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.
Funded by the Stuart Scott Memorial Cancer Research Fund with support from the Oral Cancer Cause
Voice is an incredible tool that we use every day to express our feelings and even our health. You can often tell if someone is stressed, happy, or not feeling well just by the way they sound. In fact, over 50 different diseases can cause noticeable changes in a person’s voice. One of the most serious conditions that affect the voice is laryngeal cancer, or cancer of the voice box. This type of cancer can cause major changes in a person’s voice, even in the early stages. Unfortunately, if it is not caught early, it can lead to the loss of voice, difficulty swallowing, and too many cases, death. The earlier we detect laryngeal cancer, the more treatment can preserve the voice and improve survival rates. The problem is that while many people with laryngeal cancer experience voice changes, most people who have a change in their voice do not have cancer. This creates a challenge for primary care doctors, who need to identify the rare instances where voice change suggests something more serious. To help with this, we are developing a machine learning tool that can listen to voice recordings and help doctors figure out when a patient may be at high risk for laryngeal cancer. This could help detect cancer earlier and save lives by making it easier for doctors to know when to refer patients to specialists for further testing.
Dr. Joseph Moore Excellence in Oncology Grant* Funded by Constellation Brands Gold Network Distributors
Myeloma is a blood cancer that causes bone and kidney damage. Myeloma is the second most common blood cancer. New treatments are improving patient lives, but patients have to take medicine for the rest of their life. The cancer eventually adapts to these drugs and harms patients.
We will study myeloma that has become drug resistant. We are testing new therapies that can overcome drug resistance. This new therapy targets something called a co-activator. Co-activators turn on genes that enable the cancer to grow. Our research will treat cancer models with inhibitors of co-activator to understand how they work. We will also test different co-activator inhibitors to see which are most effective. Finally, we will look for genes that cause drug resistance. These studies will help guide ongoing clinical trials in myeloma. The long-term goal of this research is to find the right combination of therapies that will stop myeloma from growing.
Funded by the Stuart Scott Memorial Cancer Research Fund
Our research looks at how hormone receptors play a role in cancer. These receptors are involved in prostate, breast, uterine, and ovarian cancers. Normally, they help control important functions in the body. But as people get older and hormone levels drop, these receptors can stop working properly and help cancer grow.
Even though there are treatments that block these receptors, many patients still see their advanced cancers return within two years. This happens because cancer cells find new ways to turn the receptors back on, which makes the treatments less effective.
To tackle this problem, we use advanced imaging tools, including high powered microscopes, to make 3D models of the hormone receptors. This helps us see how the receptors work and what goes wrong in cancer. We have already found new interactions at the molecular level that were not known before. With support from the V Foundation, we hope to create better drugs that target these receptors more effectively, helping to stop cancer from coming back and improve patient outcomes.
Our bodies are constantly exposed to a multitude of challenges, such as microbes, toxins, and injuries, especially at barrier surfaces like the skin, lungs, and intestines. These tissues serve vital and complex functions in shielding us from environmental threats while also managing body moisture, oxygen levels, and nutrient absorption. For instance, the intestine must delicately balance the elimination of harmful microbes and toxins with the absorption of essential nutrients. This requires intricate cooperation between the intestinal lining cells and the intestinal immune system. Barrier tissues, like the intestine, are particularly prone to inflammation and cancer.
Inflammatory bowel diseases are chronic inflammatory conditions affecting the intestines. They result from an interplay of genetic and environmental factors, leading to dysregulated functioning of intestinal cells and immune system. These incurable diseases can significantly increase the risk of developing colon and rectal cancer. Yet, the mechanisms through which environmental factors and inflammation impact the immune system and cells of the intestine to drive the progression of chronic inflammatory diseases and cancer remain largely unknown.
Within the Niec lab, innovative tools have been developed to investigate how immune cells and the intestinal barrier cells respond to environmental challenges and interact in disease. Through this project, we aim to unravel the alterations occurring in the immune system and the intestine during inflammation. By understanding these processes, we aspire to develop strategies to prevent and treat cancer that arises from inflammatory bowel disease.
Cancer must change its nutrient uptake to grow. Drugs blocking cancer’s use of nutrients have been the basis of cancer therapy. However, most of these drugs work by blocking the pathways that metabolites use. They exhibit significant toxicity since they also harm normal tissues. We are looking at metabolite-targeted therapies that are less toxic. We hope the therapy will be more specific and effective as well. We don’t seek to block metabolite pathways. Instead, we target the specific metabolites that change in the tumor microenvironment. We study and harness the power of our body’s metabolites as drugs. Our work has the potential to change how we target cancer, leading to less toxic and more effective drugs. Our work will also help to diagnose cancer.
To understand how genes change in cancer, our field has uncovered many gene mutations and deletions in patient tumors. However, we have not yet been able to create treatments that can combat many of these changes. This research proposal will test the potential for new combinations of medicines to treat tumors with a common gene many cancers need on for survival, PRMT5. A number of aggressive tumor types have PRMT5 as a drug target including lung cancer which remains the leading cause of cancer-related deaths in the U.S. and pancreatic cancer where >90% of patients with this disease will succumb to it. We need to make better medicines to treat these cancers.
We will test our ability to drug PRMT5 protein in lung tumors in combination with other new drug targets. This work will provide fundamental insights into mechanisms of PRMT5 function and reveal new strategies to treat an aggressive and deadly form of cancer. It is necessary that we test and design effective, rationale combination therapies in cancer. These efforts aim to effectively kill tumors and to avoid tumors coming back in the patient.
This work could lead to clinical trials in the future that would directly benefit cancer patients and their families. My goal is for our laboratory to contribute to mentoring young scientists and to improving cancer treatment for patients. This V scholar award will help me to achieve my goals by providing additional support, mentorship, and scientific exchanges.
Funded by the V Foundation Sonoma Epicurean in honor of Dustin and Johanna Valette
Myelodysplastic syndrome (MDS) is a blood cancer in which the bone marrow is unable to make enough healthy blood cells, and patients are at risk of developing a more aggressive leukemia. Besides stem cell transplantation, there is only one treatment option that has been proven to be effective at extending life for patients with MDS. Unfortunately, this drug still often fails, leaving patients with no other options. Recently, a new idea to enhance the immune system’s ability to fight cancer has been developed and successfully applied to other types of cancer. These new treatments (called immune checkpoint inhibitors) help the immune system better recognize and attack cancer cells. However, these treatments do not work in MDS. Here we propose a new immune checkpoint protein, which is found at high levels in the bone marrow MDS patients. Using mice transplanted with human MDS cells, we will study whether this protein hinders the ability for the immune system to fight MDS and whether we can block this protein to treat MDS. This study will let us understand how MDS avoids the immune system and help us find new treatments to enhance the immune system, leading to better outcomes for patients with MDS.
Funded with support from Hockey Fights Cancer powered by the V Foundation presented by AstraZeneca
Lung cancer is a deadly disease. This lethality is due, at least in part, to how often and how extensively these cells can spread throughout the body. My laboratory is working to understand what causes these cancer cells to spread and how they survive this process. By doing so, we hope to identify new ways to treat lung cancer.
We are interested in the nutrients cancer cells use to support growth and how these nutrients might help cancer cells spread. We are particularly interested in fats, or fatty acids. These complex nutrients play many different roles in cells, including helping to maintain cell structure, storing energy, and even acting as a method of communication with other cells. When we measured fatty acids in lung cancer, we saw that several fats and fatty acid pathways were different in tumors that spread throughout the body, compared to tumors that did not. In this study, we investigate how fatty acid metabolism supports aggressive cancer cells, and we will test whether blocking these fatty acid pathways can prevent lung cancer cells from spreading.
Glioblastoma (GBM) is the most frequent and deadly malignant brain tumor. Escape from the body’s immune response is a critical factor that makes GBM untreatable. One promising anti-GBM strategy is to augment the tumor-fighting capacity of immune cells. CD8+ T cells have the potential to kill tumors, but cancers make them not function properly. Strategies that aim to prevent this process have not been successful in GBM yet. We recently found that a molecule named dipeptidyl peptidase 4 (DPP-4) is present on dysfunctional T cells at high levels. Furthermore, we observed that DPP-4 prevents CD8+ T cells from killing tumors. In this application, we aim to determine how DPP-4 reprograms T cells to a nonfunctional state. DPP-4 inhibitors are commonly used by patients with diabetes. We seek to repurpose these drugs in combination with existing immune-activating strategies to improve T cell response against GBM. Collectively, these studies will define DPP-4 as a new treatment target in GBM.
Radio- and chemotherapy work by damaging the DNA of cancer cells, but malignant cancers, like glioblastoma, often regrow more resistant to therapy. Surprisingly, treated tumors don’t always have new mutations in their DNA, prompting the question: How did treatment change the tumor?
We believe that non-genetic chemical “scars” on DNA from therapy make cancer cells more aggressive. This theory is hard to study because radio- and chemotherapy cause random DNA damage. To overcome this, we developed an experimental system that creates DNA damage at precise locations, providing a clear map of the damage.
Our research shows that DNA damage leaves non-genetic changes in cancer cells’ blueprints, such as DNA methylation and changes in gene expression. We believe these non-genetic changes help cancer cells behave more aggressively and resist treatment. By understanding how these alterations occur, we aim to develop therapies that prevent cancer cells from adapting to treatment.
