State: Washington

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

Acute myeloid leukemia (AML) is the deadliest blood cancer. People with AML are treated with chemotherapy, a treatment intended to kill cancer cells. However, some AML cells have qualities that prevent them from being killed with chemotherapy. These cells remain in the body even after treatment. Unfortunately, these “chemotherapy-resistant” AML cells can cause relapse. People with AML achieve remission when doctors can no longer detect AML after treatment. Relapse occurs when the previously undetectable AML returns after remission. Relapse is the primary cause of death for AML patients. Unfortunately, ~30% of all AML patients will relapse within three years of their diagnosis. Our research goal is to understand why some AML cells survive chemotherapy and others do not. We aim to identify new treatments that target chemotherapy-resistant AML cells.

Certain proteins produced by many cells in the body have sugars attached to them. In AML cells, we found that the kind of sugar attached to these proteins determines growth rates and response to chemotherapy. In this proposal, we will test how specific categories of sugars control AML cell growth, chemotherapy resistance, and relapse. We will use mouse models of AML to test how drugs that change the sugars available to AML cells could be used to treat AML. We expect the proposed studies will pave the way for identifying new medicines that can be used to stop AML cells from resisting chemotherapy, prevent relapse, and support AML patient survival.

Funded with support from Steve and Tamar Goodfellow

Colorectal cancer (CRC) is the third most common cancer worldwide and ranks as the second leading cause of cancer-related deaths. Screening plays a key role in early detection and makes CRC one of the most preventable cancers. Developing an accurate risk prediction score is crucial because it helps us identify and focus on those at high risk from a young age, enabling early screening and effective intervention. Research has shown that thousands of genetic mutations can increase the risk of developing CRC. Our goal is to convert these genetic discoveries into useful tools for clinical use. We plan to utilize advanced techniques such as CRISPR screening technology and single-cell sequencing, combined with deep learning models and statistical analysis. This approach will help us understand the whole impact of these genetic mutations better. This work aims to provide deeper insights into how these mutations contribute to the development of CRC, leading to more targeted and efficient screening strategies. Ultimately, our research is directed toward developing a sophisticated method for predicting colorectal cancer risk, focusing specifically on those who are most at risk. This could significantly change how we prevent and treat colorectal cancer.

Funded by the Dick Vitale Pediatric Cancer Research Fund with support from the Scott Hamilton CARES Foundation

One major challenge in treating any type of cancer is resistance, or when a cancer stops responding to a certain type of drug or therapy. Some cancer cells may become resistant my changing the way they read and write their DNA, or the genetic blueprint in the cell nucleus. Other cells may change the way proteins are expressed on the surface, which can change their shape or ‘stickiness’ and ability to move in the body.  When doctors can understand exactly how cancer cells become resistant to a certain drug, they can sometimes combine two or more drugs together to overcome this.

For some new classes of drugs, we have not even begun to explore how cancer cells might become resistant. One of these classes is nanoparticle drugs, which usually involves bringing together molecules like fats or polymers to help delivery drugs into certain cells. The goal of this research project is to identify the ways that pediatric cancer cells can become resistant to nanoparticle drugs, and find new drug combinations that are more effective and less toxic to children with cancer. Many lab-based studies of nanoparticles are performed in common cancers of adulthood such as breast cancer, and this has led to new treatments in the clinic, but there have been very few studies of nanoparticle drugs in childhood cancer. Currently, there is only one nanoparticle drug approved for use in children. By studying resistance to nanoparticle drugs in a deadly childhood brain tumor, we can take the first step towards a new clinical treatment for these children.

Funded by the Stuart Scott Memorial Cancer Research Fund and the V Foundation Wine Celebration in honor of Leo Slattery, 2022 Volunteer Grant Honoree

A big part of the sequences that make our DNA come from viral infections that occurred in the past. These viral ‘fossils’ are typically not active to prevent damage to our genetic material, however in many diseases, including cancer, they are turned on. While it might be logical to think that the activation of these sequences would be a bad thing, evidence suggest that some of these viral fossils were repurposed to perform functions needed for a healthy life. In fact, some viral sequences participate in the formation of the placenta, in the way our genes are activated, and in the way our cells fight other viruses. Therefore, it is possible that the reason we see these viral fossils turned on in cancers is because they are helping the body fight the formation of tumors. Our goal is to test different ways by which the activation of these viral fossils could help prevent and fight cancer. To do this we will search for all the viral fossils present in our DNA, identify sequences that help our bodies find and destroy tumor cells, and test if one special viral fossil is able to prevent tumors by turning off its energy supply. We hope our findings can help the design of novel ways to treat cancer, taking advantage of the potential beneficial roles of these ancient viral sequences.