Almac Group’s Diagnostics business has identified a novel immune response mechanism in breast tumors deficient in DNA repair. The current study explains the molecular basis of this 44-gene immune based assay and demonstrates that the genes in the assay reflect activation of the innate immune response cGAS/STING/TBK1/IRF3 pathway in response to DNA damage.
 
The study provides rationale for the observed link between DNA repair deficiency and activation of the immune checkpoint PD-L1. Almac will now pursue their 44-gene assay as a means of prospectively identifying breast cancer patients likely to respond to PD-L1 targeted therapies.
 
Professor Richard Kennedy, MD, Ph.D., McClay Professor in Medical Oncology, Queens University Belfast and vice president and medical director, Almac Diagnostics said “The study provides strong justification for the underlying biology that causes enhanced PD-L1 expression. Almac will now engage with pharma and academia to investigate the potential clinical benefit for predicting response to immune checkpoint inhibitors, such as PD-L1 and IDO1 and their use in combination with DNA damaging agents.”