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
Summary
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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