Soft tissue sarcoma cells stop a key metabolic process which allows them to multiply and spread, and so restarting that process could leave these cancers vulnerable to a variety of treatments. The enzyme that controls the process is called FBP2, and researchers from the Abramson Cancer Center, who detailed their findings in Cell Metabolism, also showed that manipulating sarcoma cells to ramp up FBP2 expression slows or even stops their growth entirely. This ultimately leaves them susceptible to targeted therapies and potentially takes away their ability to develop treatment resistance.
Soft tissue sarcoma is actually a collection of distinct, rare cancer types affecting tissues that connect and surround other parts of the body, including muscle, fat, tendons, nerves, and blood vessels. While they can grow anywhere, the arms, legs, chest, and stomach are the most common sites. Because these cancers appear in so many different places in the body, their biology is incredibly diverse, making it difficult to develop one targeted treatment that can be broadly effective for all patients. Currently, the best options for treatment are surgery—which may involve amputation—chemotherapy, and radiation.
“While other cancer types associated with high mutational burden have benefitted from the development of immunotherapies, the diversity and low frequency of genetic mutations in soft tissue sarcomas have made them more difficult to treat, which is why our identification of a broadly expressed metabolic approach is potentially so exciting,” says the study’s senior author M. Celeste Simon, the Arthur H. Rubenstein, MBBCh Professor of Cell and Developmental Biology at the Perelman School of Medicine and scientific director of the Abramson Family Cancer Research Institute. The study’s lead author is Peiwei Huangyang, who performed the work while obtaining her Ph.D. in Simon’s lab.
Read more at Penn Medicine News.
