Abstract

Findings show that senescent cancer-associated fibroblasts secret excess IL8 to promote pancreatic cancer invasion and metastasis; thus, senescent CAFs represent a phenotypic subtype, challenging conventional assumptions that CAFs are a homogeneous population. Mol Cancer Res; 15(1); 3-14. ©2016 AACR.

Highlights

  • Pancreatic ductal adenocarcinoma (PDAC), the predominant form of pancreatic cancer, is a highly lethal malignancy with 5-year survival rates of less than 7% [1]

  • The desmoplasia results from the activation of quiescent pancreatic stellate cells into cancer-associated fibroblasts (CAF) in response to transforming growth factor beta (TGFb) and platelet-derived growth factor (PDGF) ligands derived from carcinoma cells and inflammatory cells [4,5,6]

  • Formalin-fixed, paraffin-embedded human PDAC tissue was obtained from adult patients diagnosed with pancreatic ductal adenocarcinoma between 2008 and 2015 who consented to have tissue allocated for research

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Summary

Introduction

Pancreatic ductal adenocarcinoma (PDAC), the predominant form of pancreatic cancer, is a highly lethal malignancy with 5-year survival rates of less than 7% [1]. PDAC is well-known to have intense stromal fibrosis (desmoplasia), which often forms the majority of the physical tumor volume [2, 3]. The desmoplasia results from the activation of quiescent pancreatic stellate cells into cancer-associated fibroblasts (CAF) in response to transforming growth factor beta (TGFb) and platelet-derived growth factor (PDGF) ligands derived from carcinoma cells and inflammatory cells [4,5,6]. The activated CAFs assume a myofibroblastic phenotype and secrete growth factors and cytokines [4,5,6]. Our understanding of the interaction between PDAC and CAFs has evolved in recent years.

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