Transcriptional anti-angiogenesis therapy of human pancreatic cancer

Cytokine Growth Factor Rev. 2006 Jun;17(3):147-56. doi: 10.1016/j.cytogfr.2006.01.002. Epub 2006 Mar 3.


Pancreatic cancer angiogenesis has been attributed to genetic and epigenetic alterations (e.g., oncogene activation and suppressor inactivation) and a chaotic tumor microenvironment (e.g., hypoxia, acidosis, free radical stress and imbalanced growth factor production). Those diverse "upstream signal" factors appear to converge their signaling pathways on limited sets of nuclear transcription factors (e.g., Sp1, Stat3 and NF-kappaB). Aberrant activities of these factors confer a tremendous survival and growth advantage to existing and/or emerging malignant cells through alteration of the expression and functions of their diverse "downstream effector" factors (e.g., VEGF and IL-8). Therefore, targeting a single transcription factor can affect the malignant phenotype more profoundly than just targeting any single upstream signal and/or downstream effector factor.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Angiogenesis Inducing Agents / antagonists & inhibitors
  • Angiogenesis Inducing Agents / metabolism
  • Angiogenesis Inhibitors / therapeutic use*
  • Carcinoma, Pancreatic Ductal / drug therapy*
  • Carcinoma, Pancreatic Ductal / genetics*
  • Humans
  • Neovascularization, Pathologic / drug therapy*
  • Neovascularization, Pathologic / genetics
  • Pancreatic Neoplasms / blood supply
  • Pancreatic Neoplasms / drug therapy*
  • Pancreatic Neoplasms / genetics
  • Signal Transduction
  • Transcription Factors / metabolism*
  • Transcription, Genetic


  • Angiogenesis Inducing Agents
  • Angiogenesis Inhibitors
  • Transcription Factors