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Drug resistance can arise through a number of mechanisms. For instance, EGFR mutation when treating with EGFR inhibitors, or compensatory activation of alternative survival pathways. But does it occur at the level of a single cell, or would it be a population effect? In other words, would cells exposed to e.g. targeted kinase inhibitors slowly compensate with other pathways (and that would happen in every such cell) or would there be a sub-population of cells that is sensitive to inhibitors and another subpopulation inherently resistant and predisposed towards amplifying other pathways.

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There certainly can be co-operation or competition among cancer cells within a tumor that can provide some types of population-based influences on cancer-cell survival. Present evidence, however, suggests that resistance to therapy is almost always due to resistant sub-populations of cancer cells within the tumor. In many cases, such as after treatment with EGFR inhibitors, the resistance mutations have been identified. Sometimes these mutations are in such a small fraction of the cancer cells that they can't be detected in the original tumor before treatment, but in most cases they probably were already present before therapy, caused by the mutations that are inevitable during tumor growth. This review on intra-tumor heterogeneity is a good place to start learning about this topic.

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