Canine acute myeloid leukemia (AML) is an aggressive blood cancer in dogs that causes severe illness and very short survival times. This project will use existing gene expression data to identify which biological pathways are “switched on” in AML and how they relate to disease features.

Dogs with AML often present with extreme tiredness, pale gums, poor appetite, weight loss, bleeding, and infections. Current treatments are based on older human protocols and usually only extend life by a few weeks to months. Unlike human leukemia, where genetic and molecular testing now guide targeted therapies, most canine AML cases are still classified only by cell appearance and a small panel of surface markers. We lack a clear, pathway-level picture of what is driving the disease in dogs.

In this study, I will analyze existing bulk RNA sequencing data from dogs with AML and other forms of acute leukemia. RNA sequencing measures which genes are active in a sample. Using this information, I will calculate pathway “activity scores” for each dog, focusing on important signaling and immune pathways. I will then compare these pathway patterns between AML and other leukemias and examine how they relate to simple clinical features such as fever, infection, or very short survival.

Potential Impact: This work will generate a pathway-level map of canine AML, identifying which signaling and immune pathways are most consistently dysregulated. The results will help identify the most promising pathways and genes to target in future mechanistic studies and drug trials. In the long term, this information could support more precise diagnosis and better, more rational treatment options for dogs with AML, and may also contribute to comparative leukemia research that benefits both animals and people.