The Blackburn lab is dedicated to tackling the challenges posed by pedantic cancers, specifically focusing on pediatric leukemias and brain tumors. We are committed to finding innovative treatments and identifying biomarkers to improve outcomes for young patients.
Our leukemia research is focused on uncovering new therapeutic approaches that specifically target the unique characteristics of these aggressive blood cancers. We aim to identify novel drug targets and develop innovative treatment strategies to minimize the long-term side effects often associated with conventional cytotoxic chemotherapies. Our ultimate goal is to improve the survival rates and quality of life for children battling leukemia.
Our research also focuses on Diffuse Intrinsic Pontine Glioma, a type of childhood brain tumor that poses a significant clinical challenge due to its location in the brain stem and aggressive nature. By studying the biology and genetics of DIPG, we hope to discover novel therapeutic targets and find new ways to make current treatments more successful.
We primarily use zebrafish as our model organism in our research. Zebrafish share remarkable genetic similarities to humans and offer unique advantages to studying cancer, its underlying mechanisms, and the best treatment methods. We generate cancers in zebrafish that closely mimic human disease. Our zebrafish are transparent, allowing us to visualize cancer progression in living animals so we can better understand how cancers develop and respond to treatment. The low cost of maintaining zebrafish enables us to use many animals for drug screening, so only the best and least toxic therapies move forward in our studies. Zebrafish cancer models provide us with valuable insight into cancer biology and potential treatment options.
Through our interdisciplinary approach that combines biochemistry, genetics, and translational research, we aim to make significant strides in pediatric cancer. Find out more about our current projects below and on our blog.
CURRENTLY FUNDED PROJECTS
The Role of PRL-3 in Cancer Progression
The National Cancer Institute gave us a two-year extension on my R37 MERIT award to study the role of PRL-3 in cancer! PRL-3 is important for cancer cells to invade and metastasize throughout the body, so is a very desirable drug target for both solid tumors and leukemias. This biochemistry-focused project will help us understand how cells regulate PRL-3 function, which will give us new insights into the best way to therapeutically target PRL-3. More details can be found on the blog!
New targeted therapies for DIPG
We are so happy to continue working with the Kentucky Pediatric Cancer Research Trust! They are generously providing funding for our project with Dr. Phoebe Glazer, in the Department of Chemistry at NC State, to develop new ways to target an important protein in DIPG called BRD4. We will use our zebrafish models to understand how a common mutation in DIPG, called H3K27M, works with BRD4 to cause tumor development and relapse. Dr. Glazer is developing a novel radiation-activated BRD4 PROTAC that we will test for activity in DIPG cells. Our hope is to shed light on DIPG biology, unveil new drug targets, and pave the way for effective treatments using cutting-edge medicinal chemistry techniques.
Mechanisms of DIPG Onset
Thanks to funding from the Chad Tough Defeat DIPG Foundation, we’re developing the first zebrafish model for DIPG! This is a devastating pediatric brain cancer with survival rates of <2%. We will create zebrafish with DIPG-related DNA mutations identical to humans to help us study how DIPG develops and why it is always resistant to radiation, the current standard of care. Zebrafish models will allow us to track DIPG progression in a way that is impossible to do in patient samples and mouse models. We will also use our models for large-scale in vivo drug screening to identify drugs that can successfully kill DIPG cells. Through this research, we hope to better understand DIPG biology and discover effective treatments to improve DIPG survival rates.
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