Margaret Miao
Research Mentor: Qing Li
Mentor Department: Medicine Division of Hematology & Oncology, Medicine
Author(s): Margaret Miao, Erin Kropp, Olivia Wang, Jineigh Grant
Session: Session 4 (1:00 PM – 1:50 PM)
Presentation Type: Poster 81
Abstract
Multiple myeloma (MM) is formed from the neoplasm of plasma cells, which normally secrete antibodies as part of the immunal response. The mutated plasma cells produce high and often uncontrollable amounts of antibodies – called M proteins. Despite advances in MM therapies, patients with MM have higher remission rates after therapies and the cancer remains incurable. A new effective first line therapy, proteasome inhibitors, are cytotoxic to myeloma through inhibiting a protein quality control pathway called Endoplasmic Reticulum Associated Degradation (ERAD), accumulating a high amount of mis-folded secreted proteins in the endoplasmic reticulum and triggers ER stress resulting in the cell undergoing apoptosis. While proteasome inhibitors are effective, developing proteasome inhibitor resistance is very common and results in proposed or refractory disease. We are attempting to target other proteins in the ERAD complex to overcome proteasome inhibitor resistance. Currently, we are trying to figure out whether targeting alternate ERAD complex proteins is cytotoxic to MM. Our laboratory performed small molecular drug screening and identified new ERAD inhibitors. Now, we will perform cell viability assays to test how these inhibitors are cytotoxic to MM as well as immunoblotting to determine the target protein in the ERAD complex. Our purpose in studying the ERAD complex is to find novel treatments for relapsed refractory MM in order to increase patient survival rates.
