Abstract| Volume 51, SUPPLEMENT 1, S1, March 2015

Download started.


ITOC2 – 002. Immunosuppressive microenvironment in pancreatic adenocarcinoma

      This paper is only available as a PDF. To read, Please Download here.
      Pancreatic ductal adenocarcinoma (PDAC) represents one of the deadliest cancers in the world. PDAC cells activate tumour-specific immune responses but simultaneously trigger a strong immunosuppression. We showed that PDAC cells produce high amount of chronic inflammatory mediators and PDAC tumours build an immunosuppressive cytokine milieu, which correlates with tumour progression. On the cellular level, we found that tumours from the murine Panc02 orthotopic model of PDAC were infiltrated with high numbers of regulatory T cells (Treg). Remarkably, these cells exhibited the effector/memory phenotype, suggesting their enhanced suppressive activity and higher proliferation capacity. With regard to the innative immune cells, we observed a pronounced accumulation of macrophages and myeloid-derived suppressor cells (MDSC) in murine PDAC tumours. Whilst macrophages seem not to play a significant role in this PDAC model in the context of immunosuppression, MDSC are highly suppressive, and their accumulation is associated with an increase in intratumoural vascular endothelial growth factor (VEGF) concentration during the PDAC progression. Thus, Treg and MDSC are strongly involved in the PDAC-associated immunosuppression and their depletion could provide the base for new approaches for therapy of PDAC.
      To read this article in full you will need to make a payment

      Purchase one-time access:

      Academic & Personal: 24 hour online accessCorporate R&D Professionals: 24 hour online access
      One-time access price info
      • For academic or personal research use, select 'Academic and Personal'
      • For corporate R&D use, select 'Corporate R&D Professionals'


      Subscribe to European Journal of Cancer
      Already a print subscriber? Claim online access
      Already an online subscriber? Sign in
      Institutional Access: Sign in to ScienceDirect