Angiogenesis and invasion in pancreatic cancer
Name, First name: Bikfalvi Andreas
Affiliation: INSERM U1029, University Bordeaux I, Avenue des Facultés, 33 405 Talence, France
Abstract (max 250 words):
Pancreatic tissue exhibits two main types of cancer, pancreatic ductal carcinoma (PDAC) and (neuro)
endocrine tumors arising from Langerhans islets. These tumors can be studied either by subcutaneous or
orthotopic tumor cell implantation or using transgenic mouse models. Many of these models have been
developed such as the PDX-Cre/KrasGD12 or the RIP-Tag model. The Rip-Tag model, besides being a
model for neuroendocrine tumors, provides insights into the general mechanisms of tumor angiogenesis
and invasion.
PDAC tumors have some specific features, which distinguish them from neuroendocrine and from many
other solid tumors. There is a strong stroma-reaction, which is represented by the so-called desmoplastic
reaction. The latter is characterized by a dense stroma surrounding carcinoma cells composed of
fibroblasts, activated stellate cells (myofibroblast-like cells), various inflammatory cells, proliferating
vascular structures, and matrix proteins. Furthermore, vessel abundance is rather low in comparison to
healthy pancreatic tissue. Thus, the use of anti-angiogenesis strategies in these tumors is rather
questionable.
There are a number of molecular players and receptors that have been proposed to drive pancreatic
tumor development, which include among many vascular endothelial growth factors, transforming
growth factor- or platelet-derived growth factors. Chemokines also seem to play a significant role in
pancreatic tumor development as evidenced by our own studies.
In this presentation, we will discuss some of these issues and illustrate this with examples from our own
studies.