This is our fourth and final instalment from the American Association for Cancer Research (AACR) meeting in Washington D.C.
A recurring challenge in cancer research is that patients can quickly develop resistance to treatments that the underlying science predicts should work. Laboratory experiments often show that blocking target X in cancer Y should kill the cancer cells and spare normal cells.
But when a drug is developed to inhibit the target and tested in clinical trials, the survival benefit is sometimes relatively modest.
There are certainly exceptions. A drug called vismodegib, designed to disrupt the curious sounding “Hedgehog” signalling pathway showed very good results in basal cell carcinoma – the most common and less serious type of skin cancer – and was approved last year.
But other drugs tend to benefit only a subset of patients with a particular cancer, and even those patients go on to become resistant to the drug.
Conceptually, there are two key routes to drug resistance – innate (or “intrinsic”) and acquired resistance.
Innate resistance is down to the tumour having a mixed population of cells (as discussed yesterday) – some which are sensitive to the drug and some which aren’t. Hence upon treatment, those cells that are inherently unresponsive to the drug continue to grow.
Conversely, acquired resistance involves the tumour cells evolving (through additional genetic mutations etc) to adopt alternative pathways to fuel their growth.
As such, there is a lot of research being carried out to rationally design combinations of existing drugs that can both overcome innate resistance and pre-emptively tackle acquired resistance.
A stock take of where we are in our fight with cancer painted a very encouraging picture. There are many hundreds of clinical trials ongoing worldwide investigating a variety of cancer drugs and combinations. Last year there was a bumper crop of 13 new anticancer drugs approved – the highest number per year since 1996.
The general feeling at the conference seems to be that soon we will have sufficient targeted drugs available to allow us to carry out the ‘mix and match’ trials we need to really benefit patients. These are exciting times.
This is my last blog from this conference. I hope you enjoyed reading my musings as much as I enjoyed writing them. This and the previous blogs have been my personal thoughts and experiences – and hence apologies for any inaccuracies that I may have inadvertently conveyed.
Good bye from Washington and Y’all have a great day.
Raj Mehta is a business development executive at Cancer Research Technology