p53 status determines the role of autophagy in pancreatic tumour development

In a mouse model of pancreatic tumours driven by Kras mutations, the outcome of suppressing autophagy is shown to depend on the status of p53: if p53 is intact, deletion of key autophagy genes blocks the progression of pre-cancerous lesions to aggressive carcinomas; however, in the absence of p53, loss of autophagy accelerates tumorigenesis, accompanied by deregulation of cancer cell metabolism.