Mechanism Of Action
The chances of developing cancer increase as a person gets older because more time has been available for mutations to accumulate.
For example, a 75-year-old person is a hundred times more likely to develop colon cancer than a 25-year-old. Because people are living longer today than they did 50 or 100 years ago, they have a longer exposure time to factors that may promote gene changes linked to cancer.
In addition to all the molecular changes that occur within a cancer cell, the environment around the tumor changes dramatically as well. The cancer cell loses receptors that would normally respond to neighboring cells that call for growth to stop. Instead, tumors amplify their own supply of growth signals. They also flood their neighbors with other signals called cytokines and enzymes called proteases. This action destroys both the basement membrane and surrounding matrix, which lies between the tumor and its path to metastasis--a blood vessel or duct of the lymphatic system.
Proteases and cytokines as well as other receptor pathways have now become a target for scientists to develop drugs that prevent the growth of the tumors and stop the cancer in its tracks.
A model of how cancer can corrupt the surrounding environment in the body
Source: National Cancer Institute Copyright ©, 2004.
Although the mechanism by which proteolytic proenzymess exert an anticancer effect is not fully known, there is evidence showing that proteolytic proenzymess are activated at the tumor site and tumor cell surface and that these in turn activate Protease Activated Receptors Type 2 (PAR2).
Activation of PAR2 results in a cascade of intracellular activities, including activation of a major component of the cell which controls its structure and architecture, the actin cytoskeleton.
In a cancer cell, proteolytic proenzymess have the effect of converting globular actin into tight filamentous actin, which causes the cancer cell structure to collapse and induce cell death. This reduces tumor volume and is often noticed in clinical practice.
Other mechanisms are thought to also contribute to the anticancer effects of proteolytic proenzymess, including inactivation of growth factors which can often contribute to cancer cell growth. Inactivation of growth factors is one of the mechanisms of action by which other anti-cancer drugs work, eg. Avastin™ which blocks a growth factor called vascular endothelial growth factor, or VEGF, and inhibits the growth of blood vessels at the site of the tumor. Data has been generated showing PRP also inhibits the growth of blood vessels. Although the mechanism by which this is achieved is not fully known, scientific data published by Desser et al in 2001 has shown oral therapy with proteolytic enzymes decreases excessive TGF-beta (tumor growth factor) levels in human blood.
Additional effects which have been observed include triggering cell necrosis (cell death), induction of apoptosis (programmed cell death), the induction of cell differentiation (i.e. inducing cancer cells to exhibit more normal cell behavior), the inhibition of angiogenesis (preventing new blood vessel formation) in tumors, and anti-metastases (prevention of tumor spreading) by increasing adhesion between tumor cells.
Bibliography
Desser L., Holomanova D., Zavadova E., Pavelka K., Mohr T., Herbacek I., Oral therapy with proteolytic enzymes decreases excessive TGF-beta levels in human blood, Cancer Chemother Pharmacol. 2001; 47 (suppl.):S10 – S15, Kleinsmith L.J., Kerrigan D., Kelly J., Hollen B., Understanding Cancer, National Cancer Institute, Copyright ©2004.