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Cytokine Growth Factor Rev. 2006 Jun;17(3):147-56. Epub 2006 Mar 3.

Transcriptional anti-angiogenesis therapy of human pancreatic cancer.

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Department of Gastrointestinal Medical Oncology, Unit 426, The University of Texas M. D. Anderson Cancer Center, 1515 Holcombe Boulevard, Houston, TX 77030, USA.


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.

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