Cancer cells gain immortality through the continual extension of the protective ends of chromosomes, packaged segments of DNA. In most cells in adults, limitations with DNA replication cause these telomeres to get shorter with each round of cell division—eventually, the cells die, called replicative senescence. However, in many cancers, an enzyme called telomerase, normally only expressed in continuously proliferating stem cells, is expressed, providing a template allowing telomeres to be continually extended and the cells to keep proliferating. However, about 15% of cancers can extend their telomeres without using this canonical process. Instead, they use a mechanism similar to homologous recombination (HR), in which the telomere of another chromosome is used as a template for elongation—this is called Alternative Lengthening of Telomeres (ALT). Some of the most intractable cancers, such as breast, pancreatic, and hematological malignancies, have a much poorer prognosis when ALT-positive. My research centers on the function of the BLM helicase, a protein that promotes ALT by unwinding DNA at the telomere and resolving intermediates to complete the process. As part of my project, I worked on characterizing the functional domains of this protein, understanding the phenotypic effects of nonfunctional BLM using IF-FISH fluorescence microscopy, and helping analyze the intermediate DNA structures that are created in the process, allowing us to understand the fundamental mechanisms driving ALT.