Institute discovery could have impact on cancer therapy
The Hormel Institute’s Drs. Adrian Mansini, Estanislao Peixoto, Suji Jin, Kristen Thelen, and SURE intern researcher Maetzin Cruz-Reyes, along with lab section leader and professor Dr. Sergio Gradilone, published groundbreaking research in the high impact journal Hepatology.
The research is “critically important” because the team discovered the mechanisms underlying the ability of tumor cells to eliminate primary cilia of healthy cells, said Gradilone.
Primary cilia, performing as a cell’s antenna, are in almost every cell of the human body. Like an antenna, cilia work as tumor suppressors. The research team found that tumor cells have a mechanism that destroys the cellular antenna.
The article was published this week in what is considered the premier publication in the field of liver disease, according to Institute officials.
Hepatology publishes research concerning all aspects of liver structure, function and disease and each month, the editorial board selects the best articles on subjects such as liver cancer, immunology, chronic hepatitis and related liver diseases in the abnormal over-production of a protein that destroys the antenna.
“We are constantly seeking new treatments for cancer and this particular study focused on bile duct cancer,” said Gradilone. “This cancer has very limited treatment options but by identifying the key mechanisms that tumor cells use to eliminate cilia, we found new targets to induce the restoration of the cellular antenna as a therapeutic approach.”
Going forward, The Hormel Institute, University of Minnesota scientific team will expand on approach, referred to as “ciliotherapy,” as it may be applicable to other tumors. The loss of primary cilia has now been described in more frequent cancers like breast, pancreatic, kidney, ovarian, and colon, among others.
In collaboration with Mayo Clinic physicians and pharmaceutical companies, The Hormel Institute team is aiming to establish the first clinical trial to test the approach.