It takes a village to overcome kras dependence in pancreatic cancer

Abstract

In this issue, Hou and colleagues present their exciting work demonstrating that, through remodeling of the local tumor microenvironment (TME), pancreatic ductal adenocarcinoma forms a tumor-supportive niche capable of liberating cancer cells from dependence on oncogenic KRAS signaling. Through extensive experimenta-tion both in vitro and in vivo, the authors reveal that the HDAC5–CCL2 axis drives the recruitment of tumor-associated macrophages to the TME to provide trophic signaling.