Anaplastic thyroid cancer (ATC) is a very dangerous type of cancer. Most people with this cancer only live a few months after doctors find it. The medicines we have now don’t work well. Sometimes the tumors get smaller at first, but the cancer almost always comes back. We need better ways to treat this disease.ATC is hard to treat because it tricks the body’s defense system. Our body has special cells that are supposed to fight cancer. But this cancer confuses some of these cells and stops them from attacking. When this happens, your body can’t fight back against the cancer. This study tests a brand-new way to treat cancer. Doctors take a small piece of each patient’s tumor and use it to make a special medicine just for that person. The medicine is packaged into tiny particles (called RNA-LPAs). These particles are designed to wake up the body’s defense system and teach it to find and attack the cancer. This treatment has never been tested on people with ATC before.In this early clinical test, patients will get the new treatment while doctors carefully check to make sure it’s safe. Doctors will collect blood and tumor samples to see if the body’s defense system is responding. This helps scientists learn if the treatment is working the way they hoped. If this works, it could help patients with ATC live longer. It might also help doctors treat other types of cancer that don’t respond to today’s medicines.
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.
The INTERCEPT‑HER2 study is testing a new vaccine for people with HER2‑positive breast cancer who have finished all standard treatments but still show tiny signs of cancer in their blood. These signs are called minimal residual disease (MRD). MRD cannot be seen on scans, but it can warn us that the cancer may return. Finding MRD gives doctors a chance to act earlier, when the cancer is very small and the immune system is still strong.The vaccine uses cancer proteins to train the immune system to find and attack cancer cells. Earlier studies showed that the vaccine is safe and can activate the immune system, so it may help stop the cancer from growing again. In this study, 45 patients who test positive for MRD in the blood will receive three monthly vaccine doses and then two booster shots. They will also have regular blood tests for up to three years to see if the cancer signals in their blood go down or disappear.The main goals are to learn whether the vaccine can delay or prevent the cancer from coming back and whether it can clear MRD from the blood. The study will also show how often people with breast cancer still have MRD after treatment. Blood samples will help researchers understand how the immune system responds to the vaccine. What we learn may guide a larger future study and could lead to new ways to stop breast cancer earlier, before it becomes harder to treat.
Funded by the St. Louis Blues in support of Hockey Fights Cancer powered by the V Foundation
Tumors of the throat (called oropharynx carcinoma or OPC) are on the rise in the US and worldwide. Most of these are caused by a virus, called human papilloma virus (HPV). Current treatment of these tumors is fairly effective. As a result, researchers have been trying to reduce treatment to avoid side effects and problems with speech, swallow, and taste. But a portion of OPC patients do not have good outcomes. We are interested in identifying these patients before treatment begins so we can give them the right treatments. We found that some cancer cells turn off virus expression and this makes them treatment resistance and causes poor survival. In this study, we will use human models of OPC to understand what turns HPV expression on and off. We will also learn how different cancer cells with or without HPV talk with other cells in the tumor environment such as fibroblasts and immune cells.
Funded with support from Calhoun Associates Abeloff V Scholar * (Tie for Top Rank)
Acute myeloid leukemia is an aggressive blood cancer. It affects thousands of people every year and often returns even after the newest targeted drugs. We have learned that, instead of dying, some cancer cells can “change their identity” to become a new blood cell type. These cells are called monocytes and they are able to escape therapy. This switch is like a costume change in a play: when the spotlight of treatment is on them, cancer cells put on a monocyte costume to hide. Later, when treatment eases, they can take off the disguise and return as cancer cells. We will test if these monocytes can turn back into cancer cells and cause disease to come back. We want to know how these cell changes happen and what helps them survive therapy. To answer these questions, we use new models that mimic patients’ cancer. We track how cancer cells looking at cell identity and genetic mutations. We also test new ways to block survival strategies, such as stopping the cells from becoming monocytes, in hopes of making current treatments work better and longer. By understanding and blocking the ways cancer escapes treatment, our goal is to develop strategies that keep patients in remission and improve survival.
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