EGFR/KRAS

In pancreatic adenocarcinoma, the EGFR/KRAS pathway is commonly mutated and is a promising area of focus for targeted treatment. A targeted drug needs to target mutations in the EGFR/KRAS pathway without halting it completely since the complete inactivation of KRAS would prevent cell proliferation in the pancreas. It would be detrimental to completely halt cell growth and division. A microRNA that would target the point mutation in codon 12 of the KRAS oncogene in PanINs could be useful in serving as a targeted treatment. This would bind to only the mutated mRNAs and halt expression by either blocking translation or destroying them.