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In breast cancer, dysregulated ERK1/2 signaling is associated with changes in cell cycle dynamics, which contribute to the aggressive behavior of tumors

UA, similar to its parent compound ellagic acid, exhibits poor absorption following oral administration and undergoes rapid elimination due to extensive first-pass metabolism and limited enterohepatic recirculation 84-86

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The dependency on KRAS signaling varies across different KRAS mutant cancer types and could reflect the variability in the tumor response, representing a possible mechanism of intrinsic resistance (75, 99)