503P - Mast cells expressing the major source of interleukin 17 predict a favorable prognosis in hepatocellular carcinoma

Date 19 December 2015
Event ESMO Asia 2015 Congress
Session Poster presentation 1
Topics Hepatobiliary Cancers
Translational Research
Presenter Jian-fei Tu
Citation Annals of Oncology (2015) 26 (suppl_9): 153-155. 10.1093/annonc/mdv534
Authors J. Tu1, J. Ji2
  • 1Radilolgy, lishui central hospital, 323000 - lishui/CN
  • 2Radiology, lishui central hospital, li shui/CN

Abstract

Aim/Background

Interleukin (IL)-17 is expressed in the tumor micro-environment where it appears to contribute to tumor development. In hepatocellular carcinoma (HCC) studies, IL-17 has been associated with poor prognosis. However, the source of the increased tumor-infiltrating IL-17 in HCC and prognostic valve remain poorly understood.

Methods

59 HCC patients were enrolled in this study, immunofluorescence double stainwas used to evaluate the colocalization of CD3+ T cells, CD4+ T cells, CD56+ NK cells, CD20+ B cells, CD68+ Macrophages, and mast cell tryptase+ mast cells (MCT+ mast cells) with IL-17. The prognostic effect of groups with high and low MCT numbers was evaluated by Kaplan-Meier analysis and Cox regression model.

Results

MCT+ mast cells, but not other cells, were the predominant IL-17-producing cell type. In HCC patients, immunofluorescence double stain showed a positive correlation between the number of MCT+ mast cells and microvessels (MCVs) and the majority of vascular endothelial cells expressing IL-17 receptor (IL-17R). Overall survival analysis revealed that the increasing intratumoral infiltrated MCT+ mast cells were significantly associated with a poor prognosis.

Conclusions

These findings indicated the major source of IL-17 in HCC were MCT+ mast cells and these cells infiltration may promote tumor progression by enhancing angiogenesis through the axis of IL-17/IL-17R. Increased IL-17-positive MCT+ mast cells was associated a poor prognosis, indicating therapy targeting MCT+ mast cells might be an effective strategy in controlling intratumor IL- 17 infiltration and MCVs.

Clinical trial identification

no

Disclosure

All authors have declared no conflicts of interest.