Researchers have identified crucial elements that influence the progression of rare lung tumors.
Pulmonary carcinoids are uncommon lung tumors that exhibit highly varied clinical behaviors. For many patients, these tumors act benignly, and surgical removal can result in a complete cure. However, other patients may experience aggressive tumor growth and spreading (metastasis), which significantly reduces the chances of recovery. The biological reasons for these different disease manifestations remain unclear. In a collaborative study, scientists from the Experimental Pediatric Oncology Department at University Hospital Cologne and the Department of Translational Genomics at the University of Cologne have found a link between the progression of pulmonary carcinoid tumors and the activation of the TERT (telomerase reverse transcriptase) gene. Their research, titled ‘TERT Expression and Clinical Outcome in Pulmonary Carcinoids,’ has been published in the Journal of Clinical Oncology.
“This study is the first to provide a molecular explanation for the aggressive behavior seen in certain pulmonary carcinoids,” said Dr. Lisa Werr, the lead author.
The TERT gene facilitates the production of telomerase, a protein crucial for maintaining chromosome ends (telomeres). This enzyme is typically inactive in most healthy cells, restricting their ability to divide. In contrast, telomerase activation in stem cells and cancer cells grants them unlimited division potential, rendering these cells effectively immortal and enabling perpetual growth.
The researchers discovered that aggressive pulmonary carcinoids show TERT gene activation, whereas telomerase remains inactive in carcinoids associated with benign behavior. They had previously observed a similar pattern with neuroblastoma, a common childhood cancer, where its poor clinical outcome was also linked to the presence of mechanisms that stabilize telomeres.
“These study findings could lead to more accurate predictions regarding disease progression, allowing for treatment intensity to be tailored to individual patient needs,” stated Professor Dr. Matthias Fischer, head of the Department of Experimental Pediatric Oncology at University Hospital Cologne and one of the study’s leading authors. Professor Dr. Roman Thomas, director of the Department of Translational Genomics at the University of Cologne, added: “These results indicate that the activation of telomere stabilization mechanisms is a significant characteristic of malignant cancers that sets them apart from benign ones. Developing targeted treatment strategies against telomere stabilization mechanisms could enhance treatment options for a variety of cancer types in the future.”
