Cancer's rapid growth hinges on its ability to hijack the body's nutrient supply, particularly glucose and fatty acids. But a novel approach is turning this strategy against tumors themselves. Researchers have developed a method that reprograms the body's own fat cells to deprive cancer of its essential fuel, effectively slowing or halting tumor progression.
This innovative technique, known as Adipose Manipulation Transplantation (AMT), does not rely on traditional cancer treatments like chemotherapy or radiation. Instead, it modifies existing fat cells to act as metabolic competitors, reducing the availability of nutrients that tumors depend on.
The research team, led by Dr. Nadav Ahituv at the University of California, San Francisco, focused on white fat cells, the type of fat most abundant in the human body and typically used for energy storage. Using gene-editing tools like CRISPRa, they activated a dormant gene known as UCP1, transforming white fat into a more metabolically active form called beige fat. Unlike its white counterpart, beige fat consumes energy to generate heat, mimicking the properties of brown fat, which is activated in cold conditions.
Once modified, these fat cells became voracious consumers of glucose and fatty acids—the very nutrients cancer cells rely on. In lab tests where the engineered fat cells were placed near cancer cells but separated by a membrane, the fat cells effectively starved the tumors, leading to a dramatic reduction in cancer cell survival. This surprising result was consistent across various cancer types, including breast, colon, pancreatic, and prostate cancers.
Following these promising in vitro results, the team moved to animal testing. They implanted clusters of engineered fat cells next to tumors in mice. Remarkably, the fat cells continued to outperform cancer cells for nutrients, even when placed at a distance from the tumor. The tumors not only stopped growing—they began to shrink.
A major advantage of this method lies in its compatibility with current medical practices. Since liposuction and fat grafting are already common in clinical settings, the process of extracting fat from a patient, genetically modifying it, and reintroducing it into the body is both practical and relatively low-risk. Fat cells are naturally biocompatible, meaning they’re unlikely to provoke immune reactions or migrate unpredictably within the body.
Dr. Ahituv and his collaborators further personalized the therapy by customizing fat cells to target specific nutrients favored by different cancer types. For instance, some pancreatic cancers rely on uridine when glucose is limited. By engineering fat cells to absorb uridine, the researchers managed to cut off a critical fuel supply for these tumors, halting their growth.
This nutrient competition model stands in contrast to conventional treatments that aim to destroy cancer cells directly. Instead, AMT weakens tumors by depriving them of the energy needed to grow and divide. This metabolic interference approach could be especially useful for cancers that are hard to reach surgically or are resistant to standard therapies.
While early results are promising, researchers caution that more work is needed before the method can be used in humans. Key questions remain, such as how long these engineered fat cells stay active, whether tumors could adapt by finding alternative nutrient sources, and how the therapy might affect healthy tissues.
Still, AMT opens exciting new avenues in cancer treatment and beyond. Fat cells could eventually be engineered for other conditions, such as diabetes or iron overload disorders. The idea of converting the body's own fat into a therapeutic tool—one that starves cancer instead of poisoning it—marks a compelling shift in how medicine might confront complex diseases in the future.
