Fighting cancer is so complicated that it rivals a major war in complexity. Cancer cells actually fight back when you try to treat them. For this reason, it is now recommended that you attack them with three different cancer treatments simultaneously, to overwhelm them.
Before cancer can begin, the bodies defenses have to be partially deactivated. Cancerous cells happen all the time and normally they are destroyed before becoming a problem. The cancer must be of a “successful” type or it will die. It must be able to divide yet produce other cancer cells that are both cancerous and functional.
Then, in a manner unique to cancer, it must actually stimulate the body to grow extra capillaries to feed it more than normal cells, as it consumes much more energy. And it must also defeat the “self-destruct” mechanism that cells have that prevents them from endlessly reproducing themselves instead of being replaced by stem cells.
Finally, it must change the chemical composition of its outer coat, to make itself slippery, so that cells can break off from each other, in metastasis, so they can travel through blood vessels to a new location where they can become a new tumor after changing back and adhering themselves to normal cells.
The complexity just keeps growing from there. And growing.
Findings from a 2005 study show that one of the procyanidins deactivates a number of proteins that likely work in concert to push cancer cells to continually divide. A research team from Georgetown University performed a variety of tests on breast cancer cells and four proteins that contribute to their division and growth. They discovered that after treating the cells with the procyanidin compound, all four proteins involved in the reproduction of the cancer cells were essentially “turned off” and the cancer cells stopped dividing. The lead researcher noted that the exciting aspect of their findings is that the procyanidin diactivated four separate regulatory proteins, greatly enhancing its inhibitory effect. Many anticaer agent only diplay a single inhibitory effect. The results were published in a 2005 issue of Molecular Cancer Therapeutics.