Page 36 - Hormel Report 2023

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
ASSOCIATE PROFESSOR
// UNIVERSITY OF MINNESOTA
Our research group is focused on better understanding the molecular and cellular mechanisms that control disease
processes, including vascular permeability, cancer progression, metastasis, acquired resistance to cancer therapy, and adverse effects of cancer 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, pulmo- nary edema, 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 focused on lung cancer research. We recently welcomed a new postdoctoral fellow, Dr. Anuradha Pandit, to our research team, and she’s already making important contributions.
Identifying New Strategies to Prevent Therapy-Refractory Lung Cancer Progression.
Lung cancer is the leading cause of cancer death in the US and worldwide. Small cell lung cancer
(SCLC) is the most aggressive form of lung cancer. We are currently studying the role of dopamine signaling in SCLC initiation, progres- sion, and acquired resistance to chemotherapy. We are investigating whether targeting dopamine signaling (through a dual cell type approach: activation of dopamine signaling in tumor-associated endothelial cells and abroga- tion of DARPP-32 isoforms in tumor cells) will inhibit SCLC progression and acquired drug resistance to improve the clinical outcome of SCLC patients. We have shown that DARPP-32 and t-DARPP promote SCLC growth and prolif- eration (British Journal of Cancer, 2020). This research is supported by a four-year Research Scholar Grant from the American Cancer Society.
We are investigating mechanisms of resistance to targeted therapies in non-small cell lung cancer (NSCLC). We recently discovered a DARPP-32-mediated, ERBB3-dependent mechanism NSCLC cells use to evade EGFR inhibitor-induced cell death, potentially paving