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J Natl Compr Canc Netw. 2017 Sep;15(9):1085-1089. doi: 10.6004/jnccn.2017.0151.

EGFR Exon 19 Deletion in Pancreatic Adenocarcinoma Responds to Erlotinib, Followed by T790M-Mediated Resistance.

Author information

1
Department of Medicine, Section of Medical Oncology, Yale School of Medicine
2
Yale Cancer Center
3
Department of Pathology, Yale School of Medicine, New Haven, Connecticut

Abstract

The prognosis of metastatic pancreatic cancer remains poor despite recent advances in treatment with multidrug chemotherapy regimens. Use of immune checkpoint inhibitors and molecular targeted therapies has so far been disappointing. This report describes a patient with chemotherapy-refractory metastatic pancreatic ductal adenocarcinoma (PDAC) whose tumor was characterized by an activating mutation in exon 19 of the epidermal growth factor receptor (EGFR). He experienced response to erlotinib for 10 months, and then developed disease progression in association with emergence of the T790M mutation. Activating EGFR mutations in cancers other than lung are uncommon, but when present may predict response to EGFR tyrosine kinase inhibitors (TKIs). Development of the T790M mutation in this case suggests that EGFR-targeted TKIs may follow similar patterns of resistance regardless of tumor type. Although actionable mutations are detected infrequently in PDAC, this case illustrates the potential benefit of offering genomic analysis to all patients with advanced disease.

PMID:
28874593
DOI:
10.6004/jnccn.2017.0151
[Indexed for MEDLINE]

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