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After aberrantly dimerizing in response to mesenchymally expressed ligands, FGFR2c S252W and P253R mutants are assumed to undergo transautophosphorylation analagous to the wild-type receptor, although this has not been explicitly demonstrated. Knock-down or chemical inhibition of other FGFR2-activating mutations identified in endometrial cancer cells has been shown to cause cell death (Byron, 2008).
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