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.
Myeloid cancers are a group of blood diseases that happen when blood-forming cells in the bone marrow become abnormal. These changes often come from genetic mutations. One important mutation occurs in a gene called ASXL1, which is linked to the development of blood cancers and associated with poor prognosis. However, it remains unclear how ASXL1 mutations could drive blood cancers in humans. We recently found that, in younger mice, ASXL1-mutant blood stem cells do not grow out of control. But in older mice, these mutated cells do grow and expand. These suggest that aged bone marrow environment (BMM) may help these abnormal cells grow and cause leukemia. We also found that in older mice, the bone marrow has more inflammation and a higher number of stromal cells (cells that support blood cell growth), which can be mitigated by anti-aging therapy. In this project, we will study how aged BMM helps these mutant cells grow and test if targeting the aged environment alters the development of blood cancers. By understanding this process, we hope to find new ways to treat or even prevent blood cancers in humans.
Funded with support from Hockey Fights Cancer powered by the V Foundation presented by AstraZeneca
Cancer cells are always growing, and they need nutrients to keep up this fast growth. An exciting idea is that we might be able to starve cancer cells without harming healthy cells by getting rid of nutrients that cancer cells need. A drug being developed right now called ADI-PEG20 destroys a nutrient called arginine, which is an amino acid that is used to make protein and is particularly important for cancer cells. My lab studies what happens when cancer cells don’t have enough arginine. We want to understand how ADI-PEG20 works, how to improve it, and which cancers to treat with it. We have found that restricting arginine disrupts ribosomes, the machines that build new protein, causing them to get stuck and abandon their jobs early. We want to study three things to figure out how this impacts ADI-PEG20 treatment. First, why is protein production in cancer cells so sensitive to arginine levels? Next, what machinery in the cell is responsible for causing “starved” ribosomes to press the eject button in the middle of doing their jobs? Finally, what effect does this have on a cancer cell? This work will help us understand how a nutrient like arginine can directly control very important processes in the cell like protein production. It will also reveal how we can take advantage of cancer’s dependence on arginine to shrink tumors.
Multiple myeloma and AL amyloidosis are incurable cancers of blood cells. These blood cells are called plasma cells. There is only one therapy that is available for AL amyloidosis patients. In severe stages, AL amyloidosis patients survive less than one year. Amyloidosis plasma cells cause damage to the body by spilling in the blood a sticky protein. These sticky proteins attach to each other and build up in the heart. Buildup of proteins in the heart causes progressive poor function. AL amyloidosis is a major cause of malfunctioning of the heart and death. To cure AL amyloidosis, we need drugs that 1- stop plasma cells from spilling sticky proteins; 2- kill the cancer plasma cells; and 3-remove the buildup of sticky proteins from the heart. These drugs do not exist, because we do not know how sticky proteins get spilled and why the build-up is not removed.Recently, our lab found out how sticky proteins get out of amyloidosis plasma cells. We also showed that if we stop this process, cancer cells die. Finally, we discovered that cleaner cells that should remove sticky proteins from the heart are reduced and do not function in amyloidosis patients. Based on these data, we will make two novel drugs. One will stop spillage of sticky proteins and kill cancer cells. The other will remove sticky protein from the heart without the need of cleaner cells. Our work is doable and will create therapeutic options for AL amyloidosis patients that could cure their disease.
Every year, over 25,000 people need to have a stem cell transplant to treat their blood cancer. While this can cure their cancer, it also weakens the immune system. A weak immune system is a problem because it means people get more infections and can experience other complications like their cancer coming back. When we are healthy, our gut is filled with helpful bacteria. During cancer treatment, many patients lose these helpful bugs. Patients who lose the good bacteria after they have a transplant, don’t recover as well as patients who keep their helpful bugs. These good bacteria are needed for strong immune system recovery. We are working in the lab to find new ways to support healthy bugs during cancer treatment. We think this will help the patients’ immune system. Having a healthy immune system means fewer infections and a longer life. If successful, this research could lead to new treatments that help patients feel better during their transplant, avoid infections, and live longer. In the future, we will run clinical trials in transplant patients, which will lead to new standard treatments.
Funded by the Stuart Scott Memorial Cancer Research Fund
Pancreatic cancer is an extremely deadly disease, due to its ability to spread to other organs early and easily, a process known as metastasis. Molecules called purines are often used to build DNA and have been shown to be used by cancer cells to grow and survive. Pancreatic cancer usually spreads to the liver, an organ rich in purines. We find that pancreatic cancer cells, which contain mutations in certain genes involved in cell growth, prefer to use purines to uncontrollably grow and survive. Our study will identify how metastatic pancreatic cancer cells use purines to spread and survive in organs such as the liver. We will also test FDA-approved drugs used to treat other purine-dependent diseases such as gout and metastatic breast cancer to treat pancreatic cancer addiction to purines.
Cancer cells often change their DNA to make more of the genes that help them grow and spread quickly. They do this with special proteins called transcription factors that read DNA, and helper proteins that change the DNA to work better. In prostate cancer cells, a protein called androgen receptor (AR) is the main cause of cancer growth. This is different from how AR works in normal prostate cells, where it helps the prostate develop properly and stops extra growth. We don’t know exactly how AR’s function changes in prostate cancer cells. My research tries to figure this out. With help from the V Foundation Award, my team will study a new protein called NSD2 that works with AR. Notably, NSD2 is only found in prostate cancer cells, not the normal ones. We’ll also test a new drug that stops NSD2 from working and see how well it kills cancer cells in different types of prostate cancer. This research will help us find more proteins that make AR cause cancer and create new medicines that target NSD2 to treat prostate cancer.
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 with support from Ken Romanzi and Nancy Major Romanzi, M.D.
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.
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