Mar 01, 2022
Volume 8Issue 3p159-258, e1-e2
In BRCA1/2-mutant cancers, genomic instability can induce Inflammatory
signaling, suggesting that these tumors may respond to checkpoint inhibitors. However,
genomically instable cancers have co-opted mechanisms to evade the immune system,
resulting in minimal patient benefit from immune checkpoint inhibitors. In this issue,
van Vugt and Parkes review the mechanisms by which genomic instability triggers
inflammatory signaling, and describe how cancer cells evade the immune system.
Cover image depicts how cancer cells ‘fly under the radar’ of the immune system.
Immune cells use radar to detect DNA damage and inflammatory signals in cancer
cells, prompting their mobilization. Cover design conceived by Danielle Loughlin and
created by Kip Lyall....Show more
In BRCA1/2-mutant cancers, genomic instability can induce Inflammatory
signaling, suggesting that these tumors may respond to checkpoint inhibitors. However,
genomically instable cancers have co-opted mechanisms to evade the immune system,
resulting in minimal patient benefit from immune checkpoint inhibitors. In this issue,
van Vugt and Parkes review the mechanisms by which genomic instability triggers
inflammatory signaling, and describe how cancer cells evade the immune system.
Cover image depicts how cancer cells ‘fly under the radar’ of the immune system.
Immune cells use radar to detect DNA damage and inflammatory signals in cancer
cells, prompting their mobilization. Cover design conceived by Danielle Loughlin and
created by Kip Lyall.
