Both researchers are members of the UC Cancer Center.
“Cancer immunotherapy uses a patient’s immune system against tumor cells,” Yeo says. “It has emerged as a crucial treatment strategy, resulting in stable outcomes for cancer patients. However, most breast cancers are not responsive to immunotherapy, and this remains a colossal hurdle.”
In this study, researchers found that targeting a protein called FIP200 could “overwrite” the nonresponsive nature of breast cancers to certain immunotherapies, called immune checkpoint inhibitors.
“Disruption of the protein’s functions in tumor cells could essentially turn ‘cold’, or nonresponsive, tumors into ‘hot’, or responsive, tumors, susceptible to immunotherapy,” Yeo says.
“Tumors that didn’t have this protein contained more T-cells, which is indicative of an immunologically ‘hot’ tumor. When coupled with immune checkpoint inhibitors in animal models with breast cancer, improved outcomes were observed when the protein wasn’t present.
“These findings indicate that targeting FIP200 could create a ‘hot spot’ for immunotherapy within these tumors.”