Mays Cancer Center identifies possible markers to detect metastatic lung cancer sooner
Mays Cancer Center Annual Report
Researchers at Mays Cancer Center at The University of Texas Health Science Center at San Antonio have identified protein markers that could signal the development of metastatic lung cancer sooner – making it possible for new treatment.
The findings led to a five-year, $1.6 million grant from the National Cancer Institute of the National Institutes of Health, paving the way for a clinical trial for patients with advanced lung cancer.
“For the trial, we are looking to recruit patients with lung adenocarcinoma, the most common primary lung cancer in the United States, and particularly those with a refractory condition for which treatment hasn’t been effective,” said Josephine A. Taverna, MD, lung oncologist at Mays Cancer Center and associate professor in the Division of Hematology and Oncology at UT Health San Antonio and principal investigator of the grant.
The research by Taverna and her colleagues indicates that certain proteins known as AXL and STAT3 together transmit signals that appear in more advanced stages of lung cancer. This signaling, triggered by lung cancer cells and cancer-associated cells, helps tumors grow and spread to other organs.
“These findings suggest the potential application of AXL-STAT3-related markers to quantitatively assess metastatic potential and inform therapeutic strategies in lung cancer,” Taverna said. “It provides a therapeutic rationale for targeting this network.”
The research may help scientists develop tools for early detection as well as new treatment strategies. The researchers analyzed 15 lung tumors from 13 patients with lung adenocarcinoma, one patient with squamous cell lung cancer and one patient with pleiomorphic carcinoma. They found predominant and consistent AXL-STAT3 signaling in the tumor and other cancer-related cells.
“Our experiments in the lab suggest that targeting the AXL-STAT3 pathway can prevent tumor cells from recruiting tumor-associated macrophages and other aggressive host cells into the tumor microenvironment, thereby inhibiting tumor growth and spread,” Taverna said.
