Tumour suppressor p53 is mutated in around 50% of human cancers and work is carried out to understand how p53 loses its tumour suppressive ability in tumours containing wild-type p53. In working to understand this concept, Paul Miller and colleagues have discovered that iASPP (inhibitor of Apoptosis Stimulating Protein of p53) is a suppressor of both inflammation and pancreatic cancer (PC) initiation.
The Lu laboratory identifies iASPP as a paradoxical suppressor of oncogenic KRAS-driven tumorigenesis and inflammation. The group investigated the ability of iASPP to regulate the pancreatic inflammatory response and PC formation. iASPP was found to suppress pancreatic cancer onset driven either by oncogene KRAS or by a combination of oncogenic KRAS and p53 – showing that it can suppress PC initiation independent of p53.
Read the full paper in Cell Death and Differentiation journal.