Poster Presentation 29th Lorne Cancer Conference 2017

The role of Interleukin-11 in pancreatic cancer progression   (#160)

Ka Yee Fung 1 , Adele Preaudet 1 , Tracy Putoczki 1
  1. The Walter and Eliza Hall Institute, Parkville, VIC, Australia

Pancreatic ductal adenocarcinomas (PDAC) are among the most lethal of cancers, with the majority of patients succumbing to the disease within 6 months of their diagnosis. As a result of limited progress in new treatment options, and the advanced stage of disease at the time of diagnosis, chemotherapy is provided with palliative intent.

Interleukin (IL)-11 is a member of the IL-6 family of cytokines that like IL-6, signals through the transmembrane glycoprotein-130 (Gp130) receptor resulting in activation of the pre-tumourigenic downstream transcription factor STAT3. While historically there has been a major focus on understanding the role of IL-6 in numerous diseases including cancer, there has been very little research into the function of its near identical sibling IL-11.

The progression of pancreatic intraepithelial neoplasia (PanIN) and PDAC has recently been linked to IL-6 mediated STAT3 activation in mouse models. We find in the same models, that IL-11 is also elevated and show that the genetic deletion of just one allele of the receptor for IL-11 signalling (IL-11Ra1) results in delayed PanIN and PDAC progression. This is associated with a more potent reduction in STAT3 activation than was shown for the genetic deletion of IL-6. These results suggested that targeting the IL-11 signalling network may provide a potential new treatment opportunity for PDAC.