[julierene]

I think it's just the theory that Herceptin and Tykerb block all the receptors, the immune system kills off all those cells, then you are left with whatever is left. They theorize that at microscopic levels, you can have many different types of cells, some having less receptors than others. Once you have effectively cleared out all the cancer with receptors, you can end up with cells that have different receptors. As receptors change to evade the immune system, so does the nature of the cancer. It's like the part of the cellular structure that works against people who have cancer. In normal healthy cells, this process is survival. But the natural programmed cellular structure, is now cancerous, and working against what we want. That's why Tykerb works when Herceptin fails. It's a new way to target when the receptors on the outside of the cell seem to not respond to Herceptin anymore. Then when Tykerb clears out the receptors that are on the inside, then there are cells left that don't respond to either... At that point, you start running out of targeted therapies. Avastin is a monoclonal antibody against vascular endothelial growth factor-A (VEGF-A).[1] It is used to inhibit tumor growth by blocking the formation of new blood vessels (angiogenesis). Since HER2 disease has shown trend to being very vascular, this makes sense. P53 targeted therapy also makes a lot of sense. But figuring out whichever direction you go after Tykerb and Herceptin fail, is a mystery to me.