Page 36 - Hormel Institute Annual Report 2021-22

Luke Hoeppner, PhD
“Our ultimate goal is to improve human health by developing better strategies to treat human disease.
Understanding the molecular basis of human disease,
including cancer, cardiovascular disease, and lung
injury, will help achieve this goal.”
Luke Hoeppner
36 | THE HORMEL INSTITUTE Cancer Biology
ASSISTANT PROFESSOR
// UNIVERSITY OF MINNESOTA
Our research group studies several aspects of human disease, including vascular per- meability, cancer progression, metastasis,
the development of resistance to cancer therapy, and adverse effects of cancer therapy. We are focused on better understanding the molecular mechanisms and signal transduction pathways that control these disease processes. One primary goal of our laboratory is identifying molecular and cellular mechanisms that enable tumors to initi- ate, grow, invade other organs, and resist therapy. Using this new knowledge, we aim to develop innovative approaches to prevent, predict, diagnose, and treat cancer. Our team is also investigating the molecular regulation of vascular permeability, a process that plays a role in the pathology of cancer, stroke, cardiovascular disease, retinal conditions, and COVID-19-asso- ciated pulmonary edema, sepsis, and acute lung injury. Our group consists of talented postdoctoral fellows, Dr. Li Wang and Dr. Joas Lucas Da Silva, who is co-mentored by Dr. Leena Hilakivi-Clarke. Dr. Sk. Kayum Alam is an outstanding Senior Scientist leading most of our group’s lung cancer research. We had the pleasure of hosting a dedicated SURE intern, Rhiannon Skauge, during the Summer of 2022, and she contributed to a new project investigating the role of cilia in the development of resistance to cancer therapy.
Combating non-small cell lung cancer resistance to targeted therapy
Many non-small cell lung cancer patients are diagnosed with advanced disease and tested for specific tumor-causing mutations, including those that frequently occur in a gene called EGFR (i.e. epidermal growth factor receptor). EGFR mutation positive advanced stage lung cancer patients benefit from treatment with drugs designed to inhibit EGFR signaling. Unfortunately, most patients develop resistance to these drugs within 12-18 months and rapid cancer progression recurs. New approaches to predict and prevent acquired resistance to EGFR inhibitors are urgently needed. We have shown that DARPP-32 is upreg- ulated as lung cancer patients develop resistance to EGFR inhibitors. This project is admirably led
by Dr. Sk. Kayum Alam with the support of a generous Fifth District Eagles Telethon Postdoc Award and The Windfeldt Cancer Research Award. We recently discovered a DARPP-32-mediated, ERBB3-dependent mechanism lung cancer cells use to evade EGFR inhibitor-induced cell death, potentially paving the way for the development