Tackling intractable targets and tumour escape/evasion

Understanding clonal evolution ought to be an essential part of figuring out how to tackle intractable or tricky targets such as KRAS.

Inevitably chronic treatment with monotherapy will exert selective pressure on a given tumour so it reacts by escaping and signalling elsewhere in order to ensure its continued survival.

If we add in another agent, it may work for a while and then the same thing happens again.

What if we could break out of this cycle and try some novel approaches, find more potent agents, or even rational combinations to try and box in the resistance?

In our third ASCO Preview we take a look at some of the progress being made and where things might be headed in the near to medium term future…

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