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CASE REPORT
Year : 2020  |  Volume : 16  |  Issue : 4  |  Page : 950-954

Epidermal growth factor receptor-activating mutation(E746_T751>VP) in pancreatic ductal adenocarcinoma responds to erlotinib, followed by epidermal growth factor receptor resistance-mediating mutation (A647T): A case report and literature review


1 Department of Oncologic Sciences, Mitchell Cancer Institute, The University of South Alabama, Mobile, Alabama, USA
2 College of Allied Health Professions, The University of South Alabama, Mobile, Alabama, USA
3 Division of Interventional Radiology, The University of South Alabama, Mobile, Alabama, USA
4 Medical Oncology, Mitchell Cancer Institute, The University of South Alabama, Mobile, Alabama, USA
5 Gynecology Oncology, Mitchell Cancer Institute, The University of South Alabama, Mobile, Alabama, USA
6 Medical Oncology, The James Comprehensive Cancer Center, The Ohio State University, Columbus, OH, USA

Correspondence Address:
Moh'd Khushman
Department of Medical Oncology, The University of South Alabama, Mitchell Cancer Institute, 1660 Spring Hill Ave, Mobile, AL 36694
USA
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/jcrt.JCRT_729_18

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Despite recent advances in treatment with multidrug chemotherapy regimens, outcomes of patients with advanced pancreatic ductal adenocarcinoma (PDAC) remain very poor. Treatment with targeted therapies has shown marginal benefits due to intrinsic or acquired resistance. Actionable mutations, while detected infrequently in patients with PDAC, are becoming increasingly used in personalized medicine. Here, we describe an epidermal growth factor receptor (EGFR)-activating mutation (E746_T751>VP) to erlotinib, a first-generation tyrosine kinase inhibitor (TKI), in a patient with metastatic PDAC. After an initial partial response to erlotinib for 12 months, the patient's disease progressed with emergence of the EGFR A647T mutation. Certainly, the patient also progressed after switching therapy to a third-generation EGFR TKI (osimertinib). This case illustrates the posttreatment evolution of EGFR A647T-mediated resistance to the first- and third-generation TKIs. To our knowledge, this is the first case to report the aforementioned activating and resistance-mediated mutations. In summary, genomic analysis performed in this patient with PDAC on the tumor biopsy and peripheral blood provided tools to understand mechanisms of response and resistance to targeted therapy with EFGR TKIs.


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