Abstract
As with other solid tumors, the growth and metastasis of pancreatic cancer is critically dependent on tumor angiogenesis. A major stimulus for a tumor's recruitment of additional blood vessels is cellular hypoxia, a condition which is especially pronounced in this neoplasm. Hypoxia induces transcriptional activation of genes that alter cellular metabolism and promote neoangiogenesis. Pancreatic cancer cells have demonstrated activation of such adaptive pathways even in the absence of hypoxia. A highly-angiogenic response in this neoplasm correlates with increased tumor growth, increased metastasis, and decreased survival. Pancreatic cancers expressing high levels of vascular endothelial growth factor, a potent pro-angiogenic cytokine, also have a higher incidence of metastasis and poorer prognosis. Pancreatic cancer cells uniquely express receptors for vascular endothelial growth factor, indicating a role for an autocrine loop in tumor proliferation and invasion. Multiple experimental anti-angiogenic strategies, many of which target vascular endothelial growth factor, reduce pancreatic cancer growth, spread, and angiogenesis. Anti-angiogenic treatments for pancreatic cancer will likely be most effective when used as an integral part of a combination chemotherapeutic regimen.
Highlights
Adenocarcinoma of the pancreas remains a most formidable malignancy
As with other solid tumors, there has been a surge in the study of pancreatic tumor neovascularization that is critical to growth and metastasis
In this article we will review the relevant data characterizing pancreatic cancer as an hypoxic tumor, and discuss the molecular mechanisms by which this neoplasm responds to hypoxia, generates new blood vessel growth, and promotes its own growth and metastasis
Summary
Adenocarcinoma of the pancreas remains a most formidable malignancy. Usually undiagnosed until reaching an advanced stage, pancreatic cancer is characterized by its predisposition to aggressively invade surrounding tissues, to metastasize early and extensively, and to resist conventional chemoradiation treatment strategies. The notion that a growing mass of tumor cells must recruit its own blood supply for the maintenance of oxygen and nutrients, termed tumor angiogenesis, was popularized by Judah Folkman in the early 1970s [2]. Since this first description of angiogenesis as a requisite process for continuous solid tumor growth, many endogenous pro- and (page number not for citation purposes). In this article we will review the relevant data characterizing pancreatic cancer as an hypoxic tumor, and discuss the molecular mechanisms by which this neoplasm responds to hypoxia, generates new blood vessel growth, and promotes its own growth and metastasis
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