An interesting piece of work came to my attention earlier this week that I think is worth sharing for a number of reasons. Firstly, I think it illustrates a way of working that really should be encouraged - it has significance beyond the specific interventions mentioned. Secondly, I think there are lessons here for those who are interested in anti-cancer agents not patented by the drug companies (such as curcumin, quercetin, resveratrol etc). Finally, it has interest for those suffering from glioblastoma (GBM) - a form of brain cancer that is particularly aggressive and hard to treat.
The work in question looked specifically at the phenomenon of immune suppression in GBM patients, and let's note at the outset that immune suppression is a problem for all cancer patients, not just those with GBM. Brain cancer patients - not just those with GBM - at the University of Colorado Hospital had blood taken and analysed, along with blood from non-cancer patients. Analysis revealed that the blood from GBM patients in particular showed lower levels of T-cell proliferation and released lower levels of interferon-gamma compared to normal blood samples - in other words they had lower levels of immune function. The specific forms of this immune suppression were worked out in a series of lab experiments that ultimately showed that one of the factors associated with this suppression was a high level of the enzyme Arginase I (ArgI). This enzyme consumes the amino acid Arginine, which is essential for T-cell activation.
So far so good - it's interesting, in an academic way, but so what? The experimenters then took the next step and looked at chemically blocking ArgI with a specific drug. Doing this improved the immune response in the test tube. Levels of interferon-gamma rose to normal levels. The next step, however, is where it gets really interesting from a patient point of view. Rather than blocking ArgI with a drug, the team looked at increasing levels of Arginine (which is what ArgI consumes). By adding more Arginine the immune response improved. In simple terms the ArgI was basically using up the circulating Arginine and thus starving the T-cells of it, but by increasing the amount of Arginine the researchers showed that they could 'feed' the ArgI and have enough left over to be used by the T-cells, which could become activated as normal.