Article Text

Download PDFPDF
When antimicrobial peptides hit the wrong target: a novel link between tumour macrophages and cancer stem cells
  1. Giuseppe R Diaferia,
  2. Gioacchino Natoli
  1. Department of Experimental Oncology, European Institute of Oncology (IEO), Milan, Italy
  1. Correspondence to Dr Giuseppe R Diaferia, Department of Experimental Oncology, European Institute of Oncology (IEO), Via Adamello 16, Milan I-20135, Italy; giuseppe.diaferia{at}

Statistics from

Request Permissions

If you wish to reuse any or all of this article please use the link below which will take you to the Copyright Clearance Center’s RightsLink service. You will be able to get a quick price and instant permission to reuse the content in many different ways.

Understanding the interplay between tumour microenvironment and cancer cells is an active research area that holds many promises for identifying stroma-derived paracrine drivers of tumour growth or progression that may thus represent possible therapeutic targets.

Pancreatic ductal adenocarcinoma (PDAC), the most common and almost invariably deadly pancreatic tumour, is characterised by a dense tumour stroma that contains a heterogeneous population of cells including stellate cells, fibroblasts, smooth muscle cells, endothelial cells, and a number of inflammatory and immune cells such as dendritic cells and macrophages.1 Indeed, infiltration by immune cells is a hallmark of most forms of malignancy and tumour-associated macrophages (TAMs) represent key regulators of the interplay between immune system and cancer, usually fostering rather than restraining tumour growth.2

TAMs produce a number of potent angiogenic and lymphoangiogenic factors, cytokines, and proteases all of which may potentiate neoplastic progression and tissue invasion, as also indicated by the therapeutic effect of macrophage depletion in specific tumour models.2 Recent evidence suggests that TAM-derived inflammatory components may also act on tissue cells to promote tumourigenesis. For …

View Full Text


  • Contributors GRD wrote the paper with contribution from all authors. GN revised the article.

  • Funding Research in this area in GN lab is supported by the Italian Association for Research on Cancer (AIRC).

  • Competing interests None declared.

  • Provenance and peer review Commissioned; internally peer reviewed.

Linked Articles