King’s College London develops imaging tool to track cancer fat use
Researchers have developed a novel imaging tool that tracks how tumors utilize fats for fuel in real time.
King’s College London develops imaging tool to track cancer fat use
Researchers at King’s College London have created a new imaging tool capable of tracking how cells utilize fats for fuel in real time. The technology introduces a tracer that reveals how tumors and healthy tissues rely on carnitine, a molecule that carries fatty acids into the mitochondria to produce energy.
Until now, scientists have lacked the means to easily observe this process inside living organisms. While doctors have long used glucose consumption patterns to detect tumors, this new study suggests that some aggressive cancers also rely heavily on fats.
To achieve this, the team developed modified versions of carnitine using fluorine, an element rare in the human body, which allows for easier tracking in scans. They produced two versions: fluoromethylcarnitine (FMC) and a radioactive form called [18F]FMC, specifically designed for positron emission tomography (PET) imaging.
"Using this novel tracer, we can look at carnitine metabolism in living subjects for the very first time,"
Professor Tim Witney, Professor of Molecular Imaging at the School of Biomedical Engineering & Imaging Sciences, via Yahoo
The tool's accuracy was verified using a human lung cancer cell line. The cancer cells absorbed the tracer quickly, but uptake dropped sharply when natural carnitine was added or when the carnitine transporter was blocked by a drug called meldonium. This confirmed that the tracer follows the same biological pathways as natural carnitine.
In live animal studies, PET scans showed the tracer spreading quickly through the bloodstream and accumulating in the kidneys, liver, and heart. The heart showed particularly strong uptake, reflecting its high energy demand from fats. In contrast, skeletal muscle showed little signal because it absorbs carnitine more slowly.
The most significant results appeared in tumor studies. Lung cancer cells implanted into mice absorbed the tracer steadily; after two hours, the levels were high enough to clearly distinguish tumors from surrounding tissue. When the carnitine transporter was blocked, tumor uptake dropped significantly.
The findings suggest that fat metabolism may play a more critical role in cancer growth than previously believed. By mapping these metabolic patterns, researchers believe they can develop more targeted therapies and potentially detect aggressive tumors more accurately. The team is currently working to scale up production of the tracer for broader research and eventual clinical use.
The Role of Fatty Liver in Cancer Progression
Parallel research from VIB, KU Leuven, and Cedars-Sinai has highlighted how metabolic conditions, specifically fatty liver disease, fuel the spread of colorectal cancer (CRC). Colorectal cancer accounts for nearly 1 in 10 cancer diagnoses and is the leading cause of cancer-related death in people under 50.
Researchers found that patients with fatty liver are significantly more likely to develop "replacement metastases," where cancer cells infiltrate healthy liver tissue. This form of the disease is far more aggressive than "encapsulated metastases," where tumors remain separated from healthy tissue. According to VIB and KU Leuven, 5-year survival rates for encapsulated metastases are around 73%, while they drop to below 44% for replacement metastases.
The mechanism involves a protein called MYC. In fatty livers, elevated fatty acids stabilize MYC, which increases the production of proline. Proline serves as a building block for collagen, creating an environment that allows tumor cells to expand within the liver.
Other studies conducted by Cedars-Sinai found that fatty livers release fat-coated "message bubbles" known as extracellular vesicles (EVs).
Additional findings from Cedars-Sinai point to the accumulation of hyaluronic acid in fatty livers, which causes fibrosis and suppresses immune cells, making immunotherapy treatments less effective. By inhibiting hyaluronic acid production in laboratory mice, investigators improved immunotherapy effectiveness.
The combined research suggests a necessary shift in oncology toward integrating metabolic health into cancer care. Potential future steps include using liver fat content as a biomarker to guide treatment and targeting the MYC protein or proline production to reduce aggressive metastases.
