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For example, mechanisms have been identified in which changes in cell state or lineage yield a substantial phenotypic change in a cancer cell such that it no longer exhibits its original oncogene dependencies (34). The first clinical evidence pointing to the role of such cell plasticity as a mechanism of resistance to targeted therapies came from non–small cell lung cancer transformation into small cell lung cancer upon treatment with EGFR kinase inhibitors (35). Similarly, some metastatic prostate cancers that progress on treatment with antiandrogen therapies appear to have undergone differentiation to a neuroendocrine phenotype that is no longer dependent on androgen signaling (36).
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