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 experimentation 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.See related article by Hou et al., p. 1058.
©2020 American Association for Cancer Research.