Katie L. Owen

TL;DR: Janus kinase-signal transducer and activator of transcription (JAK-STAT) signaling mediates almost all immune regulatory processes, including those that are involved in tumor cell recognition and tumor-driven immune escape.

TL;DR: Engagement ofMyeloma cells with the osteoblastic niche induces expression of a suite of myeloid genes that predicts disease progression and that are potential drug targets to eradicate dormant myel cancer cells.

TL;DR: Investigation of the interplay between type I IFN signaling and the PD-1/PD-L1 axis and the impact of combining IFN inducers, as immune activators, with anti–PD-1 to induce an antimetastatic immune response revealed that the type IIFN-inducer poly(I:C) was an effective immune activator and antimetASTatic agent, functioning better than anti-PD- 1, which was ineffective as a single agent.

TL;DR: It is demonstrated that loss of tumor‐intrinsic type I IFN occurs in proliferating prostate cancer cells in bone, which suppresses tumor immunogenicity and therapeutic response and promotes bone cell activation to drive cancer progression.

TL;DR: Current knowledge of the unique exchange that occurs between bone resident cells, innate immune populations and tumor cells that leads to the establishment of a tumor-permissive milieu is reviewed.