It’s a pathway that has got a lot of attention over the last few years; it’s the target of a drug called rapamycin. Rapamycin has been shown in many organisms, including mice, to prolong their lifespans so there’s a lot of excitement about how this molecule might work. I talked particularly about the role of this pathway in cancer. This is a pathway that normally senses nutrients, so glucose and amino acids, and tells a cell that it has sufficient nutrients to grow. In many cancers this pathway becomes activated aberrantly so the cancer cell thinks it always has nutrients so it no longer has a checkpoint elicited by nutrient deprivation. Increasingly we find this pathway again activated in cancer so there are many indications for using rapamycin to treat cancer. We’re starting to understand which cancers now are particularly sensitive to this compound.

Which diseases does this drug have the most promise with?

There are many, kidney cancer probably, though, is the best example and slowly we’re understanding what mutations predict sensitivity to rapamycin.

Yes, rapamycin is an mTOR inhibitor which we have known about for some time but why certain cancers respond better than others we haven’t known. We’ve tended to think of this pathway as essential in all cancers, so we would think that all cancers respond, but it’s turning out that there are some that are particularly sensitive and now we’re starting to see what mutations predict that. There are many clinical trials going on with rapamycin as well as analogues of rapamycin. Then there are newer versions of mTOR inhibitors that act through different mechanisms but that are also in clinical trials.

How does this tie in with personalised medicine?

It fits into the idea of simply knowing what mutations a cancer has and then picking the right drug to target the activities of those mutations’ cause. So it fits into that general theme.