Tomorrow's issue of Nature discusses the next steps in cancer research (subscription required for the full text):

A tumour cell is a genetic disaster area littered with mutations that differ not only from one type of cancer to the next, but from one patient to the next.... ...[which makes] new targeted drug therapies for cancer seem hopeless. And yet, the reality may be just the opposite. The richness of the data becoming available in these and other studies allows researchers to cut through the complexity. Genes work together in pathways of reactions to accomplish a particular biological function, such as cell division — and many or most of the mutated genes picked up by these cancer studies are involved in a comparatively small number of pathways. The Johns Hopkins team found that most of the mutations in their pancreatic tumours affected just 12 pathways. The Genome Atlas team found that most of its glioblastomas showed mutations in a set of three pathways. So drugs targeting these pathways might work in more patients than drugs that target only one of a pathway's myriad gene components.

This is somewhat along the lines of what I wrote yesterday:

This means that an effective drug treatment for many cancers will have to be based on a mixed strategy, such a drug regimen targeting not just one protein, but a combination of molecular players. Strategies like this can only be rationally designed when we actually understand how those molecular players work together. Basic researchers have been making steady progress towards that goal, but as I noted above, it is only within the last few years that genomics and computational biology have made such an understanding possible.

We're not losing the "War on Cancer," and some of the most effective cures are going to come out of the kind of detailed basic research that Nature is talking about.