Angiogenesis is required for solid tumours to enlarge beyond 1 – 2 mm, due to poor nutrient supply at greater distances. Angiogenesis may be neo-angiogenesis (stimulating new blood vessels to grow out from existing capillaries) or vasculogenesis (where endothelial cells are recruited to the tumour directly).
Angiogenesis is controlled by pro- and anti-angiogenesis proteins. The extracellular matrix contains pro-proteins of many pro- and anti-angiogenic proteins. When cleaved by proteases, these factors are released. Stressors such as hypoxia may lead to increased production of pro-angiogenesis cytokines, such as VEGF or bFGF. Tumour cells with malignancies in KRAS or MYC upregulate the expression of VEGF/bFGF and promote angiogenesis. TP53 induces expression of anti-angiogenic cytokines, and is frequently disabled in tumours. Tumours may also simply rely on their hypoxia to stimulate the body to produce new vessels for it.
Angiogenesis also enables tumour cells to enter the bloodstream and metastasise.
Old R04: Advanced Cell Biology
- R4.1: Major Cell Cycle Regulators
- R4.2: Signal Transduction
- R4.3: Molecular Response to Ionising Radiation
- R4.4: Tumour Kinetics
R4.5: Hallmarks of Cancer
- R4.5a: Self Sufficiency In Growth Signals
- R4.5b: Insensitivity To Growth Inhibition
- R4.5c: Resisting Cell Death
- R4.5d: Immortality
- R4.5e: Angiogenesis
- R4.5f: Invasion and Metastasis
- R4.5g: Deregulation of Cellular Energetics
- R4.5h: Immune Avoidance
- R4.5i: Genomic Instability
- R4.5j: Tumour Promoting Inflammation
- R4.6: In Vitro Features Of Transformed Cells
- R4.7: Mouse Models Of Tumour Initiation And Promotion