The All-Star Grant is a re-investment in previous V Scholar or Translational grant recipients who are invited to apply for a $1,000,000 grant payable over 5 years. Any type of cancer research is permitted. This grant also includes salary support for a mentored post-doctoral fellow, which supports the next generation of cancer researchers.
Pancreatic cancer (PC) is a leading cause of cancer death in America. PC has few treatment options. Immunotherapy is a treatment that has promise. Immunotherapy can cure cancer, but it has never worked for PC. We found that some PCs respond well to immunotherapy. These patients have a mutation in a SWI/SNF gene. We began a trial to test how SWI/SNF mutant PCs respond to immunotherapy. We will collect blood to see what changes with treatment. We will make mice with SWI/SNF mutant cancer and test if these mice respond to immunotherapy. We will also test if blocking SWI/SNF with a drug can make tumors respond to immunotherapy. We hope to identify PC patients that can benefit from immunotherapy. We will also identify new treatments for PC that may help other patients.
Ovarian cancer is one of the deadliest types of cancer and has very few treatment options. However, there is hope that new types of treatment that help the body’s own immune system fight cancer could help patients live longer. Scientists have found that ovarian cancer patients who have more T cells—special immune cells that can find and kill cancer—often survive longer than patients with fewer T cells. But we still don’t fully understand what T cells are targeting when they attack ovarian cancer cells. This lack of knowledge has slowed down the development of better immune-based treatments for this disease. Our study is trying to solve this problem. Using new technology, we plan to discover what T cells are looking for when they fight ovarian cancer. We also want to create a new treatment that helps T cells better find and kill cancer cells. To do this, we will use a method called mass spectrometry to find targets on the tumor cells. Then we will use computer tools and lab tests in animal models to see if T cells can recognize and respond to those targets. If this approach works, we will move forward with a clinical trial to test if the new treatment helps ovarian cancer patients live longer. We also believe this work could lead to new treatments for other types of cancer.
Breast cancer comes back in up to 30% of patients, sometimes many years after treatment. These recurrences cause nearly all deaths from the disease. The returning cancer comes from tiny “sleeper” cells that survive treatment. These cells stay in the body without growing, in a resting or dormant state.
If we can keep these cells from “waking up,” we may be able to stop breast cancer from coming back and save lives. In our earlier research using mouse models and patient samples, we found something surprising: breast cancer sleeper cells can change their behavior and start acting like bone-forming cells. This change may help keep them dormant and stop the cancer from returning. We also showed that this bone forming activity can be seen in animals using PET scans—a common imaging method used in hospitals.
Our project aims to build on this discovery and develop a new way to keep sleeper cells dormant. To do this, we will:
Study this bone-forming process in patient tumor samples under the microscope.
Improve how we detect the bone forming process using PET scans in animal models.
Use what we learn to design a clinical trial that looks for whether this process occurs in patients during treatment.
If successful, our work could reveal a new way the body keeps cancer cells asleep, help us find which patients are affected, and lead to new treatments to prevent breast cancer from returning.
Glioblastoma is the most common and aggressive type of brain cancer, and sadly, most people only survive 12 to 18 months after being diagnosed. This hasn’t changed in the last 20 years. One of the reasons it’s so hard to treat is that glioblastoma is very complex and different from one patient to another. To improve treatment, we need to better understand this complexity and figure out how to target each part of the cancer. The Suvà lab has spent the last decade studying glioblastoma in depth using advanced genetic tools to understand how it varies. We’ve discovered that glioblastoma can be broken down into four important parts, and each part is essential for the cancer to grow.In this research, we will develop strategies to target each of these four parts. We’ll use new technologies developed by the Bar-Peled lab that can target elements of the cancer that were once thought too hard to treat. Our first step will be to analyze tumor samples from patients to find new drug targets. From there, we will work on drug development to eventually test them in clinical trials.
Lung cancers are often discovered after they have spread throughout the body. When this happens, patients must be treated with drugs. These drugs often shrink tumors but do not cure patients. The tumor cells that survive these drug treatments are known as “residual” cells. Residual cells eventually grow back, causing death. For this reason, we are very interested in discovering drugs that can kill residual lung cancer cells. Recently we discovered that residual lung cancer cells cannot survive without an enzyme called PKN2. We have access to a drug that blocks PKN2. Further, we already know that this drug is safe for patients. We are applying for grant funds to do three things. First, we will determine which residual lung cancers are most sensitive to this drug. Second, we will determine how this drug kills residual lung cancers. Third, we will determine how well this drug prevents lung cancer from relapsing in mice. Together, these studies will advance our understanding of residual lung cancer. They will also advance a new drug therapy that can be quickly translated to clinical trials by our team of expert doctors and scientists.
Funded by the Michael Toshio Cure for Cancer Foundation Nick Valvano Translational Research Grant*
After successful treatments, cancer patients often dread their disease returning months or years down the road. Even a few cancer cells hidden in the body can find ways to grow again. We will find ways to block these cancer cells from mutating so that they cannot find ways to grow again. These studies seek to provide new ways to extend survival and improve quality of life.
Co-funded by the Dick Vitale Pediatric Cancer Research Fund and the Jeff Gordon Children’s Foundation
What big question(s) will your work answer? Rhabdomyosarcoma is a deadly cancer that occurs in children and young adults. Several decades of research points to a specific molecule (called PAX3-FOXO1) as the most compelling drug target in this disease. However, we simply do not understand the molecular details of PAX3-FOXO1 enough to made a medicine that exploits this target. The big question addressed in this project will be to understand this compelling target with atomic detail by applying innovative technology. • Why does this question matter? Children continue to die of rhabdomyosarcoma and yet the medicines used in the clinic are woefully inadequate and toxic. A new therapy tailor-made for this disease could change everything. • How will your work answer the big question? Our work has the potential to provide a basic science foundation upon which a drug discovery campaign could be launched.
Co-funded by the Dick Vitale Pediatric Cancer Research Fund and the Jeff Gordon Children’s Foundation
Children with cancer are typically treated with chemotherapy to kill all dividing cells, including tumor cells. This general treatment causes side-effects, including damaging the normal healthy cells children need to grow and thrive. An additional, devastating, long-term side-effect of the use of chemotherapy is the risk of developing a second cancer. To circumvent these toxicities, we propose a targeted treatment tailored for a subset of pediatric patients with blood cancer. We identified a gene called “CUX1” that is deleted in the blood cells of patients with certain types of leukemia. Loss of one copy of CUX1 causes blood cells to grow too fast and stop maturing. In the current proposal, we predict that a drug that increases CUX1 levels will prevent leukemia growth and restore normal blood cell maturation. The objectives of the current proposal are to identify druggable regulators of CUX1 and to use these compounds to restore CUX1 in leukemias with CUX1 loss. We have identified one candidate regulator, named GSK3. We hypothesize that inhibition of GSK3 will increase CUX1 levels, halt leukemia growth, and restore normal blood development. We will accomplish these studies using innovative genetic screening, novel mouse models of childhood leukemia, and patient leukemia samples. Accomplishing the proposed studies will aid in the development of non-toxic therapies for children. This work will help us achieve our long-term goal of devising urgently needed treatments to improve the outcome for high-risk leukemias of childhood.
Co-funded by the Dick Vitale Pediatric Cancer Research Fund and the Jeff Gordon Children’s Foundation
Neuroblastoma is a childhood cancer that can be difficult to treat. Currently, studies are needed to figure out effective and safe ways to treat this type of cancer. Using animal models who can develop neuroblastoma, we found a special type of cells present within the tumors that allow them to grow and spread to other parts of body. By creating our own version of these cells, we can reverse their role and block the growth of tumors instead. We are proposing to use these modified cells to inhibit tumor growth. We will perform further modification on these cells to increase their success on killing cancer cells with less or no off-target effect on normal cells in the body. Through these studies, a new way to treat this childhood cancer may be found.
Funded by the Dick Vitale Pediatric Cancer Research Fund in partnership with Mat Ishbia and Justin Ishbia
Years of cancer research have shown that combining therapies that work differently virtually always works better than when therapies are used alone. New medications are being discovered that change the way that genes are turned on and off. At this same time, treatments are also being developed that use the body’s own immune cells to find and attack cancers. Both of these treatments have been shown to work alone on specific cancers. But each have known limits. We are asking whether combining these treatments will result in a new approach to fight two aggressive cancers: Ewing sarcoma and osteosarcoma. We predict that combining these treatments will result in an effective and well tolerated therapy.
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