Hallmarks of a lethal form of ovarian cancer called “high-grade serous ovarian carcinoma” (HGSOC) are an immunosuppressive tumor microenvironment, insensitivity to checkpoint inhibitor immunotherapies, and elevated expression of checkpoint pathway ligands that thwart the immune system’s ability to kill tumor cells. Nearly 70% of HGSOC tumors express PTK2, a gene that encodes FAK (focal adhesion kinase), elevated levels of which signal poor survival outcomes.
In a study published in the journal Proceedings of the National Academy of Sciences (“Tumor FAK orchestrates immunosuppression in ovarian cancer via the CD155/TIGIT axis”), scientists from the University of California (UC), San Diego, School of Medicine, Moores Cancer Center at UC San Diego Health, La Jolla Institute for Immunology, and their collaborators have demonstrated how key proteins act together to suppress antitumor activity in HGSOC, revealing a new combinatorial strategy to treat this intractable malignancy.
“In HGSOC tumors, where high levels of CD155 and active FAK are common, our results provide compelling support for targeting FAK and TIGIT as part of a new immune-boosting therapeutic strategy,” said Schlaepfer.
Immunotherapy is a treatment strategy that uses a person’s own immune cells to fight malignancy and has been successfully used to treat a variety of cancers, but it has not been effective in treating HGSOC.
https://www.genengnews.com/topics/cancer/lethal-ovarian-cancer-checked-by-dual-attack-on-immune-checkpoint-in-mice/
Comments