It is known that in the pancreas and other tissues injury-induced inflammation and oncogenic mutations cooperate to drive tumorigenesis, whereas in the absence of oncogenic signals inflammation is resolved and tissues regenerate. Studying early and later time points of transformation in a mouse model of pancreatic cancer, Scott Lowe and colleagues now report that the combination of pancreatitis and Kras very rapidly induces chromatin opening at new loci that are inaccessible after injury or Kras activation alone, and that many of these loci remain accessible during tumour progression. One epigenetically upregulated gene in particular—the damage-associated cytokine IL-33—mimics the effects of tissue injury in facilitating Kras-driven transformation. These findings shed new light on the interplay of genetic and environmental insults that drives tumour development.
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