by Dr. med. Franjo Grotenhermen http://dr-grotenhermen.de/
In the past 20 years, many cellular and animal studies have been conducted to investigate which cannabinoids in which cancers are effective and could fight as cannabinoids cancer. Cannabinoids inhibit cancer growth at different levels. These include the inhibition of cancer growth through apoptosis, the suicide program of the cells, the inhibition of cancer cell proliferation, inhibition of blood vessel formation, inhibition of metastasis and the strengthening of the immune system against cancer cells.
Causation of cancer cell death and reducing cancer growth
In 2000, a research group was able to demonstrate at the Complutense University in Madrid that THC apoptosis in glioblastoma cells, very aggressive brain cancer cells caused. This was later proved to other cancers. Moreover, cannabinoids can also inhibit the growth of cancer cells in certain cancers such as melanoma, breast cancer and prostate cancer in addition to the induction of apoptosis. Remarkably, cannabinoids do not affect the viability of normal, non-transformed cells.
Interestingly, CBD that binds only weakly to cannabinoid receptors, and other cannabinoids promotes apoptosis in cancer cells. This effect is independent of CB1 and CB2 receptors. The mechanisms caused by the CBD, this effect is not yet fully understood.
Inhibition of blood vessel formation
The formation of blood vessels is critical to the growth of tumors beyond a size of 1 to 2 mm. In cancer cells, cannabinoids block the formation of new blood vessels in which they inhibit a specific growth factor (vascular endothelial growth factor). This and other mechanisms cause the vessel formation in tumors normalized. It will then be smaller and less blood vessels produced. Besides THC and CBD, a number of synthetic cannabinoids inhibit the formation of blood vessels in animal experiments with various types of cancer.
Inhibition of metastasis
The activation of CB1 or CB2 receptor agonists (or both) also reduces the formation of secondary tumors (metastases) in animal models. This includes support for the migration ability (migration) of cancer cells, their ability to attach to other tissues (adhesion) and their ability to penetrate tissue (invasion), inhibited. This has been demonstrated for glioblastoma cells, breast, lung, and cervical cancer cells in cultures.
in various animal models of cancer also CBD, which acts independently of CB1 and CB2 receptors, has the ability to inhibit metastasis. An important role in metastasis plays the inhibition of DNA binding, so-called Ids. In one study, incubation of breast cancer cells to CBD led to a reduction of Id-1, which inhibited their invasiveness.
Regulation of anti-tumor immunity
The activation of cannabinoid receptors may lead to changes in the immune system to fight cancer. These changes are called especially the increased production of anti-inflammatory messenger substances (cytokines) in the immune system and the increased formation of regulatory T cells, and suppressor T cells. Regulatory T cells are important for the suppression of unwanted immune processes. They therefore protect against autoimmune diseases and may otherwise be used by tumor cells to escape attacks the immune system. Therefore, there are reports of tumor formation was promoted by the activation of CB2 receptors in which the tumor monitoring has been impaired by the immune system.
On the other hand cannabinoids can also improve the tumor surveillance by the immune system under certain conditions. Thus, the antitumor effect of cannabinoids through the activation of CB2 receptors against melanoma in mice with normal immune systems in a study for example, was stronger than in mice with suppressed immune systems. So cannabinoids can be successfully used against cancer, the tumor-inhibiting effects must be stronger than the immune-suppressive and tumor growth potentially promoting effects.
Detailed information: New Book by Dr. Grotenhermen. Cannabis against cancer: The state of science and practical implications for therapy. Release Date: July 1, 2017th