Tanay Bhangale
Pronouns:
Research Mentor(s): Dipankar Ray
Co-Presenter:
Research Mentor School/College/Department: Radiation Oncology / Medicine
Presentation Date: April 20
Presentation Type: Oral5
Session: Session 4 – 2:40pm – 3:30 pm
Room: Breakout room 4
Authors: Tanay Bhangale, Dipankar Ray
Presenter: 3
Abstract
The exact biological mechanism underlying the progression from Barret’s esophagus (BE) to Dysplasia to Esophageal Adenocarcinomas (EAC) is highly unknown. Over the last 40 years, the incidence of EAC has increased over 700 percent in the US, making it one of the fastest-growing cancers in the world. Previous studies have shown that the majority of EAC cells contain TP53 mutations, which are heavily regulated by the Interferon-stimulated gene 15 (ISG15). ISG15 is a protein that affects other proteins in a very similar process to ubiquitination, termed ISGylation. In this study, we aim to target a specific protein, Inducible Nitric Oxide Synthase (iNOS), vital to the activation of ISG15. Using immunohistochemistry on EAC and BE cell lines, we seek to form a connection between iNOS protein levels with the levels of ISG15 levels as the progression from BE to EAC takes place. We are using the CpA, CpB, CpC, and CpD Barret’s esophagus cell lines and OE33, OE19 and Flo1 and analyzing 65 patient sample mRNA data. We expect to see a higher level of iNOS and ISG15 mRNA levels in the EAC cell lines compared with the BE cell lines using a novel method of visualizing a pathway using BioRender and Excel. Therefore, we aim to decrease the amount of iNOS protein in BE cells to curb their progression to cancer.
Biomedical Sciences, Interdisciplinary, Natural/Life Sciences
