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Peer-reviewedCC BY-NC-NDJournal of gastrointestinal oncology

Metastatic pulmonary ETV6::NTRK3 mucinous adenocarcinoma originating from an intraductal papillary mucinous neoplasm case report.

  • Nicholas P Giustini1,2
  • Eric Q Konnick3
  • Troy Hutchens3
  • Keith D Eaton1,2
  1. 1Clinical Research Division, Fred Hutchinson Cancer Center, Seattle, WA, USA.
  2. 2Division of Hematology & Oncology, Department of Medicine, University of Washington, Seattle, WA, USA.
  3. 3Department of Laboratory Medicine and Pathology, University of Washington, Seattle, WA, USA.
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Abstract

Mucinous neoplasms of the lung are difficult to differentiate from upper gastrointestinal neoplasms based on pathologic appearance and immunohistochemistry (IHC) alone. Both variably express cytokeratin 7 (CK7), cytokeratin 20 (CK20), and caudal type homeobox 2 (CDX2), while often lacking thyroid transcription factor 1 (TTF-1) and Napsin-A. This case presents a patient with a history of a resected pancreatic intraductal papillary mucinous neoplasm (IPMN) who was found to have a large mucinous neoplasm in the left lung seven years later. Following resection for presumed primary pulmonary invasive mucinous adenocarcinoma, new metastatic lung lesions developed. Comparative morphologic evaluation of the resected lung lesion and the IPMN noted similarities. Subsequent next-generation sequencing from both samples identified the same ETV6::NTRK3 fusion. The patient started systemic therapy with larotrectinib, which led to clinical improvement and resolution of all lung lesions with response ongoing at the time of publication. IPMNs are premalignant lesions with the potential to transform into invasive malignancies and subsequently metastasize. NTRK fusions, while rare, occur across the spectrum of epithelial neoplasms, including IPMNs. In this case thorough molecular testing of both the active pulmonary malignancy and the antecedent pancreatic premalignancy identified the likely etiology of the mucinous adenocarcinoma and allowed for treatment with effective oral therapy.

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Cite

BibTeXRIS
BibTeX
@article{giustini2026metastatic,
  title = {{Metastatic pulmonary ETV6::NTRK3 mucinous adenocarcinoma originating from an intraductal papillary mucinous neoplasm case report.}},
  author = {Nicholas P Giustini and Eric Q Konnick and Troy Hutchens and Keith D Eaton},
  journal = {Journal of gastrointestinal oncology},
  year = {2026},
  month = sep,
  doi = {10.21037/jgo-2026-0684},
  url = {https://europepmc.org/article/MED/42996621},
  note = {CC BY-NC-ND},
}
RIS
TY  - JOUR
TI  - Metastatic pulmonary ETV6::NTRK3 mucinous adenocarcinoma originating from an intraductal papillary mucinous neoplasm case report.
AU  - Nicholas P Giustini
AU  - Eric Q Konnick
AU  - Troy Hutchens
AU  - Keith D Eaton
PY  - 2026
DA  - 2026/09/28
JO  - Journal of gastrointestinal oncology
DO  - 10.21037/jgo-2026-0684
UR  - https://europepmc.org/article/MED/42996621
AB  - Mucinous neoplasms of the lung are difficult to differentiate from upper gastrointestinal neoplasms based on pathologic appearance and immunohistochemistry (IHC) alone. Both variably express cytokeratin 7 (CK7), cytokeratin 20 (CK20), and caudal type homeobox 2 (CDX2), while often lacking thyroid transcription factor 1 (TTF-1) and Napsin-A. This case presents a patient with a history of a resected pancreatic intraductal papillary mucinous neoplasm (IPMN) who was found to have a large mucinous neoplasm in the left lung seven years later. Following resection for presumed primary pulmonary invasive mucinous adenocarcinoma, new metastatic lung lesions developed. Comparative morphologic evaluation of the resected lung lesion and the IPMN noted similarities. Subsequent next-generation sequencing from both samples identified the same ETV6::NTRK3 fusion. The patient started systemic therapy with larotrectinib, which led to clinical improvement and resolution of all lung lesions with response ongoing at the time of publication. IPMNs are premalignant lesions with the potential to transform into invasive malignancies and subsequently metastasize. NTRK fusions, while rare, occur across the spectrum of epithelial neoplasms, including IPMNs. In this case thorough molecular testing of both the active pulmonary malignancy and the antecedent pancreatic premalignancy identified the likely etiology of the mucinous adenocarcinoma and allowed for treatment with effective oral therapy.
SN  - 2078-6891
SN  - 2219-679X
ER  -