Publication: CAF Subpopulations: A New Reservoir of Stromal Targets in Pancreatic Cancer

Thomas R. Cox, Oct 2019

CAF Subpopulations: A New Reservoir of Stromal Targets in Pancreatic Cancer

Working together with A/Prof Paul Timpson’s lab, we are pleased to announce that our recent review on targetting CAFs in pancreatic cancer has just been published in Trends In Cancer.

In this work we explore how different aspects of CAF heterogeneity are defined and how these manifest in multiple cancers, with a focus on pancreatic ductal adenocarcinoma (PDAC).

Mechanisms of CAF Heterogeneity

Abstract

Cancer-associated fibroblasts (CAFs) are one of the most significant components in the tumour microenvironment (TME), where they can perform several protumourigenic functions. Several studies have recently reported that CAFs are more heterogenous and plastic than was previously thought. As such, there has been a shift in the field to study CAF subpopulations and the emergent functions of these subsets in tumourigenesis. In this review, we explore how different aspects of CAF heterogeneity are defined and how these manifest in multiple cancers, with a focus on pancreatic ductal adenocarcinoma (PDAC). We also discuss therapeutic approaches to selectively target protumourigenic CAF functions, while avoiding normal fibroblasts, providing insight into the future of stromal targeting for the treatment of PDAC and other solid tumours.

Links

View article on the Trends in Cancer website
Read the PDF here

Citation

Pereira et al. CAF Subpopulations: A New Reservoir of Stromal Targets in Pancreatic Cancer
Trends in Cancer (2019) | doi: 10.1016/j.trecan.2019.09.010

Key Words

Cancer-associated fibroblasts; CAF heterogeneity; CAF subpopulations; Stromal targeting; Desmoplasia; Fibrosis; Pancreatic ductal adenocarcinoma (PDAC); Extracellular matrix (ECM); Tumour–stroma crosstalk

Funding

C.V. is supported by a Human Frontier Science Program (HFSP) fellowship. M.P. and C.R.C. are supported by an Australian Government Research Training Program (RTP) Scholarship. J.P.M. is supported by Cancer Research UK. T.R.C. is supported by an NHMRC R.D. Wright Biomedical Career Development Fellowship and a grant from Susan G. Komen. P.T. is supported by the Len Ainsworth Fellowship in Pancreatic Cancer Research and is a National Health and Medical Research Council (NHMRC) Senior Research Fellow. This work was made possible by an Avner Pancreatic Cancer Foundation Grant. This work was supported by Suttons, Sydney Catalyst, Australian Research Council (ARC), NHMRC, Cancer Council NSW, Cancer Institute NSW, National Breast Cancer Foundation (NBCF), St. Vincent’s Clinic Foundation.