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Tumor Suppression by p53 Is Mediated in Part by the Antiangiogenic Activity of Endostatin and Tumstatin

Recent research shows that p53 suppresses tumor angiogenesis by transcriptionally activating the α(II) collagen prolyl-4-hydroxylase gene. This results in the extracellular release of the potent endogenous angiogenesis inhibitors endostatin and tumstatin from collagens 18 and 4, respectively. The involvement of these inhibitors elucidates a molecular mechanism. By simultaneously repressing a multitude of proangiogenic pathways and by inducing antiangiogenic pathways, a tumor suppressor protein can prevent an incipient tumor from switching to the angiogenic phenotype. Thus, p53 guards the genome from cancer by controlling the three fundamental processes that are critical for growth of a primary tumor and its metastases—tumor cell proliferation, apoptosis, and tumor angiogenesis.

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Resource Type: Bibliography, Diagram, Illustration, Image, Journal article/Issue, Review
Audience Level: Undergraduate upper division 15-16, Graduate, Professional (degree program)

Author and Copyright


Authors and Editors: Judah Folkman of Children's Hospital and Harvard Medical School, MA
Publisher: American Association for the Advancement of Science
Format: application/pdf, image/gif, image/jpeg, text/html
Copyright and other restrictions: Yes
Cost: Yes

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Collection:
STKE/Science Signaling


     
   

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