anti-angiogenesis inhibitors - auto-immune mechanisms

[Fictional]

I just wanted to add that there is some data that anti-angiogenesis inhibitors work by an auto-immune mechanism as well.

On the kidney cancers responsive to Sutent, many people would quick the drug if it seem to "stop working" - but now some clinicians are continuing the medication and seeing some late responses that may be immune-mediated. I think the idea is that the anti-angiogenesis inhibitors kill off cells gradually (decreasing 15-50% or whatever), but with each cycle that some cells are dying, there is an opportunity to stimulate the body's immune response to the cancer cells. That may be why some people had an initial plateau in response (out to a year), then sudden rapid tumor death on the same or lower doses of medication. There are some patients who had left Sutent, who are now returning to it.

I mention Sutent, because that is the one our daughter is on, but I would think a similar reaction could be had with other anti-angiogenesis inhibitors. We are on our second cycle, and we continue to see changes that suggest it has shrunk the tumor. We were also a little shocked by what seemed to be a florid rebound response on the 2 week break (redness, itching, little heat), but assume that some immune effect might be at work during the break.

The problem with the GVAX is that you eventually run out of cells and can't immunize anymore. But at least theoretically, anti-angiogenesis inhibitors might also be valuable for inhibiting the formation of new metastases - as vascular changes are among the earlies pathological findings in ASPS.

Also, when I last searched "pipeline" drugs for anti-angiogenesis inhibitors, a lot of things seemed to pop up. Some patients respond to one drug more than another. Thanks so much for posting, Paul.