Pancreatic Adenocarcinoma with Co-Occurrence of <i>KRAS</i> and <i>EGFR</i> Mutations: Case Report and Literature Review

Abstract

<b><i>Introduction:</i></b> Mutation in <i>Kristin ras sarcoma virus (KRAS)</i> oncogene is the main driver in pancreatic ductal adenocarcinoma (PDAC) and is present in nearly 90% of patients with PDAC. <i>Epidermal growth factor receptor</i> (<i>EGFR</i>) mutation is rare in PDAC and is mostly present in the absence of <i>KRAS</i> mutation. Co-occurrence of <i>KRAS</i> and <i>EGFR</i> mutations is extremely rare, and the value of EGFR inhibition in these cases is unknown. <b><i>Case Presentation:</i></b> Here, we present a case of metastatic PDAC with co-occurrence of <i>KRAS</i> G12V and <i>EGFR</i> L730R. Despite primary resistance to folinic acid, fluorouracil, irinotecan, oxaliplatin, and gemcitabine/nab-paclitaxel, this patient had a biochemical response (decrease in carbohydrate antigen 19-9) and disease control of 7 months on gemcitabine/erlotinib (an EGFR inhibitor). This outcome is remarkable in the late-line PDAC treatment setting and is unusual after the progression of the tumor on gemcitabine/nab-paclitaxel chemotherapy. <b><i>Conclusion:</i></b> This case suggests that gemcitabine/erlotinib could be an effective treatment in patients with PDAC and co-occurrence of <i>EGFR</i> and <i>KRAS</i> mutations.