The American Association for Cancer Research's annual conference took place a couple of weeks ago in Washington, DC, and one particular presentation really stood out.
It's available online -- audio and a slideshow -- and it's called "Targeting CD47 with Blocking Monoclonal Antibodies in Human Hematologic Malignancies," by Ravindra Majeti of Stanford University. It's pretty heavy in terms of its science, but I can give you a quick summary.
As you know from reading the blog, much of the reserch being done on NHL is focused on Monoclonal Antibodies like Rituxan. These antibodies target specific proteins that are typically found on lymphoma cells; Rituxan targets one called CD20.
The researchers in this presentation are focused on a protein called CD47. They believe CD47 is significant because it sends a "Don't Eat Me!" signal (as they put it in the presentation) to immne system. In other words, cancer cells can develop into tumors because they can somehow fool the body into thinking they are not harmful. the researchers have found that CD47 may be the protein responsible for sending that signal when it binds with something else.
These researchers have developed a monoclonal antibody that targets CD47. Wipe out that signal, and it tells the immune system that these cells are harmful, and that they should be destroyed (in a process called "phagocytosis," which they mention a lot in the presentation, just in case you were planning on listening).
In one experiment, they combined the anti-CD47 antibody with Rituxan, and found that the combination was pretty potent, since it acts on lymphoma cells in two different ways.
The research has so far only involved mice, but it looks pretty good: 8 of the 9 mice were actually cured by the 20/47 combination. Nice numbers.
It makes sense: Rituxan + chemotherapy is effective because it targets cancer cells in two different ways. Add a third way, through RadioImmunoTherapy, and the numbers get even better. The research here seems to suggest that the anti-CD20/anti-CD47 combo can potentially cure NHL with minimal toxicity, targeting only lymphoma cells and leaving healthy cells alone.
I've been wondering for a while how all of these various monoclonal antobodies were going to be used. This seems like maybe the start of some of that research, combining them in ways that will make them more effective than they are by themselves.
Or maybe it's not the start, but the happy end?
Tuesday, May 11, 2010
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