Immune checkpoint inhibitors (ICIs) have revolutionized the landscape of cancer management. However, acquired resistance and response variability point to rational combination strategies as the goal to achieve significant improvements in the field. Investigators at the National Cancer Center of Japan have found that stimulators of the innate immune response unexpectedly activated suppressive cells of the innate immune system.

The tumor microenvironment plays a crucial role in the resistance of solid tumors to immunotherapy. In particular, fibroblast activation protein (FAP)-expressing cancer-associated fibroblasts have been shown to contribute to immune evasion.

Glucocorticoid-induced tumor necrosis factor receptor (GITR) and its ligand, GITRL, are involved in immune response regulation. GITR is mainly expressed in activated T cells while GITRL is primarily found in antigen-presenting cells.

Researchers from Walter and Eliza Hall Institute of Medical Research, The University of Melbourne and affiliated organizations presented the development of a new reporter mouse model designed to study the role of MDM2 and its transcriptional regulation in p53-mediated tumor suppression.

Stimulating the body’s immune defenses against a tumor can reduce or eliminate it. However, in cancer immunotherapy, when immune checkpoint inhibitors unleash the immune system, severe autoimmunity can result. A hematological technique, extracorporeal photopheresis (ECP), could offer a solution. It reduces the therapy-induced inflammation without altering antitumor immunity. According to scientists at the Universities of Basel and Freiburg, the key lies in adiponectin, a hormone produced by fatty tissue.

New research has uncovered a complex interplay between extracellular matrix (ECM) structure and the transcriptional responses of cancer cells, showing how they alter their gene expression to ‘escape’ from ECM. The findings will make it easier to identify tumors that are likely to metastasize at an early stage.