AUSTIN — With a new $150,000 grant from the Lung Cancer Research Foundation, Luke Hoeppner and his colleagues at the Hormel Institute in Austin are doing more research to figure out why certain lung cancers become resistant to treatment.
"We're trying to understand the basic science of how these lung cancer cells acquire resistance to a treatment that's initially very effective," said Hoeppner, associate professor and cancer biology section leader at the institute.
Hoeppner's research looks at non-small cell lung cancer, the most
common type of lung cancer and the leading cause of cancer-related death in the world. About 238,000 new cases of lung cancer are diagnosed each year in the U.S., Hoeppner said, and 127,000 Americans die from the disease each year.
"The primary reason that it is so fatal is that lung cancer is often not diagnosed early," he said. "If you think about breast cancer or prostate cancer or colon cancer, screening methods are in place for all those malignancies. Whereas in lung cancer, there's just not as much early detection for a variety of reasons."
When patients are diagnosed with non-small cell lung cancer, they are tested for a mutation in a gene called epidermal growth factor receptor (EGFR), which factors into cell growth. If a patient has a EGFR mutation, Hoeppner said they are typically treated with EGFR tyrosine kinase inhibitors that keep cancer cells from growing.
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"The EGFR inhibitor drugs work very well for the first several years of treatment," Hoeppner said. "But then many patients eventually, unfortunately, develop resistance to EGFR inhibitors, and the lung cancer progresses rapidly."
Hoeppner's research aims to understand how cancerous cells develop a resistance to that medication. That knowledge could lead to more effective treatments for this type of cancer.
"Our pilot data started uncovering that mechanism," he said. "And our new grant is focused on exploring it to a greater extent."
In his lab's preliminary research on EGFR inhibitor drug resistance, Hoeppner said a molecule similar to EGFR, ERBB3, plays a role in developing resistance to cancer treatment.
"We are using a drug that targets both EGFR and the other molecule, ERBB3, and we're showing that that can help overcome or prevent EGFR inhibitor resistance," he said.
Hoeppner's lab will explore this potential new treatment method for lung cancer patients over the next two years using cell models — lung cancer cell lines observed in petri dishes — animal models and specimens from lung cancer patients at Mayo Clinic, Minneapolis VA Medical Center and the University of Minnesota's Masonic Cancer Center.
"We're getting samples from those patients before they've been treated and then after they've unfortunately developed resistance to the drug," Hoeppner said. "And then we can do some immunostaining studies where we can assess the expression of a variety of proteins of interest ... and look at what's happening in the actual patient samples."
The ultimate goal: Predicting and preventing resistance to EGFR inhibitor treatment.
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"The long-term impact of our work lays the foundation for the development of new predictive markers to assist physicians and patients make the best treatment decisions," Hoeppner said. "Successful completion of the studies has the potential to lead to breakthroughs in predicting and preventing progression of EGFR TKI–refractory lung cancer and may lead to future clinical trials to treat NSCLC."
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