39P - Plasma levels of Interleukin-33 (IL-33) and Soluble Suppression of Tumorigenicity 2 (sST2) as a Potential Predictive Biomarker in Patients (pts) wi...

Date 08 December 2017
Event ESMO Immuno-Oncology Congress 2017
Session Lunch & Poster Display session
Topics Cancer in Adolescents
Cancer in Young Adults
Psychosocial Aspects of Cancer
Cancer in Special Situations
Presenter Markus Kieler
Citation Annals of Oncology (2017) 28 (suppl_11): xi6-xi29. 10.1093/annonc/mdx711
Authors M. Kieler1, M. Unseld1, S. Demyanets2, D. Bianconi1, G. Prager1
  • 1Department Of Medicine I, Medical University of Vienna, 1090 - Vienna/AT
  • 2Department Of Laboratory Medicine, Medical University of Vienna, 1090 - Vienna/AT



IL-33 is a proinflammatory cytokine and involved in the development of chronic inflammation and cancer. sST2 acts as a “decoy” receptor for IL-33 thereby regulating its action. Tumor development results in downregulation of IL-33 in epithelial cells but upregulation of IL33 in the tumor stroma and serum in many types of cancer. IL-33 expression was shown in PDAC cells and activated pancreatic stellate cells. We therefore explored IL-33 and sST2 as a potential predictive biomarker in 14 pts with advanced PDAC undergoing sCTX.


Plasma levels of IL-33 and sST2 of pts with locally advanced, metastatic or relapsing PDAC that underwent sCTX were determined with specific ELISAs. Serial measurements of IL-33 and sST2 were performed at baseline and 8 weeks after the start of sCTX. The baseline concentrations were compared with the values at week 8. Computertomography as efficacy assessment according to RECIST 1.1 was performed at baseline and at week 12.


Plasma levels of IL-33 decreased more than 50% and sST2 increased more than 15% in all 3 pts (21%) with a partial response. The Cut-off point (COP) for predicting a stable disease (SD) was a 10% increase for IL-33 levels and a 10% decrease for sST2 levels. Of the 6 pts (43%) that had a SD, IL-33 was not measurable in 1 pt. PLasma levels of IL-33 did not increase over the COP in the course of treatment of 4 pts with a SD. In 1 pt with a SD IL-33 levels increased over the COP. sST2 levels were not measurable in 1 pt. In 4 pts sST2 levels did not decrease over the COP. In 1 pt the levels of sST2 decreased under the COP. From the 5 pts (36%) that progressed under sCTX, IL-33 levels increased in 2 pts at least over 50%, but in 3 pts the levels decreased more than 20%. Plasma levels of sST2 decreased in 2 but increased in 3 pts.


Serial monitoring of IL-33 and sST2 plasma levels predicted treatment response in 10 of 14 pts (71%) within 8 weeks of sCTX and have a potential role as predictive biomarker in PDAC pts. With the anticipated introduction of immune modulating drugs in the treatment of PDAC, such biomarkers might be of enormous interest.

Clinical trial identification

Legal entity responsible for the study

Medical University of Vienna




M. Kieler: Travel support from Merck, Bayer, Bristol-Myers Squibb, Roche and participated in advisory board meetings from Bayer. G. Prager: Speaker’s fee from Bayer, Roche, Merck-Serono, Amgen, Servier, Celgen, Shire, MSD, Lilly, Sanofi-Aventis. All other authors have declared no conflicts of interest.