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Acute lymphoblastic leukemia (ALL), a cancer of the blood and bone marrow, is the most common cancer in childhood. Although cure rates now exceed 80 percent, cases of relapsed ALL are more common than most other forms of childhood cancers combined. Additionally, patients with early relapse of ALL face a grim prognosis. Understanding pathways of leukemia initiation, maintenance, and relapse is critical for detecting new potential therapeutic targets and predictive markers of relapse. Although extensive studies of leukemia genetics have yielded insights into the behavior of the disease and have led to improved treatment strategies, comprehensive understanding of all active and targetable pathways in ALL is far from complete. Additionally, the mechanisms of leukemia initiation are poorly understood.

In concert with his research mentor, Monica Justice, Ph.D., at Baylor College of Medicine, Dr. Simko is using mouse models on leukemia to discover mechanisms of cancer initiation. In particular, his lab is interested in novel oncogenes, which are genes that can trigger and promote cancer development when they are “turned” abnormally. By screening mice with spontaneously-forming ALL, they discovered that activation of a gene called Prdm 14 appeared to be the common pathway to leukemia development in a number of mice. This gene is active only during a short window in the early development of an embryo when cells lack specific function, can develop into multiple kinds of cells and can continuously renew themselves. This lack of specificity and ability for self-renewal, often referred to as a “stem cell-like” state, is a feature of many cancers. As Prdm14 has been shown by others to contribute to this state in the embryo, its role in cancer development became a focal point for Dr. Simko’s research.