Hallmarks of Cancer: Inducing Angiogenesis Energetics

Cancer cells stimulate the growth of blood vessels to supply nutrients to tumors. Angiogenesis is the formation of new blood vessels from pre-existing blood vessels. This plays an important role in tumor growth.

Benign tumors can exist in a dormant state, which can be driven by inadequate access to sufficient blood supply. However, the "angiogenic switch" occurs when angiogenesis is activated in a dormant tumor and growth factors are secreted to induce sprouting and chemotaxis of endothelial cells toward the tumor mass.

Within the hypoxic environment of the tumor mass, hypoxia inducible factor-1 (HIF-1) is stabilized and activates the expression of multiple genes contributing to the angiogenic process, including vascular endothelial growth factor (VEGF) and fibroblast growth factor (bFGF), or platelet-derived growth factor (PDGF).

Click the angiogenesis pathway link to learn more about the related proteins implicated in this Hallmark of Cancer:

 - Angiogenesis Pathways

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The Hallmarks of Cancer were identified by Doctors Robert Weinberg and Douglas Hanahan and were originally published in Cell¹. The authors propose the idea that the complexity of cancer can be broken down into smaller subsets of underlying principles. The information here pertains to one such subset. Other entries in this series explore the other known Hallmarks.

Read the additional blog posts in the Hallmarks of Cancer series to learn more:

• Resisting Cell Death
  
• Deregulating Cellular Energetics
• Sustaining Proliferative Signaling
  
• Enabling Replicative Immortality
  
• Evading Growth Suppressors
  
• Activation Invasion and Metastasis
  
• Tumor Promoting Inflammation
  
• Genome Instability and Mutation
• Avoiding Immune Destruction
  

1.  Hanahan D, Weinberg RA (January 2000). "The Hallmarks of Cancer". Cell. 100 (1): 57–70. doi:10.1016/S0092-8674(00)81683-9
2. Hanahan D, Weinberg RA (March 2011). "Hallmarks of Cancer: the next generation". Cell. 144 (5):646-74. doi: 10.1016/j.cell.2011.02.013.