Key Takeaways
- Research from the University of Cambridge shows that modifying hyaluronic acid could inhibit the spread of glioblastoma cells.
- The study indicates that changing the tumor’s surrounding environment may offer a new treatment approach to control brain cancer’s aggression.
- Future tests on animal models could lead to clinical trials, with the potential to extend treatment applicability to other solid tumors.
New research from the University of Cambridge offers promising insights into treating glioblastoma, one of the most aggressive forms of brain cancer. Glioblastoma is particularly challenging to manage, with a grim five-year survival rate of only 15%. Although more extensive testing is required before any potential treatments can be approved for human trials, initial findings are encouraging.
The study focuses on hyaluronic acid (HA), a crucial component of the brain’s extracellular matrix. Researchers found that glioblastoma cells depend on HA’s flexibility to bind to their surface receptors, a process that facilitates their spread throughout the brain. By stabilizing HA molecules to limit their flexibility, the researchers successfully ‘reprogrammed’ glioblastoma cells, preventing them from invading neighboring tissues.
“Hyaluronic acid molecules need to be flexible to bind to cancer cell receptors,” stated Professor Melinda Duer, who led the research. “If you can stop hyaluronic acid from being flexible, you can stop cancer cells from spreading. Remarkably, we didn’t have to kill the cells; we merely altered their environment.”
Conventional treatments for glioblastoma, including surgery, drugs, and radiotherapy, often face limitations. Even after surgical removal, residual cancer cells typically cause tumors to regrow shortly thereafter. Current drug therapies struggle to penetrate the tumor mass effectively, and radiotherapy only prolongs the inevitable return of cancer. In contrast, this research shifts focus from the tumor cells to their surrounding extracellular matrix, aiming to mitigate their spread.
Interestingly, the researchers noted that this effect occurred even at low concentrations of HA, suggesting that the cells were reprogrammed into a dormant state rather than being physically trapped. This could explain why glioblastomas frequently recur at surgical sites: an accumulation of fluid, or edema, can dilute HA, enhancing its flexibility and potentially promoting cell invasion. By ‘freezing’ HA in place, recurrence might be prevented.
“This could present a significant opportunity to slow glioblastoma progression,” Duer explained. Since the approach does not aim to target every single cancer cell, it could be adaptable for various solid tumors, where the surrounding matrix plays a role in invasion. The implication is profound: cancer cells’ behavior is influenced by their environment, and modifying this environment could change the cells’ actions.
Moving forward, the research team hopes to expand their studies into animal models, which could eventually lead to clinical trials involving human patients. While more work remains, these initial findings open the door to innovative approaches for combating glioblastoma and potentially other forms of cancer.
Source: Columbia University
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