Jarrod Moore

As a graduate student in the Emili Lab, my research focuses on discovering protein networks that drive clinical pathologies; specifically, I am investigating the aberrant signaling pathways in diseases of the cardiac and upper gastrointestinal systems. Disease phenotypes, especially those affecting whole organs systems, are derived from heterogenous perturbances in gene expression and biochemical pathways. Over the past decades, research in fields like oncology have highlighted that classical characterizations of disease may fail to capture this variation. Accordingly, medicine is challenged with providing more precise treatment, that is, therapeutics that are specific to patients’ cellular disturbances (i.e. personalized medicine). In order to help bridge this gap, I use in vitro models and patient samples to generate massive proteomic profiles, which with the aid of bioinformatic tools, help identify target pathways that potentially cause the overall phenotype.

I received my undergraduate degree at Boston University, where I gained my first research experience in the Buston Laboratory. There, my work focused on quantifying the evolutionary benefits of parental behavior via offspring viability. Through Dr. Buston’s mentorship, I was able to design my first experiments that eventually granted me funding through fellowships. More importantly, this experience introduced me to academic research, which has rewarded my curiosity and my passion for learning. Now, as an MD/PhD student, I have completed the first two years at Boston University School of Medicine and have taken USLME STEP 1. Though I am new to the doctoral program, I’ve received excellent professional guidance from Dr. Schreiber and Dr. Layne. Reflecting on my journey so far, I am confident that the biochemistry department will support me through the challenges of graduate school, and that I will be prepared to contribute to medicine and academia as a physician-scientist.

My current project is focused on Barrett’s Esophagus (BE), a disease of the lower esophagus. BE is a metaplastic change (from stratified squamous to columnar) caused by chronic acid reflux and is of clinical interest because it is believed to be a pre-cancerous lesion of esophageal adenocarcinoma (a rare, yet very morbid cancer). Perplexingly, though BE is common very few patients with BE develop this cancer. Using patient biopsies, I hope to elucidate the protein signal pathways that drive the disease and discover novel protein signatures that could help stratify patients based on cancer risk. Ultimately, I aim to study the disease mechanisms and provide biological markers to clinicians that will bolster treatment options.