EZH2i unlocks PDAC immune surveillance

Successful immune-mediated tumor control in pancreatic cancer is severely hampered by its dense desmoplastic stroma. New work shows that EZH2 inhibition relieves the suppressive effect of tumor stroma on pro-inflammatory chemokine expression after therapy-induced senescence, boosting NK and T cell recruitment and immunological tumor control.

Automated summary

The dense desmoplastic stroma in pancreatic cancer hinders successful immune-mediated tumor control. Recent research shows that inhibiting EZH2 can relieve the suppressive effect of tumor stroma, allowing for increased expression of pro-inflammatory chemokines after therapy-induced senescence. This boost in NK and T cell recruitment enhances immunological tumor control.