation for developing more precise and less toxic treatments, bringing new hope to children with high-risk cancers and their families.
Funded by the Dick Vitale Pediatric Cancer Research Fund
Osteosarcoma (OS) is the most common bone cancer in the United States. The disease impacts children and adults. Despite very hard treatment, many patients unfortunately die or have long-term side effects. Treatment has not changed much in over four decades. We need to improve treatment so that patients with OS have a better chance at healthy and long lives.Our research on patient tumors has shown that there are differences in gene expression across OS. This is most true for the disease that is the hardest to treat. The factors that drive this and how this relates to the genetics of OS remain unknown. Understanding this is important for developing better treatments.Our goal is to understand gene expression in OS and how this relates to genetics of this cancer. We will study patient tumor and normal tissue sequencing from OS patients and individuals without cancer. We will also carry out experiments on cell lines to build on our findings.We expect that what we learn will help inform new treatments for patients with OS. This will include a possible role for drugs that change patterns of gene expression to make OS more treatable. This would be an important step toward improving survival and outcomes for patients with OS.
Basal-like breast cancer is one of the most dangerous types of breast cancer. It is hard to treat because many cancer drugs do not work well against it. This cancer is common in people who inherit certain harmful gene changes, but it can also affect people with no family history of the disease. Today, treatment often includes chemotherapy or surgery to remove breast tissue. These options can be difficult for patients and do not always stop the cancer. Better ways to prevent and treat this disease are needed.Our research looks at the early changes that happen before this cancer forms. We created special mouse models to study how the disease begins. Using these models, we found an early change called chromatin priming. During this step, normal breast cells start to act differently and become more likely to turn into cancer cells. Changes in the way DNA is packed inside cells make it easier for genes linked to cancer to switch on. We also found that the same genes are active in both inherited and non-inherited forms of basal-like breast cancer. This means the two forms of the disease may start in similar ways.Our next goal is to learn what causes these early changes and how they lead to cancer. If we can block these changes, we may be able to stop tumors from growing. This work could lead to better treatments and better outcomes for patients.
Radiation therapy is used to treat many patients with cancer. Doctors can aim radiation at a tumor precisely. But radiation alone often cannot get rid of all the cancer, especially if it has spread. Immunotherapy is another type of cancer treatment. It uses the body’s own immune system to fight the disease. This strategy can work very well. However, it can also cause side effects. This happens when the immune system attacks healthy tissues. Thus, current immune treatments could benefit from improved precision against cancer cells. Our research combines the strengths of radiation and immunotherapy. Radiation is normally used to kill cancer cells. However, we will use radiation in a new way. Our approach is designed to improve how immune cells respond within tumors while limiting effects in other parts of the body. This may help protect healthy tissues. In this project, we will find ways to make immune cells perform better after radiation. We will find genes that help the immune cells grow, survive and kill cancer cells. We will also test ways to send supportive signals directly into tumors instead of the whole body. If we succeed, we establish a new type of cancer treatment. Patients could benefit from immune therapy that is more precise and powerful, with fewer side effects.
Glioblastoma is the most common and deadly type of brain cancer in adults. Even with surgery, radiation, and chemotherapy, the cancer almost always comes back. One reason is that tumor cells can spread into nearby brain tissue, making them very hard to remove completely. Our research focuses on how brain tumors take control of nearby healthy brain cells called “astrocytes”. These healthy cells normally help the brain work properly, but cancer cells can transform them into helpers that support tumor growth and spread. We want to understand how this happens and find ways to stop it.We believe brain tumors send signals that change the behavior of nearby cells and create an environment that helps the cancer grow. In this project, we will study these signals and test new ways to block them.This research could lead to new treatments that make it harder for brain tumors to spread and return after treatment. By targeting the support system that tumors build around themselves, we hope to improve the effectiveness of current therapies and help people with glioblastoma live longer and healthier lives.The knowledge gained from this work may also help researchers better understand how other cancers interact with healthy tissues and find new ways to stop cancer progression.
Manage Consent
To provide the best experiences, we use technologies like cookies to store and/or access device information. Consenting to these technologies will allow us to process data such as browsing behavior or unique IDs on this site. Not consenting or withdrawing consent, may adversely affect certain features and functions.
Functional
Always active
The technical storage or access is strictly necessary for the legitimate purpose of enabling the use of a specific service explicitly requested by the subscriber or user, or for the sole purpose of carrying out the transmission of a communication over an electronic communications network.
Preferences
The technical storage or access is necessary for the legitimate purpose of storing preferences that are not requested by the subscriber or user.
Statistics
The technical storage or access that is used exclusively for statistical purposes.The technical storage or access that is used exclusively for anonymous statistical purposes. Without a subpoena, voluntary compliance on the part of your Internet Service Provider, or additional records from a third party, information stored or retrieved for this purpose alone cannot usually be used to identify you.
Marketing
The technical storage or access is required to create user profiles to send advertising, or to track the user on a website or across several websites for similar marketing purposes.
To provide the best experiences, we use technologies like cookies to store and/or access device information. Consenting to these technologies will allow us to process data such as browsing behavior or unique IDs on this site. Not consenting or withdrawing consent, may adversely affect certain features and functions.
Functional
Always active
The technical storage or access is strictly necessary for the legitimate purpose of enabling the use of a specific service explicitly requested by the subscriber or user, or for the sole purpose of carrying out the transmission of a communication over an electronic communications network.
Preferences
The technical storage or access is necessary for the legitimate purpose of storing preferences that are not requested by the subscriber or user.
Statistics
The technical storage or access that is used exclusively for statistical purposes.The technical storage or access that is used exclusively for anonymous statistical purposes. Without a subpoena, voluntary compliance on the part of your Internet Service Provider, or additional records from a third party, information stored or retrieved for this purpose alone cannot usually be used to identify you.
Marketing
The technical storage or access is required to create user profiles to send advertising, or to track the user on a website or across several websites for similar marketing purposes.
