Tumor immunogenicity is quantified with a novel method, and the resulting tumor immunogenicity score is an effective tumor-inherent biomarker for prediction of response to immune checkpoint inhibitors.

Why does cancer develop in situations where the immune system is perfectly capable of eliminating it?

Downregulation of mitochondrial activity by immunosuppressive tumor-derived soluble factors leads to systemic unresponsiveness to the PD-1 blockade therapy.

Diverse components of the tumor microenvironment affect T cell metabolism in ways that are crucial to improving immunotherapy.

SLAMF6 is an inhibitory checkpoint of T cells, the lack of which leads to better tumor control, suggesting a new immunotherapy target.

Engineered T cell receptors enable targeted immunotherapy with a reduced risk of harmful autoimmunity.

Cancer systems immunology is a highly interdisciplinary field that is advancing our ability to understand and predict the complex behavior that orchestrates the interplay between tumors and the immune system.

Cancer cell expression of the T-cell co-stimulatory molecule CD80, or treatment with agonistic antibodies targeting the T-cell co-stimulatory receptors OX-40 or 4-1BB, enhances the anti-tumor activity of FAK inhibition.

An unrecognized regulation on MAGEA protein stability promotes pancreatic cancer progression via manipulating autophagy and may impact the clinical utility of MAGEA-targeted immunotherapy.

Harnessing female sex hormones may improve how all patients with melanoma respond to treatment.