Pathways for aberrant angiogenesis in pancreatic cancer

<p>Abstract</p> <p>Pancreatic ductal adenocarcinoma (PDAC) is a devastating disease. Althoughthe specific mechanisms that dictate its biological aggressiveness are notclearly established, it is characterized by a variety of molecularalterations as well as by the overexpression of mitogenic and angiogenicgrowth factors and their receptors. PDACs also express high levels ofvascular endothelial growth factor (VEGF). Recent studies indicate thatsuppression of VEGF expression attenuates pancreatic cancer celltumorigenicity in a nude mouse model, and that VEGF can exert directmitogenic effects on some pancreatic cancer cells. These findings suggestthat cancer cell derived VEGF promotes pancreatic cancer growth in vivo viaa paracrine angiogenic pathway and an autocrine mitogenic pathway, andprovide novel opportunities for therapeutic intervention in this deadlydisease.</p>

Abstract licence: CC BY-NC-ND

• The Current Treatment Paradigm for Pancreatic Ductal Adenocarcinoma and Barriers to Therapeutic Efficacy · 2021

• The long non-coding RNA HOTTIP promotes progression and gemcitabine resistance by regulating HOXA13 in pancreatic cancer · 2015

• Critical role of NF-κB in pancreatic cancer · 2014

• DCLK1 Regulates Pluripotency and Angiogenic Factors via microRNA-Dependent Mechanisms in Pancreatic Cancer · 2013

A person counts once a day per paper. We keep no cookie and no address: a reader is a hash that changes every day. Any month under five reads shows no number.