Saturday, August 18, 2012


One of the most important and vital understanding of cancer growth mechanism is Angiogenesis. It is this very mechanism that the body feeds cancer cells which invariably causes Metastasis; allowing cancer cells to spread to other parts of the body. Thanks to The Angiogenesis Foundation that more studies and researches are being undertaken to mitigate and arrest Metastasis. If we want to fight off Metastasis we should first understand the underlining factors in Angiogenesis.

Below are extracts from the Foundation.

1. How the body controls Angiogenesis

Angiogenesis (angio'gen'esis) -- the growth of new blood vessels -- is an important natural process occurring in the body, both in health and in disease. 

Angiogenesis occurs in the healthy body for healing wounds and for restoring blood flow to tissues after injury or insult. In females, angiogenesis also occurs during the monthly reproductive cycle (to rebuild the uterus lining, to mature the egg during ovulation) and during pregnancy (to build the placenta, the circulation between mother and fetus).
The healthy body controls angiogenesis through a series of "on" and "off" switches:
The main "on" switches are known as angiogenesis-stimulating growth factors

The main "off switches" are known as angiogenesis inhibitors
When angiogenic growth factors are produced in excess of angiogenesis inhibitors, the balance is tipped in favor of blood vessel growth. When inhibitors are present in excess of stimulators, angiogenesis is stopped. The normal, healthy body maintains a perfect balance of angiogenesis modulators. In general, angiogenesis is "turned off" by the production of more inhibitors than stimulators.

2. The Angiogenesis Process: How Do New Blood Vessels Grow?
The process of angiogenesis occurs as an orderly series of events:

Diseased or injured tissues produce and release angiogenic growth factors (proteins) that diffuse into the nearby tissues.
The angiogenic growth factors bind to specific receptors located on the endothelial cells (EC) of nearby preexisting blood vessels.
Once growth factors bind to their receptors, the endothelial cells become activated. Signals are sent from the cell's surface to the nucleus.
The endothelial cell's machinery begins to produce new molecules including enzymes. These enzymes dissolve tiny holes in the sheath-like covering (basement membrane) surrounding all existing blood vessels.
The endothelial cells begin to divide (proliferate) and migrate out through the dissolved holes of the existing vessel towards the diseased tissue (tumor).
Specialized molecules called adhesion molecules called integrins (avb3, avb5) serve as grappling hooks to help pull the sprouting new blood vessel sprout forward.
Additional enzymes (matrix metalloproteinases, or MMP) are produced to dissolve the tissue in front of the sprouting vessel tip in order to accommodate it. As the vessel extends, the tissue is remolded around the vessel.
Sprouting endothelial cells roll up to form a blood vessel tube.
Individual blood vessel tubes connect to form blood vessel loops that can circulate blood.
Finally, newly formed blood vessel tubes are stabilized by specialized muscle cells (smooth muscle cells, pericytes) that provide structural support. Blood flow then begins.

3. Excessive angiogenesis:
Occurs in diseases such as cancer, diabetic blindness, age-related macular degeneration, rheumatoid arthritis, psoriasis, and more than 70 other conditions.
In these conditions, new blood vessels feed diseased tissues, destroy normal tissues, and in the case of cancer, the new vessels allow tumor cells to escape into the circulation and lodge in other organs (tumor metastases).
Excessive angiogenesis occurs when diseased cells produce abnormal amounts of angiogenic growth factors, overwhelming the effects of natural angiogenesis inhibitors.
Antiangiogenic therapies, aimed at halting new blood vessel growth, are used to treat these conditions.

4. Known Angiogenic Growth Factors

Fibroblast growth factors: acidic (aFGF) and basic (bFGF)
Granulocyte colony-stimulating factor (G-CSF)
Hepatocyte growth factor (HGF) /scatter factor (SF)
Interleukin-8 (IL-8)
Placental growth factor
Platelet-derived endothelial cell growth factor (PD-ECGF)
Platelet-derived growth factor-BB (PDGF-BB)
Pleiotrophin (PTN)
Transforming growth factor-alpha (TGF-alpha)
Transforming growth factor-beta (TGF-beta)
Tumor necrosis factor-alpha (TNF-alpha)
Vascular endothelial growth factor (VEGF)/vascular permeability factor (VPF)

5. Known Angiogenesis Inhibitors

Angiostatin (plasminogen fragment)
Antiangiogenic antithrombin III
Cartilage-derived inhibitor (CDI)
CD59 complement fragment
Endostatin (collagen XVIII fragment)
Fibronectin fragment
Fibronectin fragment (Anastellin)
Heparin hexasaccharide fragment
Human chorionic gonadotropin (hCG)
Interferon alpha/beta/gamma
Interferon inducible protein (IP-10)
Kringle 5 (plasminogen fragment)
Metalloproteinase inhibitors (TIMPs)
Pigment epithelium derived factor (PEDF)
Placental ribonuclease inhibitor
Plasminogen activator inhibitor
Platelet factor-4 (PF4)
Prolactin 16kD fragment
Proliferin-related protein (PRP)
Prothrombin kringle 2
Soluble Fms-like tyrosine kinase-1 (S-Flt-1)
Targeting fibronectin-binding integrins
Thrombospondin-1 (TSP-1) and -2
Transforming growth factor-beta (TGF-b)
Troponin I
Vasostatin (calreticulin fragment)

Visit the foundation’s website here

Take care
Allen Lai


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  2. Thank you Mr Lenny for your input. Allen Lai

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