Virtual Summit Submission

The University of Texas at Austin
Biomedical Engineering

Biography

William Merlini is a student at The University of Texas at Austin studying Biomedical Engineering while also hoping to pursue a Materials Science and Engineering Minor. Outside of classes, he tends to be involved in societies such as Biomedical Engineering Society (BMES) and UT Austin's e-NABLE chapter (for designing, manufacturing, and testing prosthetics for patients and underserved populations). He is academically interested in the intersection between immunotherapy in cancer research and drug discovery/delivery, being part of two research groups whose work encompass non-invasive drug delivery for neurological conditions, and mRNA vaccine formulation for lipid nanoparticles delivery in cancer applications, respectively. He is also part of another lab that works primarily with behavioral neuroendocrinological animal testing to obtain relevant experience with handling and working with animals in the lab. His professional goals in the future involve likely pursuing a PhD in cancer biology or immunotherapy to study drug involvement in cancer therapeutics. Outside of work, he enjoys playing tennis, table tennis, riding his bike with his roommates around Austin, watching movies and reading manga, and most importantly, traveling around the world.

Project

Analyzing the Loss of the Y Chromosome in Lung Tumor Formation Within Genetically-Engineered Mouse Models
This summer I traveled to Heidelberg, Germany, to work with a research group in the Molecular Thoracic Tumors Department at the German Cancer Research Center (DKFZ). Under the mentorship of a PhD student in the group, I investigated what happens when mouse lung cancer cells (specifically adenocarcinoma cells) lose the Y chromosome as a spontaneous event and whether this helps tumors grow by escaping the body’s adaptive immune system. The guiding questions were: does loss of the Y chromosome (LOY) correlate with increased oncogenicity (i.e., tumor induction) in mouse lung adenocarcinoma models; what specific genes on the Y chromosome are most responsible for this development, and what is the mechanism by which LOY influences tumor-immune interactions? To address these questions, I was taught and engaged work with various mice lung tumor cell lines under sterile cell culture settings; learned molecular staining techniques (e.g., Eosin and Hematoxylin, Immunohistochemistry, FISH) for lung tumor tissues such that they could be visualized under fluorescent light microscope settings. I also learned to operate on and dissect mice in order to extract organs affected by tumor metastases, which were viewed and separated for preservation under a microscope. CRISPR-Cas9 technology was also used to accurately identify target DNA sequences and edit them at specific nucleotides, yielding immunodeficient mice through which we were able to induce tumor growth over the course of various weeks. The broader implication is that LOY, previously considered a bystander genomic change, may actively enable tumors to hide from immune surveillance, making it a potential biomarker in clinical settings to predict who might benefit from immunotherapy and a reminder that sex-chromosome changes in cancer also contribute considerably in both research and treatment planning.