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.
Funded by the Stuart Scott Memorial Cancer Research Fund with support from Hockey Fights Cancer powered by the V Foundation
Cancer happens when certain genes change and cells grow out of control. New efforts look closely at each patient’s tumor so researchers and doctors can pick treatments that shrink that tumor. This is important for finding ways to treat pathways that are hard to target with drugs. One of the hardest to fix is TP53 (also called p53), the gene most often changed in cancer. Because p53 helps normal cells work, trying to target it directly can cause harmful side effects. To get around that, our research studies two related genes, TP63 and TP73, which can do some of the same jobs as p53 to stop tumors from growing. Our earlier V Foundation funding in 2005 helped us discover new roles for TP63 and TP73, and now we plan to use the pathways they control to make up for lost p53 function. This idea may work better than trying to fix p53 directly, since those methods are often only partly effective or only work for certain mutations. We also found special non-coding RNAs that affect how tumors grow and respond to treatment. The new therapies we propose aim to target tumors precisely and cause less harm to patients. Although we focus on lung, breast, and ovarian cancers, these approaches could help any cancer with TP53 mutations.
Funded by the Stuart Scott Memorial Cancer Research Fund
Prostate cancer risk runs in families. A man’s risk of prostate cancer roughly doubles for every close family member who has been affected. Men in the family also tend to share how aggressive the cancer is. For example, how long a father survives with the cancer is strongly predictive of a how long a son will survive with the cancer. Studies have uncovered genetic risk factors for prostate cancer that distinguish which men are at high risk. But these factors poorly predict disease course. Two separate features of a cancer predict how aggressive it will be. These are 1) how abnormal the cancer cells are and 2) extent of cancer spread. Using such clinical features, two-thirds of cases are thought to be less aggressive and follow a watch-and-wait strategy. But over half advance and require active treatment. Ability to better recognize the path that the cancer is likely to take is needed. This is a study to discover the factors passed down in families that guide this path. The study also tests whether these factors predict which men followed by watch-and-wait will advance and require treatment.
Acute myeloid leukemia (AML) is a fast-growing blood cancer that is hard to cure. Even with today’s treatments, fewer than 1 in 5 people are alive five years after they are diagnosed. Many patients do well at first and are told they are in “complete remission,” which means doctors cannot find cancer with standard tests. But the cancer often comes back.This happens because a small number of leukemia cells survive treatment. These are called minimal, or measurable, residual disease (MRD). MRD cells are hard to find and hard to destroy. They can hide in the body, resist drugs, or change over time. Doctors are getting better at finding MRD, but we still do not fully understand why these cells survive or how they are different from the original cancer.This project aims to learn what makes MRD cells different and how to target them. Our early work shows that MRD is not just a smaller amount of leukemia—these cells act differently and depend on certain survival pathways. We have collected samples from more than 120 AML patients at different stages: diagnosis, remission, and relapse. Using advanced tools, we will study these cells closely to find new treatment targets. Our goal is to develop better treatments that remove MRD, stop the cancer from coming back, and help more patients stay in remission and be cured.
Some cancers are very hard to treat because they grow fast and stop responding to therapy. One example is a group of tumors called tuft-like cancers. These cancers can form in several organs, including the lung. Patients with these tumors often have few treatment options, and the disease can progress quickly.Our research focuses on finding a new way to treat tuft-like cancers. Our lab discovered a drug target that appears to be very important for the survival of these cancer cells. Early studies show that blocking this target can slow tumor growth in laboratory models.This treatment may also help the body’s immune system fight cancer. In other words, hitting this target may deliver a “one-two punch.” The drug could weaken the tumor while also helping immune cells attack it.In this project, we will study how this target helps tuft-like cancers grow and survive. We will test drugs that block it in models that closely resemble human cancer. We will also study patient tumor samples to learn how these cancers interact with the immune system.Our goal is to move this discovery closer to clinical trials. If successful, this work could lead to the first targeted treatment for tuft-like cancers and give new hope to patients facing this aggressive cancer type.
Cancer cells often live in a state of genetic chaos. This makes them hard to kill with existing drugs and allows cancer to spread to other parts of the body. We wanted to find out why this happens so we could stop it. We discovered that this chaos helps cancer cells hide from the body’s immune system. Usually, the immune system finds and kills cancer cells, but these cells stay invisible. To fix this, we created a new medicine. It targets the chaotic cancer cells but does not affect healthy cells. This drug turns the cancer against itself. Instead of hiding from the immune system, the cancer cells now send out a signal. This signal tells the immune system to come and destroy them. We are now testing this new medication on different types of cancers that are otherwise difficult to treat. If it works, it could lead to new treatments that save many lives.
Cac Patients with cancer suffer from weight loss. This loss is due to the loss in skeletal muscle. Patients with cancer are vulnerable to muscle loss. Patients with muscle loss also respond poorly to their treatment which lowers their survival. There is no cure for muscle loss in cancer. Therefore, understanding the causes of muscle loss may lead to new therapies. Our laboratory studies how cancer promotes muscle loss. In this proposal, we identify an inflammatory factor. Our goal is to determine how this factor causes muscle loss. Importantly, this same factor also promotes cancer. Thus, our studies might understand how this factor functions in both cancer and muscle loss.
Our research tries to understand the very earliest stages of blood cancer formation. The goal of this project is to use the processes by which these initial cells use to become cancer against them to develop a new treatments. In our study of the earliest stages of blood cancer development, our research has identified one way these cancer-forming cells are to live much longer than normal cells, which contributes to their increased growth in the bone marrow. We have identified a specific process these cancer forming cells use to live much longer than normal. This discovery is important because it opens up a new treatments. There is a drug that inhibits the same specific process we show these early blood cancer cells use grow faster. In this project, we will use this drug in our experiments and on cells from blood cancer patients to determine if it can preferentially kill these cells compared to healthy bone marrow cells. Most blood cancers currently have no cures. Our goal is to bring new treatment options for these patients. Ultimately, we hope that such approaches can even be used for blood cancer prevention.
All cells in the human body have the same DNA, but different types of cells do different jobs. This happens because cells follow extra instructions that tell them how to behave. These instructions are part of a system called epigenetics. One important epigenetic marker is called DNA methylation. It is a small chemical tag on DNA that helps cells work the right way.In many aggressive cancers, large parts of the DNA lose these chemical tags. When this happens, the cancer often grows faster and is harder to treat. Until now, we have not known how to use this information to help choose better treatments.We found that cancers with low DNA methylation have a weakness. Their cells depend strongly on a growth signal called AKT to survive. Drugs that block AKT can slow down or kill these cancer cells. When AKT is blocked, the cancer cells become even more dependent on another system called PRC2, which helps control which genes are turned on or off. By blocking both AKT and PRC2 at the same time, we were able to kill cancer cells much more effectively.Based on these results, we believe low DNA methylation can be used to provide a clue that helps choose the best treatment. We plan to test drug combinations in a clinical study and develop simple tests to see how well the treatment works. If successful, this approach could lead to a more personalized treatment for patients with cancer.
Funded by the Dick Vitale Pediatric Cancer Research Fund with support from Constellation Gold Network Distributors and Hockey Fights Cancer
Children with Down syndrome have a higher chance of getting blood cancer called leukemia. Many babies are born with a condition called transient abnormal myelopoiesis (TAM). TAM starts before birth and causes too many immature blood cells to grow. In most babies, TAM goes away on its own. But in some, it can be very serious or later turn into leukemia. Right now, doctors do not know why this happens or how to tell which babies are at risk.In this study, we will use new tools to look at single blood cells to learn more about how TAM starts, how it changes into leukemia, and why treatments sometimes stop working. We will study blood and bone marrow samples from children at different stages of the disease, as well as from pregnancies with Down syndrome, to find out when and where the first changes begin.Our goal is to find better ways to predict which babies with Down syndrome will get leukemia and to develop safer, more effective treatments. This work could improve survival and quality of life for children with Down syndrome and their families.
Funded by the Dick Vitale Pediatric Cancer Research Fund with support from Constellation Gold Network Distributors
Burkett’s lymphoma and neuroblastoma are two different types of childhood cancers that share a common link: the MYC gene. Chemotherapy is often used for treatment, but the side effects can be hard on young patients. Doctors and researchers now know that the side effects are mostly from blocking the growth of both cancer cells and healthy cells. Chemotherapy also does not work well for some patients. Our research focuses on drugs that target MYC to safely slow the growth of cancer cells. We will test these new drugs in the laboratory for future development into medications for patients. In the end, our work will produce better medicines to treat these cancers without giving up patient comfort.
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.
