Coexistence of P53 and KRAS mutations enhances ERK1/2 signaling by inducing EGR1 expression through mutp53 and c-JUN interaction.

Abstract excerpt

The ERK1/2 signaling pathway, one of the most frequently dysregulated oncogenic pathways, can be initiated by diverse mutations, including those in RAS, BRAF, and amplifications of ERBB2 (HER2). Co-occurrence of ERK1/2 hyperactivation and TP53 mutations is common in multiple cancer types and correlates with significantly poorer clinical outcomes. However, the direct mechanisms underlying the cooperation between...

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