Scientists hope to increase our chances of fighting cancer by using viruses that selectively infect and kill tumor cells,media reported. The technique, known as the “lysotic virus therapy”, shows both great promise and practical limitations. But understanding how tumor cells can withstand these attackers’ new discoveries could give the technology a huge boost.
The idea of using the virus to treat cancer has been around for more than a century, but recent research has made some really exciting advances in this area. A 2018 study details how a Nobel Prize-winning imaging technique could be used to observe and improve a powerful cancer virus, while another described how a virus not only attacks brain tumours but also “recruits” the body’s immune system into the fight.
While such studies continue to illustrate how these experimental viruses work and may make them more effective, only a limited number of patients respond to treatment. Currently, only one type of colon cell virus has been approved by the U.S. Food and Drug Administration (FDA) for clinical use.
However, new findings by researchers at the Francis Crick Institute in the UK may help make progress. To better understand why colon cancer viral therapy works only for a small number of patients, they began by studying the immediate environment around the tumor and how tumor cells worked with neighboring cells to repel the virus.
The key to cancer defense is cells called cancer-related fibroblasts (CAFs), which previous studies have shown play an active role in promoting cancer growth by shielding the body’s immune system. The new study delved into these sinister “organs” and used laboratory experiments to explore how contact between cancer cells and fibroblasts drives this protective effect.
The team found that when cancer cells come into direct contact with fibroblasts, they transmit small amounts of fluid called cytoplasm, triggering a chain reaction that causes inflammation of surrounding tissue. The scientists concluded that it was this inflammation that made it difficult for the virus to occupy and replicate in cancer cells, greatly limiting its role.
“This process only occurs when cancer cells come into direct contact with fibroblasts,” said study author Erik Sahai. “In healthy tissue, this type of inflammatory reaction only occurs when the injury occurs, as there is usually a membrane that separates them. This is a good example of cancer ‘hijacking’ our body’s protective mechanisms for self-interest. “
As part of their experiments on cell cultures and lab-grown tumors, the researchers blocked the signaling pathways involved in the process and found that it made cancer cells more sensitive to colon cancer viruses. The team hopes the findings could pave the way for new treatments for this form of inflammation and improve the efficacy of colon cancer viral therapies. Next, they plan to study how cytoplasm is transferred from one cell to another.
“If we can get a fuller picture of how cancer cells protect themselves from colon cancer viruses and find effective ways to stop these protection mechanisms, these viruses could become a more powerful tool for doctors to treat cancer,” said study co-author Emma Milford. “This study is an important and early step in that direction. “
The study was published in the journal Nature Cell Biology.