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New findings on influenza could help improve cancer treatments

Published on 20/03/20 at 09:48am
Photo by jarmoluk

A new study into how the body fights influenza could help improve cancer immunotherapies.

Researchers at the Fox Chase Cancer centre had clarified in their study that a fundamental host defence mechanism detects the presence of an influenza virus and rapidly destroys infected cells. The researchers believe this has wide reaching implications for a variety of medical fields including cancer treatment.

The research was collaboration between the Balachandran laboratory and laboratories at the University of Texas, St. Jude Children’s Hospital, the University of Pennsylvania, and the University of Miyazaki in Japan.

In their previous research, lead author of the study, Siddhart Balachandran, had identified a protein call ZBP1 which is essential for sensing the presence of influenza virus in lung cells. However they did not know how it was being activated. New research shows that ZBP1 is activated when it sees Z-RNA (ribonucleic acid), which is a new form of ZNA produced by influenza.

On the findings, Balachandran said: “Folks have been looking for Z-RNA for decades. This particular structure of RNA is what is called a pathogen-associated molecular pattern, and discovering a new such pattern is a major milestone. It also has significant implications for cancer immunotherapies.

“Although immunotherapy is clearly the most promising new cancer treatment approach in decades, a major problem with current immunotherapeutic drugs is that over half of all patients either are refractory to treatment or will develop resistance to the therapy. Making such resistant cancers sensitive to treatment is therefore a huge unmet need. Mimicking a virus infection in resistant tumours has the potential to fill this need, because it can rekindle the immune response to the tumour. The tumour cells now light up as ‘infected,’ and in doing so, become visible to current immunotherapeutic modalities such as the checkpoint inhibitor nivolumab.”  

Balachandran believes these treatments will use synthetic Z-RNAs by mimicking an influenza infection to activate ZBP1 in resistant tumours.

Conor Kavanagh


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