Nature: Genes and the environment work together to induce an overt genetic process that initiates tumor occurrence 

Previous studies have shown that tissue damage increases the risk of cancer, but we don't know much about the mechanisms behind it.
in mouse pancreatic cancer models, pancreatitis associated with tissue damage, in collaboration with activation mutations in kras cancer genes, can significantly accelerate the formation of early tumor lesions and eventually lead to adenocarcinoma.
Recently, researchers published in the journal Nature, in an introphy mouse model, showed that the combination of Kras mutations and tissue damage promoted a unique chromatin state in pancreatic epithal cells to distinguish it from normal cell regeneration by integrating genomics, single-cell chromatin assays, and space-time-controlled functional disturbances.
this cancer-related epigenetic state occurs within 48 hours of pancreatic injury and involves a chromatin switch from "tip cells to newborns" that helps define the early disorders of the human pancreatic cancer gene.
In the most rapidly activated factor after the damage to the prethyrocyte tissue of the pancreas, there is the alarm cytokine leucin 33, which reproduces the effect of the damage in collaboration with the mutant Kras to release the epigenetic remodeling process of early tumors and tumor transformation.
Overall, the study sheds light on how gene-environment interactions rapidly produce gene regulatory processes that determine the transformation of early tumors and provide a molecular framework to understand the interactions between genetic and environmental cues in cancer initiation.